Analysis of the Effects on Body Temperature of Intracerebroventricular Injection in Anaesthetized Dogs of Gamma‐aminobutyric Acid

Abstract

1 The cerebral ventricles of dogs under intravenous pentobarbitone sodium anaesthesia, were perfused with artificial cerebro-spinal fluid (CSF) at a rate of 0.4-0.5 ml/min from the ventricular to the aqueductal cannulae. The effluent was collected from the aqueductal cannula in 20 min samples. The animals' temperatures were recorded from the rectum.2 y-Aminobutyric acid (GABA) 0.1-5 mg when injected into the ventricles produced variable temperature effects. Doses of 0.1 and 0.5 mg always produced hyperthermia and 1 and 5 mg doses sometimes produced hyperthermia and sometimes hypothermia. 3 Intraventricular perfusion with 2-bromolysergic acid diethylamide (BOL) and hyoscine did not block hyperthermia. Tests on the rat isolated stomach strip or the guinea-pig isolated superfused ileum for the possible release, respectively, of 5-hydroxytryptamine or acetylcholine by GABA were negative. 4 When tested for the presence of prostaglandin E(PGE)-like substances on the isolated rat stomach strip, both the control effluent and the GABA effluent showed activity, the latter being much more potent. There was a temporal correlation between this effect and hyperthermia. Intraventricularly administered sodium salicylate converted the GABA-induced hyperthermia to hypothermia and blocked the release of PGE-like substances. 5Hypothermia induced by GABA alone or in the presence of sodium salicylate was associated with the release of noradrenaline into the effluent. 6 Intraventricular administration of GABA in reserpinized dogs produced hyperthermia and not hypothermia. Similar results were obtained with phentolamine perfusion in normal dogs. 7 Perfusion with calcium-free solution blocked both the noradrenaline-releasing and hypothermic actions of GABA. 8 It is concluded that hyperthermia associated with intraventricular injections of GABA is due to the release of PGE-like substance and hypothermia is due to the release of noradrenaline.

Genotype and phenotype in patients with dihydropyrimidine dehydrogenase deficiency

“…The regulation of body temperature takes place in the central nervous system in the hypothalamus and is affected by neurotransmitters such as serotonin and GABA (Dhumal et al 1974). In addition, after the administration of β-alanine to mammals, both hypothermia and hyperthermia have been reported (Gomez et al 1978;Peters et al 1987).…”

Effect on body temperature in dogs of perfusion of cerebral ventricles with artificial CSF deficient in calcium or containing excess of sodium or calcium

“…In our laboratory, during an investigation in dogs of the role of calcium in mediating noradrenaline release which follows the intraventricular injection of yaminobutyric acid, the cerebral ventricles were perfused with artificial CSF containing sodium edetate and lacking in calcium (Dhumal, Gulati, Raghunath & Sivaramakrishna, 1974 (Dhumal et al, 1974). Unless otherwise specified, the room temperature ranged between 28-330 C. The ventricles were perfused with the artificial CSF of Merlis (1940) at a rate of 0 4-0 5 ml/minute.…”