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Persistent inhibition of hippocampal long-term potentiation in vivo by learned helplessness stress

✍ Scribed by Benedict K. Ryan; Barbara Vollmayr; Igor Klyubin; Peter Gass; Michael J. Rowan

Publisher
John Wiley and Sons
Year
2009
Tongue
English
Weight
240 KB
Volume
20
Category
Article
ISSN
1050-9631

No coin nor oath required. For personal study only.

✦ Synopsis

Abstract

The persistent cognitive disruptive effects of stress have been strongly implicated in the pathophysiology of depression and post‐traumatic stress disorder. Here we examined factors influencing the time course of recovery from the inhibitory effect of acute inescapable stressors on the ability to induce long‐term potentiation (LTP) in the dorsal hippocampus in vivo. We tested different forms of LTP, different stressors and different inbred strains of rats. Acute elevated platform stress completely, but transiently (<3 h), inhibited induction of both NMDA receptor‐dependent LTP induced by a standard high frequency (200 Hz) conditioning stimulus and an additional LTP that required voltage‐dependent Ca^2+^ channel activation triggered by strong (400 Hz) conditioning stimulation. In contrast, acute inescapable footshock stress, used to study learned helplessness, inhibited LTP for at least 4 weeks. Contrary to expectations, there was no clear relationship between the ability of the footshock to trigger helpless behavior, a model of stress‐induced depression, and the magnitude of LTP inhibition. Moreover, LTP did not appear to be affected by genetic susceptibility to learned helplessness, a model of genetic vulnerability to depression. This long‐lasting synaptic plasticity disruption may underlie persistent impairment of hippocampus‐dependent cognition by excessive acute inescapable stress. © 2009 Wiley‐Liss, Inc.

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