Free radicals accelerate the decay of long-term potentiation in field CA1 of guinea-pig hippocampus.

Abstract:

:Free radicals have been implicated in a number of pathological conditions. To evaluate the neurophysiological consequences of free radical exposure, slices of hippocampus isolated from guinea-pigs were exposed to hydrogen peroxide which reacts with tissue iron to generate hydroxyl free radicals. Long-term potentiation, a sustained increase in synaptic responses, was elicited in field CA1 by high frequency stimulation of an afferent pathway. We found that 0.002% peroxide did not directly affect the responses evoked by stimulation of the afferent pathway but did prevent maintenance of long-term potentiation. Short-term potentiation and paired-pulse facilitation were not affected by peroxide treatment. Peroxide was less effective if removed following high frequency stimulation and was ineffective if applied only after high frequency stimulation. Input/output analysis showed that the increase in synaptic efficacy was reduced with peroxide treatment. Changes in the enhanced ability of the synaptic potential to generate a spike were less apparent. These data show that the interference of free radicals with long-term potentiation may contribute to pathological deficits. It is possible that intracellular calcium regulation is disrupted by peroxide treatment. A number of second messenger systems involved with long-term potentiation are potential targets for free radical attack.

journal_name

Neuroscience

journal_title

Neuroscience

authors

Pellmar TC,Hollinden GE,Sarvey JM

doi

10.1016/0306-4522(91)90060-2

keywords:

subject

Has Abstract

pub_date

1991-01-01 00:00:00

pages

353-9

issue

2

eissn

0306-4522

issn

1873-7544

pii

0306-4522(91)90060-2

journal_volume

44

pub_type

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