Dec 9, 2010 13:48 GMT  ·  By
Neuromuscular junction: 1. presynaptic terminal, 2. sarcolemma, 3. synaptic vesicles, 4. Acetylcholine receptors, 5. mitchondrion
   Neuromuscular junction: 1. presynaptic terminal, 2. sarcolemma, 3. synaptic vesicles, 4. Acetylcholine receptors, 5. mitchondrion

A team of medical researchers from the University of Bristol have found the explanation for the interaction between brain state and the neural triggers responsible for learning.

This discovery could open the way to new methods of strengthening cognitive functions in people suffering from debilitating diseases like Alzheimer’s, but also help improve memory in healthy individuals.

What makes this finding really exciting is the fact that the researchers from Bristol’s School of Physiology and Pharmacology, were able to study, in isolation, the exact neurotransmitter that enhances learning and memory – acetylcholine.

They studied the effects that drugs targeting acetylcholine receptors and SK channels have on the force of the connections between nerve cells in animal brain tissue.

They found out that administrating drugs that activate acetylcholine receptors or block SK channels, made changing the connection strength much easier, thus establishing a link between the two proteins.

Lead researcher Dr Jack Mellor, from the University of Bristol’s Medical School said that “from a therapeutic point of view, this study suggests that certain drugs that act on specific acetylcholine receptors may be highly attractive as potential treatments for cognitive disorders.

“Currently, the only effective treatments for patients with Alzheimer’s disease are drugs that boost the effectiveness of naturally released acetylcholine.

“We have shown that mimicking the effect of acetylcholine at specific receptors facilitates changes in the strength of connections between nerve cells.

“This could potentially be beneficial for patients suffering from Alzheimer’s disease or schizophrenia.”

During learning, acetylcholine is released in the brain where it boosts the capacity of acquiring new memories, by facilitating the activity of the NMDA receptors – proteins in charge of the strength of the connections between nerve cells, within the brain.

The researchers have shown that acetylcholine facilitates NMDA receptors by inhibiting other proteins called SK channels, which normally restrict NMDA receptors' activity.

They do so by preventing changes in the strength of nerve cells connections, weakening the brain's ability to encode memories.

Releasing acetylcholine removes the SK barrier, and enhances the brain’s capacity of learning and remembering information.

Still, Dr Mellor said that “these findings are not going to revolutionize the treatment of Alzheimer’s disease or other forms of cognitive impairment overnight.

“However, national and international funding bodies have recently made research into aging and dementia a top priority so we expect many more advances in our understanding of the mechanisms underlying learning and memory in both health and disease.”

The researchers were affiliated to the University of Bristol’s MRC Center for Synaptic Plasticity and the Division of Neuroscience in the School of Physiology & Pharmacology, part of the Bristol Neuroscience network, and their work was supported by the Wellcome Trust, MRC, BBSRC and GSK.

The results are described in the journal Neuron.