Insular cortex projection to the nucleus of the solitary tract and brainstem visceromotor regions in the mouse
- PMID: 7066705
- DOI: 10.1016/0361-9230(82)90040-5
Insular cortex projection to the nucleus of the solitary tract and brainstem visceromotor regions in the mouse
Abstract
Anterograde transport of horseradish peroxidase (HRP) and HRP conjugated to wheat germ agglutinin (WGA-HRP) demonstrated a substantial, bilateral projection from insular cortex to the nucleus of the solitary tract (NTS) in the mouse. Injections that labeled the projection were restricted to the cortical sector homologous to taste-visceral cortex in the rat and label was antero- and retrogradely transported to several subcortical structures along ascending taste-visceral pathways. Multiple, small injections in this cortical region labeled fibers and terminals throughout the rostro-caudal extent of NTS. Small, single injection showed that the projection is topologically organized: Rostral points along the cortical strip project to rostral parts of NTS, intermediate points to the intermediate levels of NTS and caudal parts of the cortical field to caudal parts of NTS. In NTS the primary cranial nerve afferents distribute along a rostral to caudal gradient with the VII nerve rostral, the IX intermediate and the Xth caudal [2, 6, 37]. The present results indicate that the cortical sensory representation of these cranial nerve afferents reflects their topographic distribution in NTS. This suggests that there is an organized anatomical substrate by which the cerebral cortex may selectively influence the central processing of both gustatory and visceral afferent information in the primary CNS relay for these modalities. This insulofugal pathway also terminates in parts of NTS and additional medullary areas that contain preganglionic parasympathetic motoneurons. This appears to be the first anatomical demonstration of a projection from any part of the cerebral cortex to parasympathetic motor nuclei. The pathway provides a substantial direct channel by which higher cortical activity may modulate parasympathetic function.
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