TY - JOUR
T1 - Vagal afferent integration of meal-related GI signals in rat
AU - Schwartz, G. J.
N1 - Funding Information:
In an effort to study the function of specific receptors we have used antisense oligomers to selectively "knock out" the endogenous production of receptor proteins involved in thirst and salt appetite. Three daily intracerebroventricular (ICV) injections of angiotensin (ANGII) AT1 receptor antisense attenuated drinking elicited by a pulse ICV injection of ANG II, whereas random oligonucleotides were ineffective. Water intake elicited by carbachol was unaffected in all groups. The identical procedure produced also reduced ANG II AT1 mRNA, as well as ANG II AT1 receptor binding in brain. Immunocytochemical detection ofbiotinylated ATI probe localized the sites of incorporation to the PVN, SON, OVLT and nucleus medianus. Daily bilateral injections of a mineralocorticoid receptor (MR) antisense into the amygdala prevented the arousal of 4% NaCI intake by exogenous DOCA injections for 5 days, whereas saline treated rats showed robust increases in salt intake. Collectively, these results demonstrate the utility of antisense oligomers to determine receptor mechanisms involved in the neuroendocrine controls of ingestion. (Supported by MH43787 and NS23986.)
Funding Information:
have been identified. One type, polymodal integration, occurs where peptidergic stimulation potentiates and synergizes with the vagal afferent neurophysiological response to mechanical stimulation of a single gastrointestinal compartment. The second type, polytopic integration, occurs where stimulation of one gastrointestinal site modifies the single vagal afferent response to stimulation of a different gastrointestinal compartment. Both types of vagal afferent integration may underlie the control of food intake. (Supported by NIDDK 19302 and the Whitehall Foundation.)
PY - 1995
Y1 - 1995
N2 - The vagus nerve is the primary neural link between gut sites that process ingested nutrients and central nervous system sites underlying the control of food intake. Vagal afferent fibers supplying the GI tract respond to both chemical and physical properties of ingested foods. Since ingested food may provide simultaneous chemical, peptide-induced and mechanical stimulation at multiple GI sites, we investigated the possibility that a single vagal afferent had the potential to integrate signals arising from multiple stimuli. Two types of integration have been identified. One type, polymodal integration, occurs where peptidergic stimulation potentiates and synergizes with the vagal afferent neurophysiological response to mechanical stimulation of a single gastrointestinal compartment. The second type, polytopic integration, occurs where stimulation of one gastrointestinal site modifies the single vagal afferent response to stimulation of a different gastrointestinal compartment. Both types of vagal afferent integration may underlie the control of food intake. (Supported by NIDDK 19302 and the Whitehall Foundation.).
AB - The vagus nerve is the primary neural link between gut sites that process ingested nutrients and central nervous system sites underlying the control of food intake. Vagal afferent fibers supplying the GI tract respond to both chemical and physical properties of ingested foods. Since ingested food may provide simultaneous chemical, peptide-induced and mechanical stimulation at multiple GI sites, we investigated the possibility that a single vagal afferent had the potential to integrate signals arising from multiple stimuli. Two types of integration have been identified. One type, polymodal integration, occurs where peptidergic stimulation potentiates and synergizes with the vagal afferent neurophysiological response to mechanical stimulation of a single gastrointestinal compartment. The second type, polytopic integration, occurs where stimulation of one gastrointestinal site modifies the single vagal afferent response to stimulation of a different gastrointestinal compartment. Both types of vagal afferent integration may underlie the control of food intake. (Supported by NIDDK 19302 and the Whitehall Foundation.).
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U2 - 10.1016/S0195-6663(95)80081-6
DO - 10.1016/S0195-6663(95)80081-6
M3 - Article
AN - SCOPUS:27044438852
SN - 0195-6663
VL - 24
SP - 92
EP - 93
JO - Appetite
JF - Appetite
IS - 1
ER -