3

Phelsuma pusilla Mertens, 1964

Distribution:

Phelsuma p. pusilla is widely distributed in eastern Madagascar. Phelsuma p. hallmanni is found only around Andasibe in eastern Madagascar.

Morphology & Colouration:

Phelsuma pusilla is a very small gecko species, reaching a maximum total length of 85-100 mm (100 mm in males of P. p. hallmanni). Like all Phelsuma species, these geckos have a strongly reduced first toe, round pupils, and lack claws. The tail is distinctly verticillated.

These geckos are dorsally green with red spots, although the spots are often lacking in females. There is an arrangement of these red spots on the snout similar to most species in the P. lineata clade. In P. p. hallmanni, one of these red spots forms a bar between and just anterior to the eyes, and the snout is often blue. These geckos possess a dark lateral stripe that is always noticeable. The tail can be teal or turquoise, and the ventral side is whitish. 

Habits:

These geckos are arboreal and diurnal. Phelsuma p. pusilla is frequently found on palms, banana plants, and in urban environments. It is less frequently encountered in rainforest. By contrast, P. p. hallmanni is found on trees at the edge of mid-altitude rainforest, and not on buildings, and is apparently rare.

The juveniles of P. p. hallmanni are grey with lots of tiny blue/white spots, whereas those of P. p. pusilla are greenish.

Conservation Status:

Phelsuma pusilla is listed as Least Concern on the IUCN Red List, due to its apparently wide distribution and commonness. Phelsuma p. hallmanni may be rarer and more threatened because it is not found outside forests.

Taxonomy and Systematics:

Phelsuma pusilla belongs to the P. lineata group (Rocha et al. 2010), and is closest related to P. lineataP. kely, and P. comorensis. It possesses two subspecies, P. p. pusilla, and P. p. hallmanni, which have been described above.

Phylogeny:

Animalia-Chordata-Reptilia-Squamata-Gekkonidae-Phelsuma-P. pusilla

Photo is a male P. p. hallmanni, photographed by Henry Cook.

Click here to see more TaxonFiles!

References:

Glaw, F. and M. Vences. 2007. A Field Guide to the Amphibians and Reptiles of Madagascar. Köln, Germany

Rocha, S., H. Rösler, P.-S. Gehring, F. Glaw, D. Posada, D.J. Harris and M. Vences. 2010. Phylogenetic systematics of day geckos, genus Phelsuma, based on molecular and morphological data (Squamata: Gekkonidae). Zootaxa 2429:1-28

Abstract

A new hadrosaurid is described from the Upper Cretaceous Neslen Formation of central Utah. Rhinorex condrupus gen. et sp. nov. is diagnosed on the basis of two unique traits, a hook-shaped projection of the nasal anteroventral process and dorsal projection of the posteroventral process of the premaxilla, and is further differentiated from other hadrosaurid species based on the morphology of the nasal (large nasal boss on the posterodorsal corner of the circumnarial fossa, small protuberences on the anterior process, absence of nasal arch), jugal (vertical postorbital process), postorbital (high degree of flexion present on posterior process), and squamosal (inclined anterolateral processes). This new taxon was discovered in estuarine sediments dated at approximately 75 Ma and just 250 km north of the prolific dinosaur-bearing strata of the Kaiparowits Formation, possibly overlapping in time with Gryposaurus monumentensis. Phylogenetic parsimony and Bayesian analyses associate this new taxon with the Gryposaurus clade, even though the type specimen does not possess the diagnostic nasal hump of the latter genus. Comparisons with phylogenetic analyses from other studies show that a current consensus exists between the general structure of the hadrosaurid evolutionary tree, but on closer examination there is little agreement among species relationships.

2

The marine eels and other members of the superorder  Elopomorpha have a leptocephalus larval stage, which are flat and transparent. This group is quite diverse, containing 801 species in 24 orders, 24 families and 156 genera (super diverse). 

Leptocephali have compressed bodies that contain jelly-like substances on the inside, with a thin layer of muscle with visible myomeres on the outside, a simple tube as a gut, dorsal and anal fins, but they lack pelvic fins. They also don’t have any red blood cells (most likely is respiration by passive diffusion), which they only begin produce when the change into the juvenile glass eel stage. Appears to feed on marine snow, tiny free-floating particles in the ocean.

This large size leptocephalus must be a species of Muraenidae (moray eels), and probably the larva of a long thin ribbon eel, which is metamorphosing, and is entering shallow water to finish metamorphosis into a young eel, in Bali, Indonesia.

Ladies and gentlemen I give you the worst piece my hands have ever wrought.

Sharkro. Not without Kanfish.

What started as a joke evolved into this monstrosity and all I can say is I deeply apologize.

Stai guardando qualcosa.
Non sai come, da quel qualcosa pensi a lui.
Magari anche leggendo questo post.
Pensi a come sia perfetto. In tutto.
A quanto lo vorresti.
A quanto vorresti un suo abbraccio,
Un suo bacio,
Un suo sorriso.
I suoi occhi sono il mare,
Che siano azzurri,
Verdi,
Grigi,
Marroni,
Viola, arancioni, rossi, sempre il mare.
La sua voce.
Le sue mani.
Come vorresti toccarle.
Come vorresti che toccassero te.
Pensi ai suoi vestiti,
Alla sua felpa,
Non sai quale sia, ma la vuoi.
Ma poi pensi che
Non puoi.
Non puoi avere niente di questo.
Non puoi averlo.
Sei triste.
Senti la rabbia,
Sale per la tua spina dorsale,
Hai i brividi.
Non resisti,
Hai bisogno di lui per stare bene.
Sbatti i piedi per terra,
Fai cadere tutto,
Lanci le cose in aria,
La gola ti brucia,
Gli occhi fanno male,
É che vorresti urlare.
I tuoi occhi diventano rossi.
Un mare in tempesta.
Le lacrime ti rigano il viso.
Stai male.
Hai bisogno di un antidoto.
Il problema è che l’antidoto ce l’ha lui.
—  Cit.

How to learn successfully even under stress

Whenever we have to acquire new knowledge under stress, the brain deploys unconscious rather than conscious learning processes. Neuroscientists at the Ruhr-Universität Bochum have discovered that this switch from conscious to unconscious learning systems is triggered by the intact function of mineralocorticoid receptors. These receptors are activated by hormones released in response to stress by the adrenal cortex. The team of PD Dr Lars Schwabe from the Institute of Cognitive Neuroscience, together with colleagues from the neurology department at the university clinic Bergmannsheil, reports in the journal “Biological Psychiatry”.

Predicting the weather under stress

The team from Bochum has examined 80 subjects, 50 per cent of whom were given a drug blocking mineralocorticoid receptors in the brain. The remaining participants took a placebo drug. Twenty participants from each group were subjected to a stress-inducing experience. Subsequently, all participants underwent a learning test, the so-called weather prediction task. The subjects were shown playing cards with different symbols and had to learn which combinations of cards meant rain and which meant sunshine. The researchers used MRI to record the respective brain activity.

Learning unconsciously or consciously

There are two different approaches to master the weather prediction test: some subjects tried consciously to formulate a rule that would enable them to predict sunshine and rain. Others learned unconsciously to give the right answer, following their gut feeling, as it were. The team of Lars Schwabe demonstrated in August 2012 that, under stress, the brain prefers unconscious to conscious learning. “This switch to another memory system happens automatically,” says Lars Schwabe. “It makes sense for the organism to react in this manner. Thus, learning efficiency can be maintained even under stress.” However, this works only with fully functional mineralocorticoid receptors. Once the researchers blocked these receptors by applying the drug Spironolactone, the participants switched over to the unconscious strategy less frequently, thus demonstrating a poorer learning efficiency.

Effects also visible in brain activity

These effects also became evident in MRI data. Usually, stress causes the brain activity to shift from the hippocampus – a structure for conscious learning – to the dorsal striatum, which manages unconscious learning. However, this stress-induced switch took place only in the placebo group, not in subjects who had been given the mineralocorticoid receptor blocker. Consequently, the mineralocorticoid receptors play a crucial role in enabling the brain to adapt to stressful situations.

(Image: Shutterstock)

2

Fed Up with Waiting? Timely Activation of Serotonin Enhances Patience

Lining up in a long queue for a popular restaurant or waiting for the arrival of a date requires a great deal of patience. Our lives are full of decisions involving patience, yet it needs to be exercised at the appropriate times. In order to examine the brain mechanism for controlling patience to obtain a reward, Drs. Kayoko Miyazaki and Katsuhiko Miyazaki and Prof. Kenji Doya of the Neural Computation Unit at the Okinawa Institute of Science and Technology Graduate University, used a new technique called optogenetics, where they use light to simulate specific neurons with precise timing. Their most recent research shows that activating serotonin neurons specifically during waiting promotes patience for delayed rewards. This research was published in the online version of Current Biology on August 21, 2014.

In this study, the researchers used genetically engineered mice that produce light-activated molecules only in neurons that produce serotonin. They implanted an optical fiber in a small part of the brain called the dorsal raphe, from which neural fibers releasing serotonin extend throughout the cerebrum, the largest and most highly developed part of the brain. The researchers trained five of those mice to perform a delayed reward task, meaning that if they waited at a hole, they would receive a food pellet as a reward. To show that they were waiting, each mouse needed to hold its nose inside the hole where the food pellet would appear, a posture that the researchers call a nose poke. The durations of waiting were randomly chosen from 3, 6, or 9 seconds, or infinity, meaning no reward was given no matter how long the mice waited. In half of those trials, researchers stimulated serotonin neurons by shining a light through the optical fiber while the mice were waiting. No prior signal was given to notify how long the waiting would be. The mice consistently waited for 3 and 6 seconds to receive the food. But when the mice needed to wait for 9 seconds, the mice showed difficulty and often removed their nose from the food hole. When the researchers shone a light on serotonin neurons during the nose poke position, the light stimulation significantly decreased the number of failures to wait for 9 seconds to obtain the food.

In the 25% of trials, the food pellet reward was not delivered regardless of how long the mouse waited. In these trials, without their serotonin neurons stimulated, mice waited 12.0 seconds on average. With their serotonin neurons stimulated, the mice waited 17.5 seconds on average. As control experiments, the researchers activated serotonin neurons at different timing when each mouse did not have its nose poked into the food hole, then observed that these mice behaved the same as in unstimulated cases with no evidence of simple motor inhibition. The results showed, for the first time, that the timed activation of serotonin neurons promotes animals’ patience for delayed rewards.

Serotonin is a neuromodulator that is released diffusely in the entire brain. It is involved in behavioral, cognitive, and mental functions. Classically, serotonin was believed to signal punishment and inhibit behaviors. However, serotonin enriching drugs, known as SSRI, are effective for therapies of depression, which is hard to reconcile with the classic view. Another recent study of optogenetic stimulation of serotonin neurons even reported its effect as a reward, to further complicate the story. On the other hand, another line of research, including the previous work by the OIST researchers, showed that the lack of serotonin causes impulsive behaviors. “Our previous studies have shown that serotonin levels increase when waiting for delayed rewards. We have also shown that inhibiting serotonin neurons leads to an inability to wait for a long time,” explained Kayoko and Katsuhiko Miyazaki. “By using light to stimulate neurons at specific times, this study has proven serotonin’s role in patience during delayed reward waiting, underlining serotonin’s much greater role than previously thought.” By further exploring the effect of serotonin, the researchers hope to decipher the neuronal network behind mental disorders and behaviors involving serotonin. Such studies can promote a better understanding of human emotions, including the development of software and robots and that think and act like humans.

Tinnitus discovery opens door to possible new treatment avenues

For tens of millions of Americans, there’s no such thing as the sound of silence. Instead, even in a quiet room, they hear a constant ringing, buzzing, hissing, humming or other noise in their ears that isn’t real. Called tinnitus, it can be debilitating and life-altering.

Now, University of Michigan Medical School researchers report new scientific findings that help explain what is going on inside these unquiet brains.

The discovery reveals an important new target for treating the condition. Already, the U-M team has a patent pending and device in development based on the approach.

The critical findings are published online in the prestigious Journal of Neuroscience. Though the work was done in animals, it provides a science-based, novel approach to treating tinnitus in humans.

Susan Shore, Ph.D., the senior author of the paper, explains that her team has confirmed that a process called stimulus-timing dependent multisensory plasticity is altered in animals with tinnitus – and that this plasticity is “exquisitely sensitive” to the timing of signals coming in to a key area of the brain.

That area, called the dorsal cochlear nucleus, is the first station for signals arriving in the brain from the ear via the auditory nerve. But it’s also a center where “multitasking” neurons integrate other sensory signals, such as touch, together with the hearing information.

Shore, who leads a lab in U-M’s Kresge Hearing Research Institute, is a Professor of Otolaryngology and Molecular and Integrative Physiology at the U-M Medical School, and also Professor of Biomedical Engineering, which spans the Medical School and College of Engineering.

She explains that in tinnitus, some of the input to the brain from the ear’s cochlea is reduced, while signals from the somatosensory nerves of the face and neck, related to touch, are excessively amplified.

“It’s as if the signals are compensating for the lost auditory input, but they overcompensate and end up making everything noisy,” says Shore.

The new findings illuminate the relationship between tinnitus, hearing loss and sensory input and help explain why many tinnitus sufferers can change the volume and pitch of their tinnitus’s sound by clenching their jaw, or moving their head and neck.

But it’s not just the combination of loud noise and overactive somatosensory signals that are involved in tinnitus, the researchers report.

It’s the precise timing of these signals in relation to one another that prompt the changes in the nervous system’s plasticity mechanisms, which may lead to the symptoms known to tinnitus sufferers. 

Shore and her colleagues, including former U-M biomedical engineering graduate student and first author Seth Koehler, Ph.D., hope their findings will eventually help many of the 50 million people in the United States and millions more worldwide who have the condition, according to the American Tinnitus Association. They hope to bring science-based approaches to the treatment of a condition for which there is no cure – and for which many unproven would-be therapies exist.

Tinnitus especially affects baby boomers, who, as they reach an age at which hearing tends to diminish, increasingly experience tinnitus. The condition most commonly occurs with hearing loss, but can also follow head and neck trauma, such as after an auto accident, or dental work.

Loud noises and blast forces experienced by members of the military in war zones also can trigger the condition. Tinnitus is a top cause of disability among members and veterans of the armed forces.

Researchers still don’t understand what protective factors might keep some people from developing tinnitus, while others exposed to the same conditions experience tinnitus.

In this study, only half of the animals receiving a noise-overexposure developed tinnitus. This is similarly the case with humans — not everyone with hearing damage ends up with tinnitus. An important finding in the new paper is that animals that did not get tinnitus showed fewer changes in their multisensory plasticity than those with evidence of tinnitus. In other words, their neurons were not hyperactive.

Shore is now working with other students and postdoctoral fellows to develop a device that uses the new knowledge about the importance of signal timing to alleviate tinnitus. The device will combine sound and electrical stimulation of the face and neck in order to return to normal the neural activity in the auditory pathway.

“If we get the timing right, we believe we can decrease the firing rates of neurons at the tinnitus frequency, and target those with hyperactivity,” says Shore. She and her colleagues are also working to develop pharmacological manipulations that could enhance stimulus timed plasticity by changing specific molecular targets.

But, she notes, any treatment will likely have to be customized to each patient, and delivered on a regular basis. And some patients may be more likely to derive benefit than others.

Newly-described anomalocaridid Lyrarapax unguispinus. Just 12cm long (4.7in), the fossils of this 520 million-year-old Chinese species have exquisitely-preserved brains — the structure of which help to confirm a shared ancestry with velvet worms and basal arthropods.

All the reference images I could find focus on the underside of Lyrarapax, so this reconstruction is pretty speculative regarding the head shield shape and possible dorsal flaps.

And while the brain discovery is really neat, look at those flippers! While Schinderhannes looks like an anomalocaridid trying to be a fish, Lyrarapax almost looks like one trying to be a penguin.

Researchers find new target for chronic pain treatment

Researchers at the UNC School of Medicine have found a new target for treating chronic pain: an enzyme called PIP5K1C. In a paper published today in the journal Neuron, a team of researchers led by Mark Zylka, PhD, Associate Professor of Cell Biology and Physiology, shows that PIP5K1C controls the activity of cellular receptors that signal pain.

By reducing the level of the enzyme, researchers showed that the levels of a crucial lipid called PIPin pain-sensing neurons is also lessened, thus decreasing pain.

They also found a compound that could dampen the activity of PIP5K1C. This compound, currently named UNC3230, could lead to a new kind of pain reliever for the more than 100 million people who suffer from chronic pain in the United States alone.

In particular, the researchers showed that the compound might be able to significantly reduce inflammatory pain, such as arthritis, as well as neuropathic pain – damage to nerve fibers. The latter is common in conditions such as shingles, back pain, or when bodily extremities become numb due to side effects of chemotherapy or diseases such as diabetes.

The creation of such bodily pain might seem simple, but at the cellular level it’s quite complex. When we’re injured, a diverse mixture of chemicals is released, and these chemicals cause pain by acting on an equally diverse group of receptors on the surface of pain-sensing neurons.

“A big problem in our field is that it is impractical to block each of these receptors with a mixture of drugs,” said Zylka, the senior author of the Neuron article and member of the UNC Neuroscience Center. “So we looked for commonalities – things that each of these receptors need in order to send a signal.” Zylka’s team found that the lipid PIP2 (phosphatidylinositol 4,5-bisphosphate) was one of these commonalities.

“So the question became: how do we alter PIP2 levels in the neurons that sense pain?” Zylka said. “If we could lower the level of PIP2, we could get these receptors to signal less effectively. Then, in theory, we could reduce pain.”

Many different kinases can generate PIP2 in the body.  Brittany Wright, a graduate student in Zylka’s lab, found that the PIP5K1C kinase was expressed at the highest level in sensory neurons compared to other related kinases. Then the researchers used a mouse model to show that PIP5K1C was responsible for generating at least half of all PIP2 in these neurons.

“That told us that a 50 percent reduction in the levels of PIP5K1C was sufficient to reduce PIP2 levels in the tissue we were interested in – where pain-sensing neurons are located” Zylka said. “That’s what we wanted to do – block signaling at this first relay in the pain pathway.”

Once Zylka and colleagues realized that they could reduce PIP2 in sensory neurons by targeting PIP5K1C, they teamed up with Stephen Frye, PhD, the Director of the Center for Integrative Chemical Biology and Drug Discovery at the UNC Eshelman School of Pharmacy.

They screened about 5,000 small molecules to identify compounds that might block PIP5K1C. There were a number of hits, but UNC3230 was the strongest. It turned out that Zylka, Frye, and their team members had come upon a drug candidate. They realized that the chemical structure of UNC3230 could be manipulated to potentially turn it into an even better inhibitor of PIP5K1C. Experiments to do so are now underway at UNC.

Text
Photo
Quote
Link
Chat
Audio
Video