Treece BR, Speth RC, Ritter RC, Burns GA (2003) Altered CCK binding in the dorsal vagal complex following cytotoxic lesion of the nodose ganglion. Neuroscience 2003 Abstracts 830.5. Society for Neuroscience, New Orleans, LA.
Summary: CCK reduces meal size by activating a specific subpopulation (30%-38%) of vagal afferent neurons. MK-801, attenuates reduction of food intake by CCK and increases meal size. We hypothesized that vagal afferents that are sensitive to excitatory amino acids might express CCK receptors and thereby mediate effects of both CCK and MK-801. Therefore we examined I125CCK-8 binding in the dorsal vagal complex, following unilateral nodosectomy or cytotoxic lesion of nodose cell bodies. To destroy vagal afferent cell bodies and their central projections we made unilateral intranodose injections of NMDA/kainic acid, which has been shown to destroy about 40% of vagal afferents. We also made intranodose injections of CCK-saporin (CCK-SAP), a novel cytotoxin, which appears to destroy vagal afferents when the ribosomal toxin, saporin, is selectively internalized along with the CCK/receptor complex. In some rats we completely eliminated vagal afferents on one side via nodosectomy. We found that this produced significant ipsilateral reduction in CCK binding in the nucleus of the solitary tract (NTS). Intranodose injection of NMDA/kainate or CCK-SAP also resulted in significantly reduced CCK binding in the NTS, ipsilateral to the injected nodose. The reduction of NTS CCK binding following nodosectomy, NMDA/kainate or CCK-SAP injection did not differ significantly. Interestingly, CCK binding appeared to be reduced in the vagal dorsal motor nucleus, ipsilateral to nodose removal, but was increased ipsilateral to CCK-SAP injection. We conclude that CCK-SAP destroys a subpopulation of vagal afferents that express CCK receptors and that intranodose NMDA/kainate destroys a partially overlapping afferent subpopulation that also expresses CCK receptors. Finally, our data suggest that expression of CCK binding in the dorsal motor nucleus may be controlled by feedback from CCK sensitive vagal afferents.
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