Hypothalamic control of gastric acid secretion.
Study of hypothalamic control of gastric acid secretion (GAS) has revealed GAS-related neurons, their location in the lateral hypothalamic area (LHA), their characteristics, and implications of their relations to feeding and other functions. Some LHA glucose-sensitive neurons are referred to as gastric type because of their effects on gastric oxyntic cells via specific gastric related neurons of the medulla oblongata and the vagus. The 2-deoxy-D-glucose (2-DG), or insulin induced GAS was completely abolished by bilateral subdiaphragmatic vagotomy, or micro-lesions in specific sites of the LHA. These gastric type glucose-sensitive neurons were thus believed to contribute to control of GAS. The paraventricular nucleus (PVN) was also found to affect GAS. GAS-related PVN neurons were observed in the rostral PVN. Electrophoretic application of various chemicals, especially glucose, also affected neurons in the rostral PVN. Electrophoretically applied norepinephrine (NE) increased PVN single neuron activity and suppressed GAS. Results suggest that the rostral PVN may be another site to modulate LHA control of GAS, and NE may be a transmitter or modulator.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D003847:Deoxyglucose / Q000494:pharmacology; D004558:Electric Stimulation; D005744:Gastric Acid / Q000378:metabolism*; D006885:Hydroxybutyrates / Q000494:pharmacology; D007031:Hypothalamus / Q000187:drug effects / Q000502:physiology*; D008297:Male; D010525:Peripheral Nerves / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains
D006885:Hydroxybutyrates; C041038:3,4-dihydroxybutanoic acid; D003847:Deoxyglucose