synaptic connections

🌼🌻study smarter🌻🌼

(here are some study tips straight from my psych notes)

1. interest: the brain prioritizes by meaning, value, and relevance so u remember things better if ur interested

  • find a study partner
  • do extra practice or research
  • teach it to someone else (this works so well!)

2. intent: be actively paying attention. very little learning actually takes place without attention

  • use a concentration check sheet (every time u get distracted, put a check on ur sheet. this is supposed to program ur mind to pay attention)
  • while u read, talk back to the author
  • ask questions during lectures (this is scary ik!! but do it!)

3. basic background: make connections to what u already know

  • preview and skim the material before u read it. or google it!
  • write out a list of vocab words before a lecture and leave some spaces between them to fill in during the lecture
  • read ahead of lectures
  • watch crashcourse tbh

4. selectivity: start by studying whats important

  • look for bolded words, graphics, pictures, chapter review questions in ur readings
  • listen for verbal clues like emphasis and repetition during lectures
  • make urself a study guide as u read and write down questions for urself to answer later as review (kinda like cornell notes)

5. meaningful organization: u can learn/rmr better if u group ideas into diff categories

  • apply vocab words to ur life
  • make flashcards and sort them (try not to have more than seven items in one category!)
  • use mnemonics

6. recitation: saying ideas aloud in ur own words strengthens synaptic connections! when u say something aloud u r forcing urself to pay attention

  • after u read, ask urself questions
  • talk abt what u learned w/ classmates outside of class
  • again, teach someone else

7. visualization: ur brain’s quickest and longest-lasting response is to images

  • convert info into a chart or graph
  • draw it out
  • make a mental video of a process
  • look at picture/video examples

8. association: memory is increased when facts are consciously associated w something u already know. memory = making neural connections

  • ask urself: is this something i already know?

9. consolidation: give ur brain some time to establish a neural pathway

  • make a list of what u remember from class
  • review notes at the end of the day, every day
  • stop after reading each prg to write a question in ur notes
  • make ur own practice quiz

10. distributed practice: we all know cramming doesnt work but we do it anyway! but yeah short and frequent study sections work better

  • make a daily/weekly study schedule
  • create a time budget/time tracker (track everything ur doing for a week and see how u can be more efficient w/ the time u waste)
  • divide the reading/vocab by the number of days before an exam and do a little bit each day (u can use sticky notes to divide ur reading)

other tips:

  • stop stressing! this sounds stupid and it isnt going to be easy, but anxiety causes u to lose focus. try ur best to think positively. sleep a lot. minimize ur caffeine intake. take a walk maybe
  • when u need to remember something, look upward or close ur eyes (when ur eyes are open ur using visual parts of ur brain that u might not need to be using)
  • find a rival! (like the person right above u in class rank) secretly compete w/ them (envy can improve mental persistence bc it makes u focus more intensely) but dont overdo it! 
  • walking and sleeping build memory storage in ur brain
  • eat flavonoids! (grapes, berries, tea leaves, cocoa beans make neurons in the brain more capable of forming new memories + increase blood flow to the brain)
  • obstacles force ur brain to try harder, so space learning lessons apart or create a puzzle to solve or change ur physical setting
Reasons why self dx is good from the pov of a professional
  1. Therapists/Specialists are not omnipotent. There are a lot of different mental disorders and disabilities that you could literally study for five years and still don’t know everything about. If you don’t know enough about a condition to see its signs in a person (which many therapists actually don’t because the only thing they really know about illnesses that are less common are the DSM/ICD criteria for it. However, these criteria are not enough for a diagnosis and sometimes even too vague to pick up the signs for an illness in a person. I honestly don’t want to know how many people are misdiagnosed with a common mental condition but actually have a rare one that’s just pretty similar to the common one) than you gonna miss a lot as a therapist. And many therapist do miss a lot.
  2. Therapists are biased. Therapists are only people. Just like normal people, they are not immune against stereotypes and prejudices. Because specialists hardly ever teach you at uni but only in special courses that you have to take in order to specialize as well, we actually learn a lot of stereotypes and prejudices because the people teaching us interpret the information they have in a wrong way because they don’t know more about it. A person who is currently studying to become a therapist needs to be aware of that and do their own research in order to get useful information, however most aren’t even aware of how wrong the things that they’re learning are because they have, like everyone else, the bias to trust people like professors that they actually know a 100% what they’re talking about (even though many actually ADMIT that they don’t know anything about it). This is another bias that’s pretty common in people, widely researched and again not something therapists and specialists are immune to.
    If you, for example, know that autism isn’t common in girls, then you won’t look for it  in girls and are likely to oversee the signs because you think that autism is too rare in girls. And additionally, to recognize autism in girls, a specialist needs to be aware that the symptoms show differently in afab and amab people which again, many “specialists” don’t because that’s not taught in class. You need to teach things like that to yourself or actually specialize on the condition.
  3. Literally every disorder that is known today is still being researched. And probably will not even exist like this in a few years anymore because the research might show that some symptoms are more important than those on the DSM V/ICD 10 that we have right now or they’ll maybe even find out that something that they diagnosed as one condition is actually two conditions (for example, for decades schizoid personality disorder was diagnosed as autism because both conditions create similar symptoms in many points. However, research showed that they differ in very important points and are actually two different conditions. I don’t even want to know how many people were misdiagnosed and mistreated because of that.)
  4. Therapists only have a limited view on their clients. They can’t look inside your head, they can only try to form an image of them by doing a metaphorical puzzle - they  have to look for the small things, the signs and symptoms and put the together in a way that actually makes sense and matches the symptoms of a disorder. If you don’t tell them everything - which you won’t (frankly because you don’t even remember everything when talking to your therapist or because you view some information as useless and don’t give it to your therapist that would actually be vital for the right diagnosis), - you can be sure that there will always be holes in your diagnosis. There will always be something that your therapist won’t take into account. That doesn’t mean that every diagnosis by a professional is wrong, therapists are often right. However, you know yourself better than anyone else. If you realize that you do/feel something that your therapist oversaw, than you are probably right and it might be worth digging into (even though I would advice talking about it with your therapist or someone else who knows you well enough to form an oppinion about it).
  5. Not everyone has access to a mental health specialist. (I should repeat this thirty times so that everyone gets it). Depending on where you life, you might not have enough money to afford a therapy. You might loose your complete health insurance or some of it if you go to a therapist more than three times, even if you’re not diagnosed with a condition (it’s like that in my homecountry). Getting diagnosed or attending a therapist literally makes it easier for people to instutionalize you against your will because speaking up against it gets interpreted as a person “not having insight in their own condition" by neurotypicals (even though they might have last beeen in treatment a deade ago… They don’t care, they say that the said person is insane because they say that they need treatment and when they deny it, it just prooves their point) [you would not believe how many therapists I already met who actually think like this].
    Our society is still hugely biased against mentally ill people. Getting a diagnosis can be expensive or impossible for other reasons. Not in every country you can attend a therapist without getting an official diagnosis (some people might do “off record”-diagnoisis, meaning that they confirm that you have a certain condition but don’t give you a diagnostic paper because they know how this can affect you. However, this highly depends on how the therapist is paid - if they only receive payment for diagnosed conditions, then they have no choice but diagnose you).
  6. Self-dx can be just as accurate and good as professional dx. There are a lot of free ressources all around the internet, libraries and so on that are actually written for professionals. Reading and applying these things is what maks a professional a professional. It’s exactly how you turn into a professional - your professors hand you the ressources, the rest is your own job. It doesn’t make much of a difference if you read all the books that you need for yourself or if you attend courses at college/university. The only difference is that professionals know a lot about other areas of human behavior and thus are better at evaluating how strongly it differs from normal behavior and in which points a person exactly differs. That doesn’t really have a big impact on the diagnostic process though, it’s just important for a general understanding of this weird species we call homo sapiens. If you feel better about it, you can read those ressources, too, but I wouldn’t deem it nesscessary.
  7. Self-dx actually helps improvement. If a person is not able to consult a specialist, it doesn’t really do any good for them to sit around and wait until they have the oportunity to do so (if that ever happens, which is again not the case for everyone). Because mental illnesses/conditions are just like physical ones - if you don’t treat them, they get worse and worse and worse. Mental health issues lead to different neurons firing in the brain, strengthening different synaptic patterns and thus patterns of thinking and behaving. The longer a person uses their synaptic connections, the more intense they become while others that aren’t use weaken. Not intervening means not stopping this process. And depending on how long a person has been following some of those patterns, they might take twice the time to “rewire” themselves or might even be unable to do so ever.
    It is important to treat mental illnesses as soon as possible in order to prevent further damage. Being against self-dx is being against people who don’t have a possibility to get help helping themselves which is frankly the only thing that might save them or give them the chance to live their life how they want to. Knowing about what illness you have is important in order to know how to cope with what. Sometimes it’s even essential to know what you need to cope with in the first place (e.g. my autism diagnosis… I was born autistic and didn’t know that I was autistic. The first thing I had to learn is what exactly makes me different from other people which I couldn’t know because I didn’t even know that I was different. I didn’t know what exactly made me feel bad, what stressed me out, and so on. But finally having a diagnosis, finally knowing what I’m dealing with helped me improve my life a whole damn lot.) 
  8. Self-dx is not a short process. I’ve always known that I wasn’t neurotypical, that’s for sure. However, it took me years to finally figure out which conditions I actually have and which are just results of other conditions I had. In order to do that, I needed to research everything that was somehow related to anything that I could be affected by. Self-dx takes time and extensive screening of information because, guess what, mis-self-diagnosing is just as unhelpful as professional mis-diagnosing. Only that it’s much easier to figure out if you’ve wrongly misdiagnosed yourself and went about it the wrong way than actually getting a specialist to admit that they misdiagnosed you (because therapists actually like to forget that they’re not omnipotent themselves).
  9. No one actually thinks that self-dx should replace professional-dx. Nobody actually wants to deny that professional diagnosis are valid by self-dxing. They don’t want to make fun of a disorder or “try to be edgy by having a mental condition”. Just like od-people don’t have the condition to be cool or edgy. The only difference is that od-people have a sheeet of paper that a human signed and that is saying “you have this disorder, congratulations, here is why I know”.
  10. Neurodivergent people actually know that they are neurodivergent! Everyone who has been diagnosed with anything later in life that they actually had since they were little should understand that not the diagnosis makes you have a condition but that actually having a condition gets you your diagnosis. Everyone remembers signs and symptoms they showed prior to their diagnosis. And it’s the same for self-dx people. Only because they didn’t have the chance to get a professional to check their claim, it doesn’t mean that they never noticed that they are mentally ill or in which ways they are. Neurodivergent people are not dumb. They actually know that they’re not neurotypical. So of course they start to look for an explanation, for a label in order to understand what they’re dealing with! And who are you to decide if the label they picked is right or wrong? You don’t know them. And even if it’s wrong… than they will definitely notice and not stick with it becaue “this condition is so much cooler than the one I actually have omg like autism is far more edgy than bpd”. Nobody who seriously self-diagnosed would say anything like that because that’s not the resaon you put so much effort in your self-diagnosis!! It’s because you want to know what’s going on with you and how to cope with it.
    (Being against self dx is actually further pushing the narrative that neurodivergent people don’t know that they aren’t neurotypical which is frankly such a harmful and toxic rethoric that is used against everyone who says that they’re mentally ill [because how bad can it be if you notice, right?] and those who have made enough progress that they wouldn’t consider themselves ill anymore [e.g. instutionalization, as mentioned above]. What is even worse about the rethoric is that in order to get diagnosed [and to diagnose yourself], you have to actually notice how the condition influences your quality of life. If it doesn’t have any impact on that, then you aren’t considered mentally ill. You probably all see now how this is actually the opposite of the rethoric that many people still push and believe in)


Honestly, I could probably continue this list forever, but I’ll stop now. If you feel like you have anything to add, just do it! It’s important to speak out for our self dx friends.

Pulse | Prologue

Medical Jargon \ Medical Inaccuracies \ Blood \ Angst \ Smut \ Fluff \ Medical Doctors \ Pneumothorax \ Taehyung \ All of BTS \ Swearing \ NSFW 

Typically felt at an artery, such as in the neck and wrist, the rhythmical throbbing of the arteries, caused by the successive contractions of the heart, are subject to environmental and behavioural stimulus and response, such as panic, love and nostalgia of the aforementioned. You fell in love with Kim Taehyung in medical school and believed you’d never see him again when you specialised. How wrong you were. ❞

⌬  Chapter Index

We are composed of 270 bones at birth that make up our human skeleton. Over time our bones fuse together, decreasing in quantity to 206. Most of these bones are in our hands and our feet: 26 in each foot and 27 in each hand.

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Be Still, Wanderer: A Story of Love, Loss, & Science


The human brain weighs as much as six human hearts. But sometimes the heart feels so heavy there might as well be no brain at all. Looking at a picture of her—the person who, for the past five years, I’ve variously known as Pooh Bear, Starmate, My Love, and Freckles—I use my finger to trace the outline of her face. Our past life together flickers in my thoughts. Tears and laughter and pain and joy, I see it all playing out in my brain, I feel it all in my heart. Things are over between us now, our relationship ending right along with our twenties. Good things must come to end, that’s what a refrigerator magnet told me once. Why should my relationship be any exception? It’s all for the better, I tell myself. But I don’t believe it. Instead, I just feel frozen. I stare at her picture, the room motionless, my memories alive. The freeze is interrupted only by my heartbeat. Someone tapping from inside, awakening me, reminding me I’m not dead, pounding out the old Plathian brag: ‘I am, I am, I am.’ The room is still, apparently serene—but here’s my heart pattering away, indifferent to the stillness of its surroundings. 

My mind feels overwhelmed with thoughts of loss. I want to think about something else—anything else. I decide to think about my thoughts. I have thoughts. Here they are, there they go, zipping around inside me. Here, like every other human, I have this three-pound mass of wrinkly, electrified meat trapped inside my skull, and it is busy. Busy sending signals throughout my nervous system—more signals than all the phones in the world combined—busy serving as the organic epicenter of my thoughts and actions, busy making me. My thoughts, the result of innumerable neurons and more synaptic connections than stars in the universe, coming together to create a self, an identity. I want to reach inside and pluck out one of these mysterious thoughts, but they are too elusive. The entire brain—no, the whole damn system— is at work, the brain just a bulbous gob situated at the top of a spinal cord that stretches and connects through all of me. I have a nerve—the vagus nerve—coupled to my hindbrain that snakes its way through my heart, lungs, and gut, never taking a break from its role as bodily regulator. ‘Vagus’ is Latin for 'wanderer’, and it’s largely thanks to this wandering nerve and its detours through my digestive tract that I felt butterflies in my stomach as I fell in love, and that I felt aches in my stomach as I fell out of love. 

And it’s not just the tortuous nerves and blood vessels that are hard at work. Here, like every other human, I have within me an entire ecosystem of living creatures. There are more bacterial cells in my body than human cells, which means I am more alien than me. My gut alone acts as the home for enough bacteria that if each one were a human being they could populate 15,000 planet Earths. Flowering flora alive and wriggling and eating and farting and breathing, none of them able to exist without me, and me unable to exist without them. Most are helpers, some enemies, generations living out their lives within me, subsisting on my existence. I am the God of a microbial cosmos. So much life and motion inside, and so much motion inside of that motion. All of them, all of me, and all that’s around me, everything that makes up this frozen tableau, is at its most basic level utterly dynamic. The subatomic scaffolding of these stolid and solid walls, if we could look close enough, would be jittering and jiggling and racing, particles with all sorts of exotic names—bosons, gluons, charm quarks, and muons—popping in and out of actuality, moving at incredible and erratic speeds, blurry and vibrant and empty, abstract entities not even existing in the way we like things to exist, but as probabilities, as potential thing-like things, ghostly and ever-moving, never stopping, forever in an ethereal dance that is, starting now, called the quantum shuffle.

All this invisible motion around me, I decide I need to move as well. 

I stand. 

Everything still seems so still. 

I take a deep breath. 

My feet are firmly planted, but the ground underneath—not so much. 

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3. How to study effectively!

Studying should be enjoyable because it only takes you closer to your goals and isn’t that fun? :D Once you think it’s fun, it will no longer feel like a burden.

These are some tips that works for me, but you should always stick to what works for you.

1. Enjoy.

By studying, you are becoming smarter. Therefore, it is making you a better person so you are more equipped to contribute to society! I mean who doesn’t like to be knowledgeable? For me, I feel like I am putting my life into good use when I learn new topics. I also feel very accomplished when I get good grades because it shows myself that I can be awesome just by investing time. The feeling of accomplishment is extremely enjoyable!!

The purpose of studying is to learn and become better at the subject. If you make it your priority to learn, then good grades will come with it.

For me, studying can be really fun because I like to use colorful pens to make my notes look appealing to my eyes. I also find drawing diagrams/writing with pens super enjoyable because everything comes out so neat.

2. Eliminate.

I take sample tests and pay attention to the topics that I missed and only study those. I also write down things that I missed/not comfortable with on a piece of paper and look at that everyday, rather than the whole textbook. By eliminating all the information that you already know, it makes the content a lot more approachable because everything is more concise. After narrowing down the content that you must study, you can also dedicate most of your time to the topics you struggle with.

Always start with the big picture, then go into the details. I always go over chapter summaries first before reading the actual chapter.

3. Reward yourself.

Rewards motivate people to work because they offer a sense of accomplishment. Rewards can be anything that makes you happy. My parents used to reward me with money when I get good grades, but I don’t ask for that anymore because I feel that it is unnecessary. For me, the reward of getting good grades is self accomplishment and nothing beats being happy with myself. I feel like money doesn’t make me as happy as the feeling self pride in the form of an accomplishment. I also like to reward myself daily with drawing/internet time when I know that I have worked hard that day.

Something I look forward to every day is dinner with my books. I know that this is not the most I guess socially acceptable thing to do, but it’s what really motivates me to do something that satisfies me more. For example, I’ll read and take notes of one paragraph, take a bite, read and take notes of another paragraph, and take another bite. This is why it can take me hours to finish a meal but it works for me.

4. Take breaks/Break it up

If you don’t take breaks in anything you do, you are going to experience a burnout and feel unwilling to work for a long time. Therefore, taking breaks are ultimately more productive than working through the whole thing in one go.

Because I know that I am the type of person who can not physically be still for a very long time, I get up every 30-45 mins to walk around when I study. On weekends, when I have the whole day, I will always alternate between tasks. For example, I’ll study for 45 mins, wash the dishes, study for 45 mins, and mop the floor. Therefore, I am getting multiple tasks done at the same time, leaving me feeling awesome at the end of the day. Constantly switching between tasks enables me to begin each task with a recharged brain, which also increases the quality of my work.

4. Use your resources.

But be careful of distractions. The internet is a wonderful sea of answers but you are just one click away from a black hole. For me, I usually have a clear objective of what I want to accomplish during a certain time which enables me to stay focused. But I know that distractions can be a major issue for a lot of people. There are some websites that can block social media from your computer, or you can study with a friend/parents around so you have people around you that can keep you in check.

My phone is my best friend and I can not lie. I love my phone so much because it enables me to take any information that I need anywhere I go which enables me to be productive everywhere I go and productivity is my favorite thing. I’m always taking pictures of textbook pages so I can work on homework anywhere, without having to wait till I get home so I can do something more fun instead when I get home! Sometimes, all the computers at school are filled and I can always rely on my phone to get some good research done!

Some of my favorite apps for productivity include podcasts and pocket. I enjoy listening to downloaded podcasts and audiobooks to listen when I run/walk home so I can learn something at the same time so I feel smarter and productive. I love pocket because I can save any content from the internet/certain news apps to it for offline use. So when I’m waiting for something in an offline environment, I always have something interesting to read at my fingertips and learn something new!

5. Live healthily.

Just because it’s finals week or you have a big test coming up, that doesn’t give you an excuse to sit around all day with junk food next to you as you spend hours trying to get information into your head.

If you eat healthy food, your body will reward you with the ability to better retain information because your body likes healthy food and if you give your body what it likes/needs, it will give you what you want. Avoid refined simple sugars aka fast release carbs such as candy and soda. Instead, stick to complex aka slow release carbs such as fruits and vegetables so you will not experience a sugar crash.

Exercise is also important because it gets your blood flowing, delivering more oxygen to all the mitochondria in all the interneurons in your brain, enabling them to efficiently make ATP which powers them to make more synaptic connections, so you become smarter. Your body also really likes it when you exercise so it will thank you.

6. Don’t stress

Nothing good ever comes easy so you can never expect success without putting in the work for it. It’s going to be hard, but it’s worth it. There is no shortcut to success, because if there was one, everyone would be equally successful.

Your brain is like a muscle, the more you use it, the stronger it becomes. You should be confident because you can achieve anything with consistency and dedication. Therefore, you shouldn’t stress about it because you already know what you have to do.

Procrastination is a stress that can be easily avoided by simple planning. Procrastination is unnecessary stress.

7. Find a great spot.

Have a spot in your house where you can study with no distractions around. Make sure you are either standing or sitting upright so you will stay focused. Don’t study on the comfort on your bed because your brain will just want to rest, therefore not work in such a comfortable environment.

I turned my dresser into a standing desk because it helps me stay more focused than I am if I sit. If sitting makes you feel tired, you should try standing.

Listening to music is also something that really helps me stay focused, but can be a distraction for some people. The music I like to listen to is usually in japanese/korean so there is no way my brain can pay attention to the lyrics so that helps me focus on what’s in front of me. Music also helps me tune out other people in my environment so they won’t have to be a distraction to me.

8. Make connections.

People learn best when they can apply concepts to previous experiences/different things. For example, the hormone glucagon is secreted by the pancreas when blood glucose levels drop below homeostasis. Glucagon is released when glucose is gone! :)

9. Flash cards.

If you’re like me and you’re too lazy to make actual ones on paper, quizlet.com is an awesome website I use to create flashcards. They also have games hat you can play to help you to learn your terms.

How Stress Affects the Brain

Are you sleeping restlessly, feeling irritable or moody, forgetting little things, and feeling overwhelmed and isolated? Don’t worry. We’ve all been there. You’re probably just stressed out. Stress isn’t always a bad thing. It can be handy for a burst of extra energy and focus, like when you’re playing a competitive sport, or have to speak in public. But when its continuous, the kind most of us face day in and day out, it actually begins to change your brain. Chronic stress, like being overworked or having arguments at home, can affect brain size, its structure, and how it functions, right down to the level of your genes.

Stress begins with something called the hypothalamus pituitary adrenal axis, series of interactions between endocrine glands in the brain and on the kidney, which controls your body’s reaction to stress. When your brain detects a stressful situation, your HPA axis is instantly activated and releases a hormone called cortisol, which primes your body for instant action. But high levels of cortisol over long periods of time wreak havoc on your brain. For example, chronic stress increases the activity level and number of neural connections in the amygdala, your brain’s fear center. And as levels of cortisol rise, electric signals in your hippocampus, the part of the brain associated with learning, memories, and stress control, deteriorate.

The hippocampus also inhibits the activity of the HPA axis, so when it weakens, so does your ability to control your stress. That’s not all, though. Cortisol can literally cause your brain to shrink in size.

Too much of it results in the loss of synaptic connections between neurons and the shrinking of your prefrontal cortex, the part of your brain the regulates behaviors like concentration, decision-making, judgement, and social interaction. It also leads to fewer new brain cells being made in the hippocampus. This means chronic stress might make it harder for you to learn and remember things, and also set the stage for more serious mental problems, like depression and eventually Alzheimer’s disease.

It’s not all bad news, though. There are many ways to reverse what cortisol does to your stressed brain. The most powerful weapons are exercise and meditation, which involves breathing deeply and being aware and focused on your surroundings. Both of these activities decrease your stress and increase the size of the hippocampus, thereby improving your memory.

So don’t feel defeated by the pressures of daily life. Get in control of your stress before it takes control of you.

From the TED-Ed Lesson How stress affects your brain - Madhumita Murgia

Animation by Andrew Zimbelman

Comic 14: The Closet Story (Part 2)

NOTES ON COMIC 14
- “We have your back, man. Always.” Yes yup if you want to see me get sentimental and weepy allow me to talk to you about the stupid adamantium-strength friendships slowly building between these five dumb college hockey players.
- Back when I was starting CP! and thought it was going to be like, four comics long, I wasn’t thinking about how annoying it would be to have two characters whose names rhyme. *sighs* Shitty and Bitty??? Really??? What are you guys, dwarves??? (╯°□°)╯︵ ┻━┻.
- Speaking of things I didn’t think through when I was starting the comic: remember the first posts I ever made about CP? Waaay back when? (Don’t loiter.) I described Shitty as “best friend of bitty, loves romcoms, smokes so much fucking pot”. Yikes, was kinda groping for characterization there. At the beginning of this school year Shitty is definitely Jack’s best friend, and probably becomes Bitty’s closest friend after this comic. (Shitty is definitely a confidant for both Jack and Bitty.)
- Also, Holster’s obviously the one who likes romcoms. What was I even thinking???


CAMPUS
- Comic 14 takes place right on the river (map) which is–OKAY more like a glorified stream at most places–but is the other cool geographical feature on Samwell’s campus. Other than being a lovely scenic route to class, it’s a great place for, say, a lovely morning run! Or maybe a romantic, lamp-lit evening walk? Or perhaps you and your best friend have a death wish and like waking up the geese under one of the bridges when you’re drunk on Saturday nights? Perhaps.
- That giant church-like building in the background is Founder’s, the main library (there are quite a few libraries) on Samwell’s campus. It is super-blatant ripoff of one of my favorite buildings in the world, Sterling Memorial Library. Founder’s is one of the places where the Boys meet up to study (or rather, disrupt the studying of other Wellies #Why-Everyone-At-Samwell-Hates-The-Hockey-Team) and it actually first made an appearance in Comic #6 - The Tale of the Hockey Prince where you can see The Pond, Lake Quad and Faber too. YOOOO certified crazy person running this webcomic.


???
“Bro. Like. You just made room in your brain about a fictional place and the fictional bros inhabiting it. Isn’t it weird how your brain indiscriminately wires those synaptic connections? Real or not? Bro!! Freaky, right? Truth is biological programming!…Hey, I’d really wish they’d bring the puck down the ice, I haven’t gotten to make a save in ages.”


Donate!
Comics is hard work! If you’re not a broke college student like me and like CP! I’d really appreciate it! (It usually results in a little gift doodle? ~non-merchandise incentives.~)

And speaking of merchandise…I’m thinking pucks? Shirts? Stickers? Samwell penants?? Would people buy things? Life-sized Shitty body pillows with real ‘stache action?


Tapastic
LAST THING: In addition to Tumblr, I’ll be posting Check, Please! to Tapastic!

It sounds silly, but to Bruce Bridgeman – and probably only Bruce Bridgeman – Hugo was a legitimately life-changing film. Watching it literally helped him see again.

Bridgeman was born with partially impaired stereovision – better known as “lazy eye” – wherein one’s eyes have a tendency to drift independently, making your brain unable to accurately process depth. But when Bruce saw Hugo in 3D, he was not only able to see the “depth” in the film, but he also came out of the theater suddenly able to perceive, in his words, “a riot of depth” in the outside world.

This sudden dramatic breakthrough did have scientific precedent. A 2011 study documenting five people with impaired stereovision who later learned to see in 3D concluded that people “were most likely to have a breakthrough if the stereoscopic images were reinforced by monocular cues like relative size and shading.” In short, Hugo was so effective at creating the illusion of depth that it helped Bridgeman’s mind establish the necessary synaptic connections to bridge the gap to fully-functioning stereovision.

5 True Stories About Films (Too Far Fetched For Movie Plots)

anonymous asked:

What kind of biology advice would you give people who are trying to create alien races for science fiction, those who want to be a little more on the "hard sci-fi" spectrum/more scientifically accurate with their stuff? I know it can kinda sorta slide because fiction but I imagine there's some stuff you'd like to see more or less of.

Okay first off make your alien race based off of fucking carbon

Because even though I guess you could have things based off of other chemicals carbon is the easiest thing because it has the maximum number of covalent bonds (four) without having extra electron shells that fuck up everything (silicon, I’m looking at you). 

Second off for the love of god, your alien race cannot reproduce any way whatsoever with Earth-based lifeforms

Because guess what? They probably have a different fucking genetic code. 

The genetic code is, for those not in the know, the matching up of nucleotide bases (DNA/RNA, our genes) to different amino acids (proteins that basically make up our entire bodies okay that’s the structure to life)

This is the fucking code for us

And I am sorry, but even though some of the matching up of nucleotides-aminos is based on chemical structure, a lot of it is just random chance of evolution and the odds of another alien race having the same code as we do is approximately the size of the ULTRA-ULTRA SUB-SUB atomic particle 

So if all of your aliens from different planets can reproduce with one another you better fucking have them all have a common ancestor or something, like they all came form the same damn planet originally. Otherwise they can’t have the sex and I’m sorry

Also don’t be afraid to have the genetic material be a different set of nucleotide bases or even a different sort of organic molecule, and same for the building block material (aka proteins and to a lesser extent carbs and lipids). 

Also remember: evolution is not a fucking perfect process. It can only work with what it is given and that is why we are all so fucked up, our genes are honest to god terrible and horrifying. So your aliens should not be perfect. They should not be able to do everything. They should have a respiratory chain that can get fucked by a molecule that is better at binding to active sites on enzymes than the thing you want bound there (fucking carbon monoxide I swear to fucking god). Like there should be ways to fuck things up

Also don’t fucking forget the microbiome. It’s a delicate thing and aliens probably need similar things. Hell in general don’t ignore ecology and the fact that having one thing per general ecological category doesn’t actually fucking work. Monocultures don’t work. Diversity exists for a fucking reason. 

Stop making all intelligent aliens humanoid there is nothing fucking “special” about human body shape the only thing you need is a high number of synaptic connections or whatever the equivalent is in your alien race for high processing power in the brain jesus fucking christ make some weird ass looking aliens

Ultimately have an explanation for everything. Every single damn fucking thing ultimately has a cause both in biology and in history. Have an explanation for why your aliens looked the way they do and evolve the way they did and have the history they do. Nothing - skin color, hair style, historical dominance - evolves in a vacuum. Europeans fucked everyone’s shit up because somehow they managed to get all the fucking really good domesticate-able animals on their damn continent, fucking lucky-ass shitheads. People from hot climates have more melanin to prevent skin cancer from all the damn sunlight. Mammals became the megafauna of the Cenozoic because all the damn non-Neornithean dinosaurs had to go and die out 66 million years ago because of a fucking asteroid. Literally everything in biology is due to luck, chance, and having the right fucking genes at the right fucking time and to have a good story you need to have a damn well-built world and backstory for the whole thing. 

Connectomics—How The Emerging Revolution In Neural Wiring Diagrams Is About To Change Biology Forever

Wiring diagrams just got significantly more interesting

One of the great challenges in modern science is to understand the structure of the human brain. In particular, neurologists want to work out the complete map of connections between neurons, it’s a wiring diagram and a structure known as the human connectome.

That’s a significant challenge. So far, researchers have successfully constructed the connectome of only one creature, the nematode worm C. elegans with the grand total of 302 neurons and 8000 connections between them. By contrast, the human cerebral cortex contains some 10^10 neurons linked by 10^14 synaptic connections.

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Our current diagnostic system — the main achievement of the biomedical revolution in psychiatry — drew a sharp , clear line between those who were sick and those who were well, and that line was determined by science. The system started with the behavior of persons, and sorted them into types. That approach sank deep roots into our culture, possibly because sorting ourselves into different kinds of people comes naturally to us.

The institute is rejecting this system because it does not lead to useful research. It is starting afresh, with a focus on how the brain and its trillions of synaptic connections work. The British Psychological Society rejects the centrality of diagnosis for seemingly quite different reasons — among them, because defining people by a devastating label may not help them.

Both approaches recognize that mental illnesses are complex individual responses — less like hypothyroidism, in which you fall ill because your body does not secrete enough thyroid hormone, and more like metabolic syndrome, in which a collection of unrelated risk factors (high blood pressure, body fat around the waist) increases your chance of heart disease.

The implications are that social experience plays a significant role in who becomes mentally ill, when they fall ill and how their illness unfolds. We should view illness as caused not only by brain deficits but also by abuse, deprivation and inequality, which alter the way brains behave. Illness thus requires social interventions, not just pharmacological ones.
Much like a snowflake, every thought we have is entirely unique. This may not seem to be the case—indeed, many of our thoughts seem repetitive and trite—but the uniqueness reveals itself when we factor in the sheer immensity and complexity of our neurophysiology. Every neuron triggered, every neurotransmitter released, and every synapse flooded conspires in a statistically unique way to create each and every thought we have. Each thought is a vastly complex chemistry experiment with its own unique signatures, pathways, and life-cycles. We have over one hundred billion neurons hiding in our noggins and some several hundred TRILLION synaptic connections (allowing for more combinations than the number of stars in the known universe). So next time you’re feeling bored, or think that nothing unique ever happens to you, just follow some of those neurons down the rabbit hole and savor the fact that no other being in the universe, before or ever again, will get to experience this identical trek through your grey matter.
—  N.P. Krause
Supporting the damaged brain

A new study shows that embryonic nerve cells can functionally integrate into local neural networks when transplanted into damaged areas of the visual cortex of adult mice.

(Image caption: Neuronal transplants (blue) connect with host neurons (yellow) in the adult mouse brain in a highly specific manner, rebuilding neural networks lost upon injury. Credit: Sofia Grade, LMU/Helmholtz Zentrum München)

When it comes to recovering from insult, the adult human brain has very little ability to compensate for nerve-cell loss. Biomedical researchers and clinicians are therefore exploring the possibility of using transplanted nerve cells to replace neurons that have been irreparably damaged as a result of trauma or disease. Previous studies have suggested there is potential to remedy at least some of the clinical symptoms resulting from acquired brain disease through the transplantation of fetal nerve cells into damaged neuronal networks. However, it is not clear whether transplanted intact neurons can be sufficiently integrated to result in restored function of the lesioned network. Now researchers based at LMU Munich, the Max Planck Institute for Neurobiology in Martinsried and the Helmholtz Zentrum München have demonstrated that, in mice, transplanted embryonic nerve cells can indeed be incorporated into an existing network in such a way that they correctly carry out the tasks performed by the damaged cells originally found in that position. Such work is of importance in the potential treatment of all acquired brain disease including neurodegenerative illnesses such as Alzheimer‘s or Parkinson’s disease, as well as strokes and trauma, given each disease state leads to the large-scale, irreversible loss of nerve cells and the acquisition of a what is usually a lifelong neurological deficit for the affected person.

In the study published in Nature, researchers of the Ludwig Maximilians University Munich, the Max Planck Institute of Neurobiology, and the Helmholtz Zentrum München have specifically asked whether transplanted embryonic nerve cells can functionally integrate into the visual cortex of adult mice. “This region of the brain is ideal for such experiments,” says Magdalena Götz, joint leader of the study together with Mark Hübener. Hübener is a specialist in the structure and function of the mouse visual cortex in Professor Tobias Bonhoeffer’s Department (Synapses – Circuits – Plasticity) at the MPI for Neurobiology. As Hübener explains, “we know so much about the functions of the nerve cells in this region and the connections between them that we can readily assess whether the implanted nerve cells actually perform the tasks normally carried out by the network.” In their experiments, the team transplanted embryonic nerve cells from the cerebral cortex into lesioned areas of the visual cortex of adult mice. Over the course of the following weeks and months, they monitored the behavior of the implanted, immature neurons by means of two-photon microscopy to ascertain whether they differentiated into so-called pyramidal cells, a cell type normally found in the area of interest. “The very fact that the cells survived and continued to develop was very encouraging,” Hübener remarks. “But things got really exciting when we took a closer look at the electrical activity of the transplanted cells.” In their joint study, PhD student Susanne Falkner and Postdoc Sofia Grade were able to show that the new cells formed the synaptic connections that neurons in their position in the network would normally make, and that they responded to visual stimuli.

The team then went on to characterize, for the first time, the broader pattern of connections made by the transplanted neurons. Astonishingly, they found that pyramidal cells derived from the transplanted immature neurons formed functional connections with the appropriate nerve cells all over the brain. In other words, they received precisely the same inputs as their predecessors in the network. In addition, they were able to process that information and pass it on to the downstream neurons which had also differentiated in the correct manner. “These findings demonstrate that the implanted nerve cells have integrated with high precision into a neuronal network into which, under normal conditions, new nerve cells would never have been incorporated,” explains Götz, whose work at the Helmholtz Zentrum and at LMU focuses on finding ways to replace lost neurons in the central nervous system. The new study reveals that immature neurons are capable of correctly responding to differentiation signals in the adult mammalian brain and can close functional gaps in an existing neural network.

Scientists design peptide to promote functional recovery following spinal cord injury

Case Western Reserve scientists developed a new chemical compound that shows extraordinary promise in restoring function lost to spinal cord injury. The compound, which the researchers dubbed intracellular sigma peptide (ISP), allowed paralyzed muscles to activate in more than 80 percent of the animals tested. The remarkable study, partly funded by the National Institutes of Health, appears in the Dec. 3 edition of the journal Nature.

Case Western Reserve University School of Medicine Professor of Neurosciences Jerry Silver, the senior author, led an international team of scientists in the research in which 21 of 26 animals with spinal cord injury regained the ability to urinate, move or both. In the experiments, the peptide appears to allow nerve fibers to overcome scarring that normally blocks their regrowth.

“This recovery is unprecedented,” Silver said. “Each of the 21 animals got something back in terms of function. For any spinal cord-injured patient today, it would be considered extraordinary to regain even one of these functions, especially bladder function. ISP additionally has treatment potential for diseases where the body produces destructive scarring such as heart attack, peripheral nerve injury and multiple sclerosis (MS).” (Silver’s team now is testing the effectiveness of ISP in animal models of these disorders.)

Immediately after a central nervous system (CNS) injury, molecules known as proteoglycans collect in scar tissue at the injury site and in the perineuronal net (PNN). In healthy tissue, proteoglycans are key components in the matrix between cells and play a key role in maintaining the structure of the nervous system. However, following injury, proteoglycans are overly abundant in scar tissue and the impenetrable nets around synapses throughout the brain and spinal cord. The consequence is a formidable barrier preventing regeneration and new nerve connections. Proteoglycans produce a sticky quagmire, trapping and restricting the cut nerve fiber tips (called growth cones) from making their journey back to their proper synaptic connections. It is these connections that transmit critical information through electrical impulses to nerve cells that enable a person or animal to control bodily functions.

“There are currently no drug therapies available that improve the very limited natural recovery from spinal cord injuries that patients experience,” said Lyn Jakeman, a program director at the NIH’s National Institute of Neurological Disorders and Stroke, Bethesda, Md. “This is a great step toward identifying a novel agent for helping people recover.”

The investigators designed the ISP peptide to turn off the neuron’s proteoglycan receptor on/off switch. In addition, they added a shuttle called TAT (trans-activator of transcription) to send ISP throughout the nervous system and across cell membranes. ISP travels to and penetrates the membranes of cells, including the scar tissue-covered injury site. Because the peptides can penetrate tissue, ISP can be delivered systemically rather than with a direct injection to the spinal cord.

“Our treatment strategy was designed to be easily translatable,” said Bradley Lang, a Silver lab graduate student and lead author on the study. “Our goal is to progress this treatment forward for use as a therapeutic following spinal cord injury.”

For this study, 26 severely spinal cord-injured animals (rats) received daily injections for seven weeks. During that time, the animals were assessed for their ability to walk, to balance and to control when and how much they urinate. The results showed that 21 of the 26 animals regained one or more of the functions well after injections began. Some animals regained all three behaviors and others one or two out of three.

“We don’t know why a particular animal regained a specific function,” Silver said. “That is one of the big remaining questions.”

One clue may be the small amounts of nerve tracts spared in the animals’ spinal cords. These remaining tracts are differentially damaged by bleeding or inflammation sustained just after the original injury. One especially important tract that responded robustly to ISP contains serotonergic fibers. These fibers release the neurotransmitter serotonin into the spinal cord, which, in turn, greatly enhances functional activity of the scant numbers of remaining fiber tracts that control the behaviors that were restored.

Each animal had different serotonergic sprouting patterns and variable tract sparing, which probably accounts for the different functions they were able to regain. “Sprouting is a critical phenomenon,” Silver said. “Even if there are just a few intact fibers left after the injury, it could be one critical piece that brings back an important function.”

Silver also commented about a next research step regarding ISP. “Our goal is to progress this treatment forward for use as a therapeutic following spinal cord injury,” he said.

Neuroscientists discover new learning rule for pattern completion

IST Austria Professor Peter Jonas and team identify a new learning rule.

“Fire together, wire together” is the famous abridged version of the Hebbian rule. It states that neurons in the brain adapt during the learning process, a mechanism which is called neuronal plasticity. Hebb’s theory dates back to the 1940s and subsequent research in neuroscience has further corroborated it. Today, we also know that different factors play a critical role, such as timing of firing, order of activity, and functional connectivity, as cutting-edge technologies allow examining subcellular processes with extraordinary precision.

Recently, scientists at the Institute of Science and Technology Austria (IST Austria) discovered a new learning rule for a specific type of excitatory synaptic connection in the hippocampus. Their study was now published in the renowned journal Nature Communications on May 13. These synapses are located in the so-called CA3 region of the hippocampus, which plays a critical role for storage and recall of spatial information in the brain. One of its hallmark properties is that memory recall can even be triggered by incomplete cues. This enables the network to complete neuronal activity patterns, a phenomenon termed pattern completion.

Professor Peter Jonas and his team, including postdoc José Guzmán and PhD student Rajiv Mishra, investigated how the strength of connections between neurons is adjusted, taking into account the relative timing of firing neurons. In neuroscience, this is known as spike-timing-dependent plasticity or STDP. According to the STDP rule, neuron A has to fire just before neuron B so that the synaptic connection becomes stronger with time. In the case of a reverse order—neuron B fires before neuron A—the connection between the neurons may become weaker.

Yet in apparent contrast to this rule, the team of Professor Jonas discovered in their experiments that a reverse order also leads to stronger connections between the investigated synapses (CA3–CA3 recurrent excitatory synapses). Surprisingly, a potentiation takes place independent of the order of firing. So if the sequence is not important at these particular synapses, why is this the case?

To address this question, the authors performed various cutting-edge measurements with extremely high precision. These included patch-clamp recordings to control which neurons fire at what time, imaging of calcium molecules, which play a critical role in synaptic plasticity, and subcellular recordings of electrical signals in dendrites. All data resulted in the same symmetric summation curves. Thus, the unusual induction curve of potentiation is generated by the properties of calcium signaling, which is in turn explained by the characteristics of electrical signaling in dendrites.

The scientists subsequently investigated what happens if a huge number of neurons is being connected via excitatory synapses in a network model. To this end, they ran computer simulations after incorporating different plasticity induction rules. They compared the results of simulations with the new symmetric plasticity induction rule with those of a conventional rule. The outcome clearly demonstrated that patterns could be better restored from partial cues when the new symmetric rule was applied. Professor Jonas: “The new plasticity induction rule may explain why learning in vivo occurs robustly under a variety of behavioral conditions. For example, it may explain storage and recall of cell assembly patterns of freely moving animals in open fields, as previously found by the systems neuroscience groups of IST Austria (O’Neill et al., 2008)”.

The new data seem to be in contrast to classical STDP induction rules at other glutamatergic synapses. Do they violate the Hebb rule? Professor Jonas: “If you read the classical Hebb text carefully, it states: ‘If the axon of a cell A is near enough to excite cell B […], A’s efficiency, as one of the cells firing B, is increased’. However, there is no mentioning of depression. So the new data do not violate Hebb’s postulate, but may confirm it in the literal sense”.

New role for immature brain neurons in the dentate gyrus identified

University of Alabama at Birmingham researchers have proposed a model that resolves a seeming paradox in one of the most intriguing areas of the brain — the dentate gyrus.

This region helps form memories such as where you parked your car, and it also is one of only two areas of the brain that continuously produces new nerve cells throughout life.

“So the big question,” said Linda Overstreet-Wadiche, Ph.D., associate professor in the UAB Department of Neurobiology, “is why does this happen in this brain region? Entirely new neurons are being made. What is their role?”

In a paper published in Nature Communications on April 20, Overstreet-Wadiche and colleagues at UAB; the University of Perugia, Italy; Sandia National Laboratories, Albuquerque, New Mexico; and Duke University School of Medicine; present data and a simple statistical network model that describe an unanticipated property of newly formed, immature neurons in the dentate gyrus.

These immature granule cell neurons are thought to increase pattern discrimination, even though they are a small proportion of the granule cells in the dentate gyrus. But it is not clear how they contribute.

This work is one small step — along with other steps taken in a multitude of labs worldwide — towards cracking the neural code, one of the great biological challenges in research. As Eric Kandel and co-authors write in Principles of Neural Science, “The ultimate goal of neural science is to understand how the flow of electrical signals through neural circuits gives rise to the mind — to how we perceive, act, think, learn and remember.”

Newly formed granule cells can take six-to-eight weeks to mature in adult mice. Researchers wondered if the immature cells had properties that made them different. More than 10 years ago, researchers found one difference — the cells showed high excitability, meaning that even small electrical pulses made the immature cells fire their own electrical spikes. Thus they were seen as “highly excitable young neurons,” as described by Alejandro Schinder and others in the field.

But this created a paradox. Under the neural coding hypothesis, high excitability should degrade the ability of the dentate gyrus — an important processing center in the brain — to perceive the small differences in input patterns that are crucial in memory, to know your spatial location or the location of your car.

“The dentate gyrus is very sensitive to pattern differences,” Overstreet-Wadiche said. “It takes an input and accentuates the differences. This is called pattern separation.”

The dentate gyrus receives input from the entorhinal cortex, a part of the brain that processes sensory and spatial input from other regions of the brain. The dentate gyrus then sends output to the hippocampus, which helps form short- and long-term memories and helps you navigate your environment.

In their mouse brain slice experiments, Overstreet-Wadiche and colleagues did not directly stimulate the immature granule cells. They instead stimulated neurons of the entorhinal cortex.

“We tried to mimic a more physiological situation by stimulating the upstream neurons far away from the granule cells,” she said.

Use of this weaker and more diffuse stimulation revealed a new, previously underappreciated role for the immature dentate gyrus granule cells. Since these cells have fewer synaptic connections with the entorhinal cortex cells, as compared with mature granule cells, this lower connectivity meant that a lower signaling drive reached the immature granule cells when stimulation was applied at the entorhinal cortex.

The experiments by Overstreet-Wadiche and colleagues show that this low excitatory drive make the immature granule cells less — not more — likely to fire than mature granule cells. Less firing is known in computational neuroscience as sparse coding, which allows finer discrimination among many different patterns.

“This is potentially a way that immature granule cells can enhance pattern separation,” Overstreet-Wadiche said. “Because the immature cells have fewer synapses, they can be more selective.”

Seven years ago, paper co-author James Aimone, Ph.D., of Sandia National Laboratories, had developed a realistic network model for the immature granule cells, a model that incorporated their high intrinsic excitability. When he ran that model, the immature cells degraded, rather than improved, overall dentate gyrus pattern separation. For the current Overstreet-Wadiche paper, Aimone revised a simpler model incorporating the new findings of his colleagues. This time, the statistical network model showed a more complex result — immature granule cells with high excitability and low connectivity were able to broaden the range of input levels from the entorhinal cortex that could still create well-separated output representations.

In other words, the balance between low synaptic connectivity and high intrinsic excitability could enhance the capabilities of the network even with very few immature cells.

“The main idea is that as the cells develop, they have a different function,” Overstreet-Wadiche said. “It’s almost like they are a different neuron for a little while that is more excitable but also potentially more selective.”

The proposed role of the immature granule cells by Overstreet-Wadiche and colleagues meshes with prior experiments by other researchers who found that precise removal of immature granule cells of a rodent, using genetic manipulations, creates difficulty in distinguishing small differences in contexts of sensory cues. Thus, removal of this small number of cells degrades pattern separation.

Missing gene linked to autism

The team already knew that some people with autism were deficient in a gene called neurexin-II. To investigate whether the gene was associated with autism symptoms, the Leeds team studied mice with the same defect.

They found behavioural features that were similar to autism symptoms, including a lack of sociability or interest in other mice.

Dr Steven Clapcote, Lecturer in Pharmacology in the University’s Faculty of Biological Sciences, who led the study published in the journal Translational Psychiatry today, said: “In other respects, these mice were functioning normally. The gene deficiency mapped closely with certain autism symptoms.”

Dr Clapcote added: “This is exciting because we now have an animal model to investigate new treatments for autism.”

The researchers also looked at how the absence of neurexin-II was affecting the brain.

Co-author Dr James Dachtler, Wellcome Trust Junior Investigator Development Fellow in the Faculty of Biological Sciences at Leeds, said: “We found that the affected mice had lower levels of a protein called Munc18-1 in the brain. Munc18-1 usually helps to release neurotransmitter chemicals across synaptic connections in the brain, so neurotransmitter release could be impaired in the affected mice and possibly in some cases of autism.”

Research by Professor Thomas Südhof, a Nobel prize-winning biochemist at Stanford University, previously established a link between autism symptoms and neuroligin-1, another gene associated with synapse signalling. The Leeds-led study is the first to find a connection with neurexin-II.

Dr Clapcote said: “Not all people with autism will have the neurexin-II defect, just as not all will have the neuroligin defect, but we are starting to build up a picture of the important role of genes involved in these synapse communications in better understanding autism.”