Research finds neural activity changes in the amygdala affect ingestion of quinine in transgenic mice, suggesting key roles in taste processing.
Several forebrain areas project to the rostral gustatory portion of the nucleus of the solitary tract (rNST), where they modulate processing of oral gustatory signals. Among them, the central nucleus of the amygdala (CeA) provides descending input via somatostatin-expressing (Sst) neurons, where suppression of CeA/Sst-to-rNST neural activity alters ingestion of the bitter tastant quinine. Together, these results indicate that the regulation of ingestive behavior involves descending neuromodulatory processes. Yet, the postsynaptic targets of CeA/Sst and non-Sst-expressing neurons in rNST, as well as the projection targets of rNST neurons receiving CeA input remain unknown. Using a combination of transmission electron microscopy and transsynaptic viral tracing in transgenic mice, we show that CeA axon terminals in the rNST are GABAergic and form synapses with Phox2b-, glutamate-, calretinin-, and GABA-expressing neurons in distinct proportions. rNST neurons receiving CeA input were distributed across the medial, central, and ventral subdivisions and projected primarily to the ipsilateral reticular formation (RF) and parabrachial nucleus (PBN). These findings suggest that CeA input to rNST neurons influences both ascending gustatory information and orosensory motor functions, including licking, mastication, and salivation.
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Bartonjo et al. (2025) studied this question.
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