Ritter S, Flynn FW, Dinh TT (2004) Immunotoxic destruction of hindbrain catecholamine neurons impairs the vasopressin response to hypovolemia. Neuroscience 2004 Abstracts 660.4. Society for Neuroscience, San Diego, CA.
Summary: In order to better understand the involvement of hindbrain catecholamine neurons in hypovolemia-induced vasopressin secretion, we lesioned these neurons selectively using anti-dopamine beta-hydroxylase (dbh) conjugated to the ribosomal toxin, saporin (DSAP). When injected into catecholamine terminal sites, this neurotoxin is selectively internalized by and retrogradely transported in dbh-containing neurons, destroying cell bodies that innervate the injection site. We microinjected DSAP or unconjugated saporin (SAP) control bilaterally into the medial hypothalamus of female rats to destroy catecholamine neurons innervating the magnocellular areas of the paraventricular nucleus (PVH). The lesion was verified at the conclusion of the experiment by analysis of dbh-immunoreactive terminals in the PVH and cell bodies in hindbrain catecholamine cell groups. Two weeks after DSAP injection, hypovolemia was induced by remote withdrawal of blood (1 ml/min for 4.5 min) using a chronically implanted intra-atrial catheter. Blood was sampled between 0-2 and 2-4.5 min and at 20 and 50 min after the start of blood withdrawal. Plasma vasopressin was extracted and analyzed using ELISA. The DSAP lesion severely impaired the vasopressin response. Responses at 20 min were 35 pg/ml in the SAP control and 21 pg/ml in the DSAP rats. Responses at 50 min were 45 pg/ml in the SAP and 23 pg/ml in the DSAP lesioned rats. Results indicate that hindbrain catecholamine neurons play a crucial role in full expression of the vasopressin response to hypovolemia.
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