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Potassium-induced long-term potentiation in area CA1 of the hippocampus involves phospholipase activation

✍ Scribed by Julie Bernard; Ahmed Lahsaini; Dr. Guy Massicotte

Publisher
John Wiley and Sons
Year
1994
Tongue
English
Weight
781 KB
Volume
4
Category
Article
ISSN
1050-9631

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✦ Synopsis

Abstract

Previous studies have shown that potassium‐induced long‐term potentiation (LTP) of the Schaffer collateral/commissural synapses in area CA1 of the hippocampus shares common properties with tetanus‐induced LTP. In the present investigation, we performed electrophysiological and binding experiments on CA1 hippocampal slices to evaluate the location and nature of the changes underlying potassium‐induced LTP. Paired‐pulse facilitation, which represents an index of transmitter release, was markedly reduced by potassium‐induced LTP. In addition, KC1‐induced LTP was associated with an increase in ^3^H‐AMPA ([^3^H]‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate) binding to CA1 synaptic membranes when measured 40 min after high‐potassium exposure; however, no changes were detected in binding of an antagonist ([^3^H]‐6‐cyano‐7‐nitroquinoxaline‐2,3‐dione; ^3^H‐CNQX) to AMPA receptors in slices expressing KC1‐induced LTP. Administration of the phospholipase A~2~ (PLA~2~) inhibitor bromophenacyl bromide (BPB) prior to potassium application prevented LTP formation as well as the changes in paired‐pulse facilitation and ^3^H‐AMPA binding that characterized this type of potentiation. Taken together, these data indicate that potassium‐in‐duced LTP may be related to modifications in both pre‐and postsynaptic properties and confirm the hypothesis that PLA~2~ activation is an important mechanism in long‐term changes of synaptic operation. © 1994 Wiley‐Liss, Inc.

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