Central control of gastric acid secretion by extralateralhypothalamic nuclei.
Whether secretion of gastric acid (GAS) is in response to peripheral and/or central administration of chemical or electrical stimuli can be differentiated by vagotomy. GAS has been shown to be controlled by specific lateral hypothalamic (LHA) neurons. Application of 2-deoxy-D-glucose (2-DG) or insulin to the LHA by microinjection or iontophoresis has experimentally induced GAS. The paraventricular nucleus (PVN) has now been found to also affect GAS. GAS was produced more copiously and more quickly by rostral PVN lesion than by lesion of the ventromedial (VMH) or dorsomedial (DMH) nucleus, and nearly as much by caudal PVN lesion. Microinjection of 2-DG into the LHA induced GAS more potently in animals with rostral PVN lesions than in those with caudal PVN, VMH or DMH lesions, or in intact animals. Results indicate that the PVN may be an additional central site from which GAS is affected.
D000818:Animals; D003847:Deoxyglucose / Q000494:pharmacology; D004558:Electric Stimulation; D004594:Electrophysiology; D005744:Gastric Acid / Q000378:metabolism*; D007026:Hypothalamic Area, Lateral / Q000187:drug effects / Q000502:physiology*; D007328:Insulin / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000502:physiology; D010286:Paraventricular Hypothalamic Nucleus / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains
D007328:Insulin; D003847:Deoxyglucose