'Rewired brain' revives patient after 19 years | New Scientist
newscientist.com(03 July 2006) A study of the “miraculous” recovery of a man who spent 19 years in a minimally conscious state has revealed the likely cause of his regained consciousness.
The findings suggest the human brain shows far greater potential for recovery and regeneration then ever suspected. It may also help doctors predict their patients’ chances of improvement. But the studies also highlight gross inadequacies in the system for diagnosing and caring for patients in vegetative or minimally conscious states.
Reduced use of a limb proves the power of brain elasticity
Swiss scientists have shown that breaking your arm can greatly affect your brain. It appears that immobilising the broken limb reduces the thickness of part of the cerebral cortex. Professor Lutz Jäncke and colleagues at the University of Zurich in Switzerland report their findings in the journal Neurology this week.
The motor cortex on the left side of the brain controls the right arm, and the team found that its thickness had decreased significantly in response to the arm’s lack of use. They also found thinning in the fibre tract.“What we have found so far from studies on the plasticity of the brain is that we need to use it or lose it”, says Jäncke.
Jäncke thinks his findings may have relevance for ‘constraint-induced therapy’ which is often used in stroke victims. In this therapy, when a stroke has affected one arm of a patient, the remaining (good) arm is immobilised using a sling, forcing the patient to use and improve their stroke-affected limb. Jäncke’s work suggests that the motor cortex controlling the good arm will thin with disuse.
(via DiscoveryNews)
Bursts of Brain Activity May Protect Against Alzheimer's Disease
TAU reveals the missing link between brain patterns and Alzheimer’s
Evidence indicates that the accumulation of amyloid-beta proteins, which form the plaques found in the brains of Alzheimer’s patients, is critical for the development of Alzheimer’s disease, which impacts 5.4 million Americans. And not just the quantity, but also the quality of amyloid-beta peptides is crucial for Alzheimer’s initiation. The disease is triggered by an imbalance in two different amyloid species — in Alzheimer’s patients, there is a reduction in a relative level of healthy amyloid-beta 40 compared to 42.
Now Dr. Inna Slutsky of Tel Aviv University’s Sackler Faculty of Medicine and the Sagol School of Neuroscience, with postdoctoral fellow Dr. Iftach Dolev and PhD student Hilla Fogel, have uncovered two main features of the brain circuits that impact this crucial balance. The researchers have found that patterns of electrical pulses (called “spikes”) in the form of high-frequency bursts and the filtering properties of synapses are crucial to the regulation of the amyloid-beta 40/42 ratio. Synapses that transfer information in spike bursts improve the amyloid-beta 40/42 ratio.
This represents a major advance in understanding that brain circuits regulate composition of amyloid-beta proteins, showing that the disease is not just driven by genetic mutations, but by physiological mechanisms as well. Their findings were recently reported in the journal Nature Neuroscience.
Tipping the balance
High-frequency bursts in the brain are critical for brain plasticity, information processing, and memory encoding. To check the connection between spike patterns and the regulation of amyloid-beta 40/42 ratio, Dr. Dolev applied electrical pulses to the hippocampus, a brain region involved in learning and memory.
When increasing the rate of single pulses at low frequencies in rat hippocampal slices, levels of both amyloid-beta 42 and 40 grew, but the 40/42 ratio remained the same. However, when the same number of pulses was distributed in high-frequency bursts, researchers discovered an increased amyloid-beta 40 production. In addition, the researchers found that only synapses optimized to transfer encoded by bursts contributed towards tipping the balance in favor of amyloid-beta 40. Further investigations conducted by Fogel revealed that the connection between spiking patterns and the type of amyloid-beta produced could revolve around a protein called presenilin. “We hypothesize that changes in the temporal patterns of spikes in the hippocampus may trigger structural changes in the presenilin, leading to early memory impairments in people with sporadic Alzheimer’s,” explains Dr. Slutsky.
Behind the bursts
According to Dr. Slutsky, different kinds of environmental changes and experiences — including sensory and emotional experience — can modify the properties of synapses and change the spiking patterns in the brain. Previous research has suggested that a stimulant-rich environment could be a contributing factor in preventing the development of Alzheimer’s disease, much as crossword and similar puzzles appear to stimulate the brain and delay the onset of Alzheimer’s. In the recent study, the researchers discovered that changes in sensory experiences also regulate synaptic properties — leading to an increase in amyloid-beta 40.
In the next stage, Dr. Slutsky and her team are aiming to manipulate activity patterns in the specific hippocampal pathways of Alzheimer’s models to test if it can prevent the initiation of cognitive impairment. The ability to monitor dynamics of synaptic activity in humans would be a step forward early diagnosis of sporadic Alzheimer’s.
will-we-ever-have-a-fully-digital-brain
technologyreview.comfunny to phrase this as a question when the answer is a hearty maybe
What Fragile X Syndrome Tells Us About Brain Plasticity
Basically, this means that FXS syndrome is directly related to impaired plasticity of these synaptic connection, which is necessary for normal learning and cognition. FXS brains appear less flexible, which supports the idea that certain genes are necessary for normal brain functioning.
Research has clearly been established showing that post-synaptic processes, meaning processes on the receiving neuron, are crucial for plasticity. A new study in FXS mice shows that pre-synaptic processes, which occur on the transmitting neuron, are also crucial. While post-synaptic processes control long-term plasticity, pre-synaptic processes control short-term plasticity. The new study shows that both are disrupted in FXS.
I've been looking for scholarly articles on neurotransmitters and their relations to learning, and memory. Would you be able to recommend any? Greatly appreciated.
Mol Neurobiol. 2011 Dec;44(3):449-64. doi: 10.1007/s12035-011-8214-0. Epub 2011 Nov 11.
Serotonin and prefrontal cortex function: neurons, networks, and circuits.Source
The Picower Institute for Learning and Memory and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. mvpuig@mit.edu
Abstract
Higher-order executive tasks such as learning, working memory, and behavioral flexibility depend on the prefrontal cortex (PFC), the brain region most elaborated in primates. The prominent innervation by serotonin neurons and the dense expression of serotonergic receptors in the PFC suggest that serotonin is a major modulator of its function. The most abundant serotonin receptors in the PFC, 5-HT1A, 5-HT2A and 5-HT3A receptors, are selectively expressed in distinct populations of pyramidal neurons and inhibitory interneurons, and play a critical role in modulating cortical activity and neural oscillations (brain waves). Serotonergic signaling is altered in many psychiatric disorders such as schizophrenia and depression, where parallel changes in receptor expression and brain waves have been observed. Furthermore, many psychiatric drug treatments target serotonergic receptors in the PFC. Thus, understanding the role of serotonergic neurotransmission in PFC function is of major clinical importance. Here, we review recent findings concerning the powerful influences of serotonin on single neurons, neural networks, and cortical circuits in the PFC of the rat, where the effects of serotonin have been most thoroughly studied.
Mol Brain. 2010 May 13;3:15. doi: 10.1186/1756-6606-3-15.
Emotional enhancement of memory: how norepinephrine enables synaptic plasticity.Source
Department of Psychiatry, McLean Hospital, Harvard Medical School, 115 Mill Street, Belmont, Massachusetts 02478, USA. ktully@mclean.harvard.edu
Abstract
Changes in synaptic strength are believed to underlie learning and memory. We explore the idea that norepinephrine is an essential modulator of memory through its ability to regulate synaptic mechanisms. Emotional arousal leads to activation of the locus coeruleus with the subsequent release of norepineprine in the brain, resulting in the enhancement of memory. Norepinephrine activates both pre- and post-synaptic adrenergic receptors at central synapses with different functional outcomes, depending on the expression pattern of these receptors in specific neural circuitries underlying distinct behavioral processes. We review the evidence for noradrenergic modulation of synaptic plasticity with consideration of how this may contribute to the mechanisms of learning and memory.
Neuropharmacology. 2010 Jun;58(7):951-61. doi: 10.1016/j.neuropharm.2010.01.008. Epub 2010 Jan 21.
Neurotransmitter roles in synaptic modulation, plasticity and learning in the dorsal striatum.Source
Laboratory for Integrative Neuroscience, NIAAA/NIH, 5625 Fishers Lane, Rockville, MD 20852, USA. lovindav@mail.nih.gov
Abstract
The dorsal striatum is a large forebrain region involved in action initiation, timing, control, learning and memory. Learning and remembering skilled movement sequences requires the dorsal striatum, and striatal subregions participate in both goal-directed (action-outcome) and habitual (stimulus-response) learning. Modulation of synaptic transmission plays a large part in controlling input to as well as the output from striatal medium spiny projection neurons (MSNs). Synapses in this brain region are subject to short-term modulation, including allosteric alterations in ion channel function and prominent presynaptic inhibition. Two forms of long-term synaptic plasticity have also been observed in striatum, long-term potentiation (LTP) and long-term depression (LTD). LTP at glutamatergic synapses onto MSNs involves activation of NMDA-type glutamate receptors and D1 dopamine or A2A adenosine receptors. Expression of LTP appears to involve postsynaptic mechanisms. LTD at glutamatergic synapses involves retrograde endocannabinoid signaling stimulated by activation of metabotropic glutamate receptors (mGluRs) and D2 dopamine receptors. While postsynaptic mechanisms participate in LTD induction, maintained expression involves presynaptic mechanisms. A similar form of LTD has also been observed at GABAergic synapses onto MSNs. Studies have just begun to examine the roles of synaptic plasticity in striatal-based learning. Findings to date indicate that molecules implicated in induction of plasticity participate in these forms of learning. Neurotransmitter receptors involved in LTP induction are necessary for proper skill and goal-directed instrumental learning. Interestingly, receptors involved in LTP and LTD at glutamatergic synapses onto MSNs of the “indirect pathway” appear to have important roles in habit learning. More work is needed to reveal if and when synaptic plasticity occurs during learning and if so what molecules and cellular processes, both short- and long-term, contribute to this plasticity.
(c) 2009. Published by Elsevier Ltd.
Curr Med Chem. 2009;16(7):796-840.
Neuro-transmitters in the central nervous system & their implication in learning and memory processes.Reis HJ, Guatimosim C, Paquet M, Santos M, Ribeiro FM, Kummer A, Schenatto G, Salgado JV, Vieira LB, Teixeira AL, Palotás A.
Abstract
This review article gives an overview of a number of central neuro-transmitters, which are essential for integrating many functions in the central nervous system (CNS), such as learning, memory, sleep cycle, body movement, hormone regulation and many others. Neurons use neuro-transmitters to communicate, and a great variety of molecules are known to fit the criteria to be classified as such. A process shared by all neuro-transmitters is their release by excocytosis, and we give an outline of the molecular events and protein complexes involved in this mechanism. Synthesis, transport, inactivation, and cellular signaling can be very diverse when different neuro-transmitters are compared, and these processes are described separately for each neuro-transmitter system. Here we focus on the most well known neuro-transmitters: acetyl-choline, catechol-amines (dopamine and nor-adrenalin), indole-amine (serotonin), glutamate, and gamma-amino-butyric acid (GABA). Glutamate is the major excitatory neuro-transmitter in the brain and its actions are counter-balanced by GABA, which is the major inhibitory substance in the CNS. A balance of neuronal transmission between these two neuro-transmitters is essential to normal brain function. Acetyl-choline, serotonin and catechol-amines have a more modulatory function in the brain, being involved in many neuronal circuits. Apart from summarizing the current knowledge about the synthesis, release and receptor signaling of these transmitters, some disease states due to alteration of their normal neuro-transmission are also described.
Prog Brain Res. 2008;172:567-602. doi: 10.1016/S0079-6123(08)00927-8.
Serotonin/dopamine interaction in learning.Olvera-Cortés ME, Anguiano-Rodríguez P, López-Vázquez MA, Alfaro JM.
Source
Laboratorio de Neurofisiología Experimental, Centro de Investigación Biomédica de Michoacán, Instituto Mexicano del Seguro Social, Morelia, México. maesolco@yahoo.com
Abstract
Dopamine (DA)-serotonin interactions dealing with learning and memory functions have been apparent from experimental approaches over the past decade. However, since the former evidence showing that these cerebral neurotransmitter systems are involved in the regulation of the same cognitive processes, few experimental studies have been done to further clarify the nature of DA-serotonin interactions for cognitive processes sharing common brain structures. Nevertheless, a regulatory role of 5-HT/DA interactions in cognition and the prefrontal cortex (PFC) and the striatum as a neuroanatomical substrate for these DA/5-HT interactions, are now recognized. Experimental evidence indicates that pharmacological disruption of serotonin neurotransmission results in a facilitative effect on the processing of mnemonic information by cerebral regions under strong, functional DA modulation, such as the striatum and the PFC; on the other hand, increased serotonin neurotransmission appears to have a detrimental effect on cognitive functions integrated in these structures. These effects seem to occur through the interaction of different pre- and postsynaptic DA and serotonin receptor subtypes acting as opposite systems underlying cognitive abilities. Some studies, focused on DA-serotonin interactions underlying the pathophysiology of neurological and psychiatric diseases, which evolve with cognitive dysfunctions in human beings, have shown that drugs that are able to modify DA or serotonin neurotransmission may exert beneficial effects on cognitive functions, even though improvement of motor, mood and behavioural disturbances are the main objectives of pharmacological treatment of these diseases. The complete significance of DA-serotonin interactions in cognitive functions could be addressed by future experimental and clinical studies.
Hi!
I searched and found these on PubMed. The first 3 are available as free downloads. Enjoy!
Our brain structure changes after two hours of learning.
mindblog.dericbownds.netby Deric Bownds
Sagi and colleagues have provided the first evidence that rapid structural plasticity can be detected in humans after just 2 hr of playing a video game. To assess brain structure they used diffusion magnetic resonance imaging, a technique sensitive to the self-diffusion of water molecules that depends on tissue architecture (how freely water diffuses depends on the space between the objects such as neurons, glia, and blood vessels, that it is moving through). They showd that only two hours of learning can cause a mean diffusivity reduction in the human hippocampus. In a similar supporting study on rats, the authors were able to show that changes in brain derived neurotropic growth (BDNF) factor correlated with the structural change measured by MRI. I’m passing on the abstract, and for those of you who like data, one of the figures from their paper.
The timescale of structural remodeling that accompanies functional neuroplasticity is largely unknown. Although structural remodeling of human brain tissue is known to occur following long-term (weeks) acquisition of a new skill, little is known as to what happens structurally when the brain needs to adopt new sequences of procedural rules or memorize a cascade of events within minutes or hours. Using diffusion tensor imaging (DTI), an MRI-based framework, we examined subjects before and after a spatial learning and memory task. Microstructural changes (as reflected by DTI measures) of limbic system structures (hippocampus and parahippocampus) were significant after only 2 hr of training. This observation was also found in a supporting rat study. We conclude that cellular rearrangement of neural tissue can be detected by DTI, and that this modality may allow neuroplasticity to be localized over short timescales.
Figure (Click on figure to enlarge it) - Structural Remodeling of Brain Tissue, Measured by DTI as Changes in MD after 2 hr of Training on a Spatial Learning and Memory TaskThe following statistical analyses were employed: paired t tests between the MD maps before and after the task in the learning group (A and F); planned comparisons analysis of the learning versus control groups with respect to scan time with predicated effect in the learning group only (B and G); and linear effect between groups (C and H) as well as a group by time interaction following ANOVA (D and I). The effects were found in the left hippocampus (A–D) and right parahippocampus (F–I). The parametric maps in these images were generated at a significance level of p less than 0.005 (uncorrected). The enlarged subset in those images indicates the significant voxels following correction for multiple comparisons (p less than 0.05, corrected). In the enlarged subset the corrected p value color scale is between 0.005 and 0.05. L indicates the left side of the brain. (E) and (J) show the MD values in the clusters in the subset of (A) and (F) (mean ± SEM). (K) shows the correlation analysis between subjects’ improvement rates (see Figure 1) and decrease in MD in the right parahippocampus (of the cluster in F).
Random Fact #24: Plasticity.
Oh come on, sinong hindi? Hahaha! I mean, lahat ng tao may traits na ganyan, maging sino ka man. Presidente, mga politiko, mga pari o madre, o maging ordinaryong tao ka man. Lahat ng tao, PLASTIC.
At, oo, aminado ako na ganito rin ako. Di naman maiiwasan. Di naman kasi lahat ng tao magugustuhan mo, mapplease mo at pwede mong pakisamahan ng maayos. Kaya nga kahit sabihing plastic ka, tanggapin nalang, totoo naman kasi. Wag nang i-deny. Act of man yan, hindi moral act. :)))
The synaptic web concept
The Internet is constantly evolving. As the speed, flexibility and complexity of connections increase exponentially, the Web looks more and more like a biological brain.
In the brain, it is the density and flexibility of the connections between neurons, not simply neurons themselves, which are the root of intelligence. The chemically-mediated connections are called “synapses”.
Even if the total number of brain cells, or neurons, begins to diminish in early adulthood, our ability to generate new connections between neurons – what neurologist call “plasticity” – persists throughout life. And plasticity can increase with exercise.
Neurology provides a metaphor for the web organization so called “the synaptic web” in that the connections between objects are more important than the object themselves.
In that web, plasticity (the speed and flexibility of connection making) and the synapse (the bridge that occurs between the gap of two neurons) are critical to forming bundles of connections (the thing that scientists believe determines intelligence).
In a web of connections (of data, people, information, profiles, communities, etc), the way connections bundle and un-bundle to form ever-changing, emergent properties provides intelligence
Neural Plasticity of Development and Learning
onlinelibrary.wiley.comthis is an interesting article using detailed neuro-imaging, behavioral studies, and developmental studies that describes the interaction between two of the underlying mechanisms for neural plasticity, both in adults and children.
it’s interesting to see the timetables of plasticity for children and adults at certain tasks (for example, learning a language has a timetable that is biased towards youth), which makes me wonder what other things we’ll discover (in terms of tasks that adults are more suited to learning with experience-dependent mechanisms).
