Abstract
Although conditioned fear has been shown to involve mechanisms of synaptic plasticity in the amygdala, the association with afferent input systems is not yet clear. Here we report on homosynaptic long-term depression (LTD) of excitatory responses after stimulation of putative thalamic input fibers, but not of cortical inputs, to the rat lateral amygdala in vitro. LTD is induced by theta frequency stimulation and involves postsynaptic calcium-dependent mechanisms and group II metabotropic glutamate receptors. These input-specific changes in synaptic strength represent potential cellular sources, which regulate the balance between sensory thalamic and cortical input signals to the amygdala. This regulation would function to reduce the influence of relatively undiscriminated stimulus information carried by thalamic afferents in favor of discriminated sensory information mediated by the cortex during fear responses.
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