Abstract
It was recently found that temporary inactivation of the dorsal hippocampus with lidocaine impaired fear memory, whereas temporary inactivation of the ventral hippocampus did not. These site-specific deficits, however, may have resulted from disruption of axonal signals arriving from structures outside of the hippocampus, or from disruption of axons that pass through the hippocampus entirely. This is problematic because the hippocampus receives extensive afferent input from both the amygdala and the septum, which also play very important roles in fear and fear memory. To mitigate this problem, rats were infused with the GABA(A) receptor agonist muscimol, into either the dorsal or the ventral hippocampus, just after an "acquisition" session in which the rats were shocked from an electrified probe. A "retention" test in the same apparatus was conducted 24h later, when the hippocampus was no longer inactivated, and the probe was no longer electrified. Dorsal hippocampal inactivation just after acquisition impaired conditioned fear behavior (probe avoidance) during the retention test, whereas ventral hippocampal inactivation after acquisition did not. However, muscimol inactivation of the ventral hippocampus during an "acquisition"...Continue Reading
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