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Pharmacological evidence for a role of long‐term potentiation in memory
Author(s) -
Izquterdo Ivan
Publication year - 1994
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.8.14.7958619
Subject(s) - long term potentiation , neuroscience , hippocampus , ampa receptor , memory consolidation , nmda receptor , long term depression , glutamate receptor , entorhinal cortex , metabotropic glutamate receptor , chemistry , biology , receptor , biochemistry
Memory processes and long‐term potentiation (LTP) are blocked at the time of their initiation by antagonists of glutamate NMDA or metabotropic receptors, by drugs that hinder the activity of carbon monoxide or the platelet‐activating factor, and by GABA type A receptor agonists. In the next 2 h, memory and LTP are accompanied by an enhancement of the activity of calcium/calmodulin‐dependent protein kinase II and of protein kinase C, and are blocked by inhibitors of these enzymes. At the time of expression, memory and LTP are blocked by antagonists of glutamate AMPA receptors. The effects of drugs on memory are seen upon their infusion into areas of the brain known to be responsible for the storage and retrieval of declarative memories (hippocampus, amygdala, medial septum, entorhinal cortex) and are both task‐ and structure‐specific. When put together with other pharmacologic findings, with lesion and recording studies, and with data on transgenic animals showing deficits of both memory and LTP, the data reviewed here lend strong support to the hypothesis that LTP in these brain areas underlies memory processes.—Izquierdo, I. Pharmacological evidence for a role of long‐term potentiation in memory. FASEB J. 8, 1139‐1145 (1994)