CHOLINERGIC NEUROTRANSMISSION AND SYNAPTIC PLASTICITY CONCERNING MEMORY PROCESSING

The brain is able to change the synaptic strength in response to stimu li that leave a memory trace. Long-term potentiation (LTP) and long-te rm depression (LTD) are forms of activity-dependent synaptic plasticit y proposed to underlie memory. The induction of LTP appears mediated b y glutamate acting on AMPA and then on NMDA receptors. Cholinergic mus carinic agonists facilitate learning and memory. Acetylcholine depolar izes pyramidal neurons, reduces inhibition, upregulates NMDA channels and activates the phosphoinositide cascade. Postsynaptic Ca2+ rises an d stimulates Ca-dependent PK, promoting synaptic changes. Electroencep halographic desynchronization and hippocampal theta rhythm are related to learning and memory, are inducible by cholinergic agonists and eli cited by hippocampal cholinergic terminals. Their loss results in memo ry deficits. Hence, cholinergic pathways may act synergically with glu tamatergic transmission, regulating and leading to synaptic plasticity . The stimulation that induces plasticity in vivo has not been establi shed. The patterns for LTP/LTD induction in vitro may be due to the lo ss of ascending cholinergic inputs. As a rat explores pyramidal cells fire bursts that could be relevant to plasticity.