Electrical stimulation of the salivatory nucleus in the rat.
Unilateral electrical stimulation of the salivatory nucleus evoked a secretion from the ipsilateral parotid gland which was well maintained. Flow rate was not affected by sympathetic decentralization or by adrenoceptor antagonists but was abolished by atropine. Protein secretion was reduced by beta-adrenoceptor antagonists but not by sympathetic decentralization or adrenalectomy. In support of previous histochemical findings it is concluded that the cells of the reticular formation are the origin of the preganglionic parasympathetic fibres to the salivary glands but that a beta-adrenoceptor mechanism as yet unidentified is also involved in the protein secretion.
D000315:Adrenalectomy; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D004087:Dihydroergotamine / Q000494:pharmacology; D004558:Electric Stimulation; D008297:Male; D010306:Parotid Gland / Q000378:metabolism; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012154:Reticular Formation / Q000187:drug effects / Q000502:physiology*; D012471:Salivary Proteins and Peptides / Q000378:metabolism; D012472:Salivation / Q000187:drug effects; D013562:Sympathectomy; D013564:Sympathetic Nervous System / Q000502:physiology
D012471:Salivary Proteins and Peptides; D004087:Dihydroergotamine; D001285:Atropine; D011433:Propranolol