Cholinergic neurotransmission and synaptic plasticity concerning memory processing

被引:126
作者
Jerusalinsky, D [1 ]
Kornisiuk, E [1 ]
Izquierdo, I [1 ]
机构
[1] UNIV FED RIO GRANDE SUL, INST BIOCIENCIAS, CTR MEM, BR-90049 PORTO ALEGRE, RS, BRAZIL
关键词
cholinergic transmission; muscarinic receptors; memory; synaptic plasticity; LTP;
D O I
10.1023/A:1027376230898
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The brain is able to change the synaptic strength in response to stimuli that leave a memory trace. Long-term potentiation (LTP) and long-term depression (LTD) are forms of activity-dependent synaptic plasticity proposed to underlie memory. The induction of LTP appears mediated by glutamate acting on AMPA and then on NMDA receptors. Cholinergic muscarinic agonists facilitate learning and memory. Acetylcholine depolarizes pyramidal neurons, reduces inhibition, upregulates NMDA channels and activates the phosphoinositide cascade. Postsynaptic Ca2+ rises and stimulates Ca-dependent PK, promoting synaptic changes. Electroencephalographic desynchronization and hippocampal theta rhythm are related to learning and memory, are inducible by cholinergic agonists and elicited by hippocampal cholinergic terminals. Their loss results in memory deficits. Hence, cholinergic pathways may act synergically with glutamatergic transmission, regulating and leading to synaptic plasticity. The stimulation that induces plasticity in vivo has not been established. The patterns for LTP/LTD induction in vitro may be due to the loss of ascending cholinergic inputs. As a rat explores pyramidal cells fire bursts that could be relevant to plasticity.
引用
收藏
页码:507 / 515
页数:9
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