Forebrain projections to the rostral nucleus of the solitary tract in the hamster

Abstract

The rostral nucleus of the solitary tract (NST) is the first central site of taste information processing. Specific anatomical subdivisions of the NST receive taste afferent input and contain interneurons and projection neurons that engage ascending or premotor taste pathways. The forebrain projects to the NST and can influence taste responses, but the anatomical relationship between forebrain inputs and the subdivisions of the NST and their cellular elements is not understood. To evaluate this, in this study, we used cholera toxin B (CTb) as a retrograde and anterograde marker. CTb was injected into the rostral NST to label, by retrograde transport, the sources of forebrain inputs. Cells were labeled bilaterally in the lateral and paraventricular hypothalamic nuclei, bed nucleus of the stria terminalis, central nuclei of the amygdala, and the agranular and dysgranular divisions of insular cortex. Within the medulla, labeled cells were located in the parvicellular reticular formation and spinal trigeminal nuclei. In addition, labeled cells and anterograde axonal labeling were present in the rostral NST contralateral to the injections. Injections of CTb centered in the dysgranular insular cortex, the site of most forebrain-NST cells, labeled axon endings confined to the rostral NST. These endings were concentrated in the rostral central and ventral subdivisions. Corticofugal endings in the rostral central subdivision are positioned to influence microcircuits that include taste afferent synapses, presumed inhibitory interneurons, and neurons that project to the parabrachial nucleus. The many corticofugal endings in the ventral subdivision synapse among premotor neurons that ultimately influence salivatory and oromotor outflow. Intramedullary CTb labeling after NST injection indicates that the rostral central subdivision also receives projections from the contralateral rostral NST. J. Comp. Neurol. 422:429–447, 2000. © 2000 Wiley-Liss, Inc.