Intrinsic ability to brain learning discovered emphasis (science daily)

PharmaLive.com (13 December 2010) - medical researchers have discovered a missing link which explains the interaction between the State of the brain and triggers neurons responsible for learning, potentially open new ways to stimulate cognitive function in the face of diseases like Alzheimer's as well as strengthen memory in healthy people.

Much is known processes neurons which occur in learning so far was not clear why it occurs in some States of the brain, but not others. Now researchers at the University of Bristol were able to study specific neurotransmitter that promotes learning and memory in isolation.

Acetylcholine is released into the brain to learning and is essential for the acquisition of new memories. Its role is to facilitate the activity of NMDA, protein receptors that control the strength of the connections between nerve cells in the brain.

Currently, the only effective treatment for the symptoms of cognitive impairment seen in diseases like Alzheimer's disease is through the use of drugs that increase the amount of the release of acetylcholine and thereby improve cognitive functions.

Describing their findings in the journal Neuron, Physiology and pharmacology of Bristol school researchers demonstrated acetylcholine facilitates NMDA receptors by inhibiting the activity of others channels SK whose normal role is to limit the activity of the NMDA receptor proteins.

This Discovery Channel SK role provides new insights into the mechanisms underlying learning and memory. SK channels normally act as an obstacle to the function of the NMDA receptor, preventing changes in resistance of the connections between nerve cells and therefore limit the ability of the brain to encode souvenirs. This most recent search results show that canal SK barrier can be removed by the release of acetylcholine in the brain to enhance our ability to learn and recall information.

Principal investigator, Dr. Jack Mellor, Faculty of medicine at the University of Bristol, said: "these findings will not revolutionize the treatment of Alzheimer's disease or other forms of cognitive impairment from one day to the next." However, national and international funding agencies have recently been aging and dementia research a priority so we expect many progress more in our understanding of the mechanisms underlying learning and memory in health and disease. »

The team studied the effects of drugs that target acetylcholine receptors and SK channels on the resistance of the connections between nerve cells in the animal brain tissue. They found that changes in the strength of connection was facilitated by the presence of drugs which activate acetylcholine receptors or block channels SK revealing the relationship between the two proteins.

Dr. Mellor said: "therapeutic point of view, this study suggests that certain medications that affect specific acetylcholine receptors can be very attractive as potential treatments for cognitive disorders." Currently, only effective treatments for patients with Alzheimer's disease are drugs that boost the effectiveness of the naturally released acetylcholine. We have shown that mimic the effect of the acetylcholine to specific receptors that facilitates change in resistance of the connections between nerve cells. This could potentially be beneficial for patients with schizophrenia and Alzheimer's disease. »

CRM Center of the University of Bristol in synaptic plasticity and Division of neurosciences in the school of Physiology involved research team & Pharmacology, part of the Bristol neuroscience network. This work was supported by the Wellcome Trust, CRM, BBSRC and GSK.

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Source of the story:

The story above is reproduced (with drafting adaptations by staff at PharmaLive.com) materials provided by University of Bristol.

Reference of the review:

Buchanan KA, Petrovic MM, SEL de Chamberlain, M. NV & Mellor. facilitation of M1 muscarinic receptor long-term potentiation is mediated inhibition of SK channels. Neuron, DOI: 10.1016/j.neuron.2010.11.018

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