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Activation of muscarinic receptors induces protein synthesis‐dependent long‐lasting depression in the perirhinal cortex
Author(s) -
Massey P. V.,
Bhabra G.,
Cho K.,
Brown M. W.,
Bashir Z. I.
Publication year - 2001
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.0953-816x.2001.01631.x
Subject(s) - perirhinal cortex , neuroscience , long term depression , chemistry , muscarinic acetylcholine receptor m1 , muscarinic acetylcholine receptor , muscarinic acetylcholine receptor m4 , muscarinic acetylcholine receptor m2 , receptor , biology , nmda receptor , recognition memory , biochemistry , ampa receptor , cognition
There is strong evidence that decrements in neuronal activation in perirhinal cortex when a novel stimulus is repeated provide a neural substrate of visual recognition memory. There is also strong evidence that muscarinic acetylcholine (ACh) receptors are involved in learning and memory. However, the mechanisms underlying neuronal decrements in the perirhinal cortex and the basis of ACh involvement in learning and memory are not understood. In an in vitro preparation of rat perirhinal cortex we now demonstrate that activation of ACh receptors by carbachol (CCh) produces long‐lasting depression (LLD) of synaptic transmission that is dependent on muscarinic M1 receptor activation. Crucially, the induction of this form of LLD requires neither N ‐methyl‐ d ‐aspartate receptor activation nor synaptic stimulation. CCh‐induced LLD was not blocked by the protein kinase C inhibitors staurosporine or BIM, or by the protein phosphatase inhibitor okadaic acid. However, each of cyclopiazonic acid (an agent that depletes intracellular calcium stores) and anisomycin (an inhibitor of protein synthesis) significantly reduced the magnitude of CCh‐induced LLD. These mechanisms triggered by muscarinic receptor activation could play a role in the induction and/or expression of certain forms of activity‐dependent long‐term depression in perirhinal cortex. An understanding of CCh‐induced LLD may thus provide clues to the mechanisms underlying lasting neuronal decrements that occur in the perirhinal cortex and hence for neural substrates of visual recognition memory.