Effect of unpredictable stress on cognition and brain acetylcholinesterase activity in adult and aged mice

Long-term potentiation (LTP) is a long-lasting enhancement of synaptic function induced by a brief high-frequency tetanus. Excitatory amino acids (EAA), particularly glutamate and aspartate are a topic of increasing research interest with regard to their proposed involvement in the pathogenesis of a variety of neurological and psychiatric disorders, some of which are associated with a loss of learning and memory abilities. LTP of excitatory synaptic transmission is a candidate for the neural mechanism underlying learning and memory. LTP has certian properties and characteristics that coincide with voltage-dependent properties of N-methyl-D aspartate (NMDA) receptor. In hippocampal CA1 area, there are at least two forms of LTP, one is NMDA receptor-dependent LTP, and the other is NMDA receptor-independent LTP. Excitatory pathways that utilize NMDA receptors are also involved in the initiation of seizures and their propagation. These NMDA-induced convulsions can be reversed by anticonvulsant drugs or NMDA antagonists. There are reports suggesting that a significant number of people with epilepsy have cognitive difficulties and impaired memory. Some epileptic patients show memory dysfunctions associated with chronic anticonvulsant therapy. Some anticonvulsant drugs which interfere with NMDA receptor system directly or indirectly, possibly influence the expression of LTP. Long-term depression (LTD) is also being considered as a candidate mechanism for memory formation in hippocampus. LTP and LTD also share a few common features. Some areas which remain to be explored include:- Will LTP and the NMDA receptor turn out to be the true molecular foundations of human memory? To what extent the link between LTP and NMDA systems mediate epilepsy