Rinaman L, Wonders CP (2001) Targeted destruction of A2/C2 catecholamine neurons alters hypothalamic responses to vagal stimulation. Neuroscience 2001 Abstracts 131.4. Society for Neuroscience, San Diego, CA.
Summary: Central catecholamine (CA) pathways participate in viscerosensory modulation of hypothalamic neuroendocrine function. Different brainstem CA cell groups may relay different types of viscerosensory signals to different classes of hypothalamic effectors. The present study sought to determine the role of dorsal medullary A2/C2 neurons in hypothalamic responses to exogenous cholecystokinin (CCK), which activates gastrointestinal vagal sensory inputs to the caudal brainstem. Saporin toxin conjugated to dopamine-beta-hydroxylase antibody (anti-DbH-sap; 10 ng in 100 nl) or control toxin was microinjected unilaterally or bilaterally into the A2/C2 region of the dorsal vagal complex in adult male rats. After 10-14 days, rats were injected i.p. with CCK (10 ug/kg) and perfused with fixative 1 hr later. Brainstem and forebrain sections were processed for dual immunocytochemical detection of cFos (a marker of neural activation) and DbH (to define the lesion). Additional forebrain sections were processed for cFos and either oxytocin (OT), vasopressin (AVP), or corticotropin-releasing factor (CRF) to identify hypothalamic neurons activated by CCK. Anti-DbH-sap destroyed the majority of A2/C2 neurons within the microinjection site(s), with minimal non-specific damage. A2/C2 lesions markedly attenuated CCK-induced activation of OT neurons and, to a lesser extent, attentuated CRF activation. Conversely, CCK-induced cFos expression was significantly increased in AVP neurons. The latter effect was observed only after bilateral lesions. These results indicate that A2/C2 neurons participate in vagal sensory-mediated stimulation of OT neurons and CRF neurons, and inhibition of AVP neurons.
Related Products: Anti-DBH-SAP (Cat. #IT-03)