Abstract
GABAergic neurons regulate different aspects of information processing in the amygdala. Among these are clusters of intercalated cells (ITCs), which have been implicated in fear-related behaviors. Although a few of the ITC clusters have been studied, the functional role of apical ITCs (apITCs) is unknown. Here, we combine monosynaptic rabies tracing with optogenetics and demonstrate that apITCs receive synaptic input from medial geniculate nucleus (MGm), posterior intralaminar nucleus (PIN), and medial dorsal nucleus of the thalamus and from a diverse range of cortical areas including temporal association, entorhinal, insular, piriform, and somatosensory cortex. Upon fear learning, PIN/MGm inputs are strengthened, indicative of their involvement in fear behaviors. 3-D reconstruction of apITCs reveals local arborization and innervation of the dorsal striatum and lateral amygdala. We further show that apITCs provide sensory feedforward inhibition to LA principal cells, a putative mechanism for controlling plasticity during fear learning.
Highlights
Fear and anxiety are adaptive responses expressed in anticipation of, or while experiencing stimuli perceived as threatening (Pape and Pare, 2010)
The medial part of the medial geniculate nucleus (MGm) and temporal association cortex (TeA) are thought to relay the necessary auditory information, whereas somatosensory information arrives from posterior intralaminar nucleus of the thalamus (PIN) (Romanski et al, 1993; Shi and Cassell, 1998)
This convergence of auditory and somatosensory information enables the strengthening of CS inputs via N-methyl D-aspartate (NMDA) receptor-dependent associative long-term potentiation (LTP) in the amygdala, which is required for fear learning (Nabavi et al, 2014; Pape and Pare, 2010)
Summary
Fear and anxiety are adaptive responses expressed in anticipation of, or while experiencing stimuli perceived as threatening (Pape and Pare, 2010). The medial part of the medial geniculate nucleus (MGm) and temporal association cortex (TeA) are thought to relay the necessary auditory information, whereas somatosensory information arrives from posterior intralaminar nucleus of the thalamus (PIN) (Romanski et al, 1993; Shi and Cassell, 1998). This convergence of auditory and somatosensory information enables the strengthening of CS inputs via N-methyl D-aspartate (NMDA) receptor-dependent associative long-term potentiation (LTP) in the amygdala, which is required for fear learning (Nabavi et al, 2014; Pape and Pare, 2010)
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