Aspartic acid in the arcuate nucleus attenuates the depressive effects of naloxone on ventilation.
Ventilation, oxygen consumption, the ventilatory equivalent for oxygen, and ventilatory responses to hypoxia and to hypercapnia were evaluated in conscious male rats who received each of four treatments: (1) microinjection of artificial cerebrospinal fluid (aCSF) into the arcuate nucleus and subcutaneously saline (CS); (2) aspartic acid into the arcuate nucleus and saline subcutaneously (AS); (3) aCSF into the arcuate nucleus and naloxone subcutaneously (CN); and (4) aspartic acid into the arcuate nucleus and naloxone subcutaneously (AN). Rats treated with CN exhibited a depression of ventilation, ventilatory equivalent, ventilatory response to hypercapnia, and tidal volume response to hypoxia and to hypercapnia. AS had no effect on any parameters. Administration of both aspartic acid and naloxone attenuated all the effects of CN except the depression of minute ventilation in response to hypercapnia. Therefore the naloxone (a mu opioid receptor antagonist) induced a depression of ventilation that was attenuated by aspartic acid acting on N-methyl-D-aspartic acid receptors in the arcuate nucleus.
Schlenker
E H
EH
Department of Physiology and Pharmacology, University of South Dakota, School of Medicine, Vermillion 57069, USA. eschlenk@usd.edu
D000818:Animals; D001111:Arcuate Nucleus of Hypothalamus / Q000502:physiology*; D001224:Aspartic Acid / Q000494:pharmacology*; D006935:Hypercapnia / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology; D007279:Injections, Subcutaneous; D008297:Male; D008845:Microinjections; D009270:Naloxone / Q000037:antagonists & inhibitors* / Q000494:pharmacology*; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D012119:Respiration / Q000187:drug effects*; D012965:Sodium Chloride / Q000494:pharmacology
D001224:Aspartic Acid; D009270:Naloxone; D012965:Sodium Chloride