Afferents from the auditory thalamus synapse on inhibitory interneurons in the lateral nucleus of the amygdala.
Woodson W., Farb CR., Ledoux JE.
Physiological studies suggest that afferents to the lateral nucleus of the amygdala (LA) from the auditory thalamus initiate feedforward inhibition [Li et al. (1996b)]. This model of neural processing requires that thalamic afferents synapse directly onto inhibitory interneurons. To determine whether such synaptic contacts occur, we combined anterograde tract tracing with interneuron immunocytochemistry. The anterograde tracer biotinylated dextran amine (BDA) was injected into the auditory thalamus. Inhibitory interneurons in the LA were identified using antibodies directed against gamma aminobutyric acid (GABA) or one of the calcium binding proteins (CBPs), parvalbumin (PARV), calbindin (CALB), or calretinin (CALR), since CBPs identify distinct populations of GABAergic cells within the amygdala. The distribution of GABAergic and CBP interneurons in each subregion of the LA was examined by light microscopy and the relationships between thalamo-amygdala terminals and interneurons were examined by confocal and electron microscopy. Immunoreactive cells were distributed in all three subdivisions of LA, except for CALR-ir neurons, which were sparse in the dorsal subregion and were found mainly in the ventromedial and ventrolateral subregions. Confocal microscopy revealed some thalamo-amygdala terminals in close proximity to LA interneurons, while electron microscopy showed that thalamo-amygdala terminals made direct synaptic contacts onto distal dendritic processes of inhibitory neurons. These data provide morphological evidence that thalamic afferents synapse directly onto inhibitory interneurons in LA, and are consistent with the possibility that inputs from the auditory thalamus initiate feedforward inhibition in LA. This architecture could play an important role in the suppression of background neural noise, thereby enhancing the response of LA cells to incoming auditory stimuli.