Afferents from rat temporal cortex synapse on lateral amygdala neurons that express NMDA and AMPA receptors.

The lateral nucleus of the amygdala (LA) is a critical component of the circuitry through which environmental stimuli are endowed with emotional meaning through association with painful or threatening events. Individual cells in LA receive convergent input from auditory processing areas in the thalamus and cortex, and the excitatory amino-acid L-glutamate (Glu) participates in synaptic transmission in both pathways. Previously, we characterized the ultrastructure of pre- and postsynaptic processes in the thalamo-amygdala pathway, and showed the relation of presynaptic inputs to N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydoxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor subunits. In the present study, we examined the nature of cortico-amygdala synaptic interactions with Glu receptors in LA and determined whether they are similar or different from those in the thalamo-amygdala pathway. Cortical afferents to the LA were identified by anterograde transport of biotinylated-dextran amine (BDA) and postsynaptic sites were labeled immunocytochemically using antisera directed against the R1 subunit the NMDA receptor, and the R1 and R2/3 subunits of the AMPA receptor. Electron microscopy revealed that the vast majority of cortical afferents (99%) synapse onto distal dendritic processes and most of these processes (62%) contained at least one glutamate receptor subtype. Cortical afferents synapsed on approximately the same proportion of immunoreactive targets for each glutamate receptor subtype examined. These data provide morphological evidence that cortical afferents form direct synaptic contacts with LA neurons that express both NMDA and AMPA receptors and are consistent with recent physiological studies demonstrating the participation of NMDA and AMPA receptors in cortico-amygdala-transmission. These results are nearly identical to those obtained in the studies of the thalamo-amygdala pathway. Copyright 1999 Wiley-Liss, Inc.