Dinh TT, Huston NJ, Ritter S (2009) Caudal hindbrain catecholaminergic projection to the ventrolateral bed nucleus of the stria terminalis (vlBNST): Assessment of role in glucoprivic and CCK feeding responses and corticosterone secretion. Neuroscience 2009 Abstracts 87.16/CC80. Society for Neuroscience, Chicago, IL.
Summary: Catecholamine neurons in the caudal hindbrain provide a significant innervation of the vlBNST and some of these neurons co-innervate the paraventricular nucleus of the hypothalamus (PVH). We previously found that PVH injections of the retrogradely-transported immunotoxin, anti-dopamine beta hydroxylase (DBH) saporin (anti-DBH-sap), profoundly reduced feeding and corticosterone responses to glucoprivation, but did not alter CCK-induced satiety, which has been linked to catecholamine neurons in the A2 cell group. In this experiment, we examined the origin of the vlBNST/PVH catecholamine projection and assessed its role in responses to glucoprivation and CCK. Retrograde tracing from vlBNST and PVH revealed dually-projecting DBH-ir (norepinephrine or epinephrine) neurons primarily in A2, A1 and caudal C1, with a few cells also present in C2. Dually-projecting PNMT-ir (epinephrine) were also present in C1 and in small numbers in C2. Overall, the relative numbers of DBH- and PMNT-ir neurons with projections to both vlBNST and PVH and the locations of these triply-labeled neurons indicate that the dually-projecting neurons are predominantly noradrenergic. Injections of anti-DBH-sap into the vlBNST produced cell losses in the hindbrain that were anatomically consistent in distribution and number with the tracing results. This immunotoxin caused a loss of DBH neurons in the dorsal hindbrain that was concentrated in the A2 cell group (14.6 – 13.68 mm caudal to bregma), where a maximum of 50% of DBH neurons were lesioned: 50% loss at 14.6 mm caudal to bregma, 25% at 13.24 mm and 0% at 11.96 mm. In ventral hindbrain, loss of DBH cell bodies was predominantly in the A1 cell group (14.6 – 12.8 mm caudal to bregma), where a maximum of 60% of DBH-ir neurons were lesioned: 60% loss at 14.6 and 13.68 mm, 22% at 13.24 and and 0% at 12.8 mm. In the dorsal hindbrain nearly all cells retrogradely labeled from the vlBNST were ipsilateral and DBH-ir. In ventral hindbrain there was a significant contralateral projection to vlBNST that was not DBH-ir. Anti-DBH-sap lesions did not impair the feeding, blood glucose or corticosterone responses to 2-deoxy-D-glucose (250 mg/kg) and did not impair the suppression of feeding by CCK-8 (4 ug/kg), indicating that the catecholamine projection to the vlBNST, including the dually-projecting neurons that innervate both the vlBNST and the PVH, is not required for these responses.
Related Products: Anti-DBH-SAP (Cat. #IT-03)