Abstract
Acute swim stress of mice produces increases in the density of high and low affinity binding sites in the brain for the inhibitory neurotransmitter γ-aminobutyric acid (GABA), together with analgesia as measured by an increase in tail flick latency. Apparent tolerance develops an repeated swimming with analgesia and GABA binding returning towards control levels. The time course of analgesia and Increases in GABA binding following a single swim are also similar. Acute swim stress does not alter diazepam binding. GABA systems may be important in analgesia and in responses to environmental stress.
Published Version
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