Sympathetic inhibition of thermogenesis in the infant rat: possible glucostatic control

Abstract

Nonshivering thermogenesis (NST) was examined during cold exposure (30 degrees C) in 5-day-old rats, during food deprivation. NST in the fed state doubled the O2 consumption observed at neutral temperatures. With fasting, the additional O2 consumption stimulated by cold dropped to that observed at thermoneutrality within 6 h, and colonic temperature (Tco) dropped concomitantly. Blood glucose (BG) concentration was halved. Oxygen consumption and Tco in the cold varied linearly with BG changes during food deprivation. 6-Hydroxydopamine transiently stimulated norepinephrine release and elevated metabolism nonadditively with cold stimulation in fed animals, and also stimulated O2 consumption. The drug also partially restored BG concentration, after it had declined during fasting. NST and BG were also restored by gastric infusion of glucose. These data suggest that the decline of NST, and the subsequent hypothermia during food deprivation, is in large part a sympathetically mediated reflex response to low cerebral BG concentration. However, glucose injection in doses sufficient to restore BG after fasting did not restore NST, nor was NST abolished by intracellular glucoprivation with 2-deoxy-D-glucose in fed rats. Thus, it is not argued that BG concentration is in itself an adequate signal for controlling NST.

The effects of 24‐hr maternal separation and of litter‐size reduction on the isolation‐distress response of 12‐day‐old rat pups

“…It seems possible that 24 hr of maternal and nutrient deprivation may uncouple the usual relationship between USV and thermal conditions. Such a hypothesized uncoupling of thermal stimuli and USV may be linked to the uncoupling of thermogenic responses to cold that has already been studied extensively by Bignall et al (1974Bignall et al ( , 1975Bignall et al ( , 1977. These investigators showed that 18-24 hr of nutrient deprivation abolished the thermogenic response of rat pups to cold as measured by oxygen consumption (Bignall et al, 1974).…”

“…These investigators showed that 18-24 hr of nutrient deprivation abolished the thermogenic response of rat pups to cold as measured by oxygen consumption (Bignall et al, 1974). This effect was found to be the result of loss of nutrient effects on gastric interoceptors (Bignall et al, 1977) and appears to be mediated centrally, since the effect was abolished by midpontine transections (Bignall et al, 1975). More recently, others have found that the normal thermogenic response of brown adipose tissue (BAT) to cold is absent in 24-hr-deprived rat pups during isolation at gradually reduced ambient temperatures (Blumberg & Alberts, 1991;Hofer & Shair, 1991).…”

“…Rates of brown adipose tissue (BAT) thermogenesis have been correlated with levels of pups' USV under some circumstances (Blumberg & Alberts, 1990, 1991 but not in others (Hofer & Shair, 1991, 1993. And intragastric nutrient has been shown to regulate central autonomic control of BAT thermogenesis over 18-to 24-hr maternal separation (Bignall, Heggeness, & Palmer, 1974,1977. Thus, orosensory and intragastric nutrient components of the maternal interaction and direct maternal thermal input are hypothetical pathways for maternal regulation of the pups' USV response.…”

Protection against 3,4‐methylenedioxymethamphetamine‐induced neurodegeneration produced by glutathione depletion in rats is mediated by attenuation of hyperthermia

“…Measurement of the rectal temperature of the animals during the 6 h after MDMA treatment revealed that DEM pre‐ and post‐treatment also attenuated the hyperthermia induced by MDMA. The mechanism of DEM‐induced hypothermia is not fully understood but it is thought that its effect on temperature is independent of its GSH depleting effect (Costa and Murphy 1986) and could possibly be related to its impairment of glycogen synthesis and metabolism leading to an impairment of energy production (Bignall et al . 1977; Krack et al .…”

“…Measurement of the rectal temperature of the animals during the 6 h after MDMA treatment revealed that DEM pre-and post-treatment also attenuated the hyperthermia induced by MDMA. The mechanism of DEM-induced hypothermia is not fully understood but it is thought that its effect on temperature is independent of its GSH depleting effect (Costa and Murphy 1986) and could possibly be related to its impairment of glycogen synthesis and metabolism leading to an impairment of energy production (Bignall et al 1977;Krack et al 1980;Steffen and Musacchia 1985). Prevention, or even attenuation, of the hyperthermic response to MDMA has been widely shown to be neuroprotective against the degeneration induced by MDMA (Farfel and Seiden 1995a;Malberg et al 1996;Colado et al 1998Colado et al , 1999aColado et al , 1999b and other substituted amphetamines (Farfel and Seiden 1995b), leading to the question of whether or not the attenuation in hyperthermic response to MDMA induced by DEM treatment might have produced non-specific protection.…”