Abstract
Fear-conditioning is a model of fear learning and anxiety. The lateral nucleus of the amygdala (LA) provides a critical link for relaying thalamic and cortical auditory information to the rest of the amygdala during the fear conditioning process. Alterations in excitatory synaptic transmission in the thalamic to LA pyramidal cells was studied using whole-cell patch clamp recordings in brain slices from fear-conditioned animals. Following paired stimulation of the thalamic afferents, paired-pulse depression (PPD) could be recorded at 200-ms to 2-s intervals. Increasing transmitter release by decreasing the Mg 2+/Ca 2+ ratio enhanced PPD suggesting that PPD is reflective of changes in release probability. Analysis of the pairs of composite, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl- d-aspartate (NMDA) receptor-mediated excitatory postsynaptic currents (EPSCs) showed that there was no correlation between EPSC pairs suggesting that PPD may be mediated through a release-independent mechanism of presynaptic origin. However, AMPA and NMDA receptor mediated PPD had a different time course and magnitude suggesting postsynaptic factors may be involved in PPD. After fear-conditioning PPD of the composite and AMPA receptor-mediated EPSCs was enhanced suggesting that neurotransmitter release may be increased in learned fear. The NMDA receptor-mediated PPD was however not altered in fear-conditioned animals. The differences in response of AMPA and NMDA receptor-mediated PPD suggest that postsynaptic mechanisms may also be involved in the expression of fear conditioning.
Published Version
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