Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of surgical adrenalectomy were investigated on behavioural responses produced by the selective D-1 agonist, SK&F 38393, alone, and in combination with the D-2 agonist, quinpirole (LY171555). Further, stereotyped responses to apomorphine and LY171555 were assessed following treatment with either the D-1 or the D-2 antagonists, SCH 23390 and raclopride, respectively. There was no difference between sham-adrenalectomized (sham) and adrenalectomized (ADX) groups in responses to SK&F 38393. Although concomitant stimulation of both receptor subtypes increased the incidence of stereotyped sniffing behaviour, there was no difference in the magnitude of this effect between the sham and ADX groups. Raclopride reduced LY171555-induced sniffing and hypothermia less in ADX rats than in sham controls, which was consistent with the hypothesis that adrenocortical hormones affect D-2 receptor responsiveness. SCH 23390 had a greater inhibitory effect on LY171555 responses, but a smaller effect on apomorphine responses in the ADX group compared with their sham controls. It is concluded that the amplified D-2-stimulated response observed in ADX rats may be more dependent on tonic D-1 receptor activation than the control D-2 response of shams.
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PMID:Effects of adrenalectomy on responses mediated by dopamine D-1 and D-2 receptors. 256 98

The control of weaning was studied in rat pups aged 17-24 days. The influence of two hormones, thyroxine (T4) and corticosterone, and the effect of declining intestinal lactase activity were evaluated. Hypothyroidism was induced by administration of n-propylthiouracil and hyperthyroidism was induced by injection of T4. Hypothyroid pups failed to begin nibbling chow while littermates injected with T4 weaned normally. Two abnormalities resulting from hypothyroidism, hypothermia and stunted incisors, were not responsible for the lack of weaning in hypothyroid pups. Hyperthyroidism did not cause precocious weaning. Glucocorticoid levels were manipulated by both adrenalectomy (ADX) and administration of corticosterone. ADX pups exhibited a delayed pattern of weaning while both ADX pups injected with corticosterone and sham-operated pups weaned normally. Corticosterone injected before its normal developmental surge did not cause precocious weaning. Lactase activity, measured throughout these experiments, did not consistently reflect the degree of weaning progression. We conclude that 1) the hormones, T4 and corticosterone, are necessary for the onset of weaning, but neither is a sufficient stimulus to initiate weaning, and 2) low lactase activity does not initiate weaning.
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PMID:Weaning in the rat: a study of hormonal influences. 640 84

Substantial evidence suggests that stress can alter the general toxicological properties of the substituted amphetamines (AMPs) as well as their psychostimulant properties. Research concerning the interactions between stress and the neurotoxicity associated with the AMPs is, however, limited. Our previous work demonstrated that a variety of AMPs, including d-METH, d-MDA, d-MDMA but not d-FEN are able to damage dopaminergic elements of the striatum as shown by decreases in dopamine and tyrosine hydroxylase. The neurotoxic capabilities of these AMPs appear linked to their hyperpyrexic actions as diverse manipulations able to block AMP-induced hyperthermia are also neuroprotective. Surprising, since stress usually potentiates the actions of the AMPs, it is our finding that restraint, a commonly used stressor, is protective against the injurious actions of all neurotoxic AMPs evaluated to date. In the mouse restraint acts to elevate blood levels of corticosterone (CORT) by activating the hypothalamic-pituitary-adrenal (HPA) axis as well as inducing a profound hypothermia. The role CORT may play in the neuroprotective actions of restraint, if any, is unknown. Here, data is presented showing the impact of several HPA axis manipulations, including restraint, supplementation with CORT in the drinking water and removal of CORT by adrenalectomy (ADX) on the striatal dopaminergic neurotoxicity of d-AMP. As strain is known to be a powerful determinant of the actions of stress an essential element of these experiments was the evaluation of both an inbred, C57BL/6J and outbred, CD-1, mouse strain. Exposure to d-AMP caused hyperthermia and substantial striatal dopaminergic neurotoxicity in both strains suggesting that an elevation in body temperature is as important a component of the neurotoxicity of d-AMP, as it is of the other neurotoxic AMPs. Restraint was equally effective in both strains and completely blocked the hyperthermia and striatal neurotoxicity induced by d-AMP. CORT supplementation, evaluated in only the C57BL/6J mouse at dosages not capable of involuting either the thymus or the spleen, did not alter d-AMP-induced neurotoxicity. Although the immune system organs of the two strains responded differentially to the removal of CORT, ADX provided equivalent partial protection against the loss of dopaminergic elements in striatum for both strains. Adrenal status clearly affects d-AMP neurotoxicity but the interaction is complex. Future work should examine the roles of the cortical and medullary components of the adrenal gland in the neuroprotective actions of ADX. A precise assessment of the role of circulating CORT In the neurotoxicity of the AMPs will require additional work in which a wider range of CORT dosages, including those capable of involuting thymus and spleen, are evaluated.
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PMID:Neurotoxicity of d-amphetamine in the C57BL/6J and CD-1 mouse. Interactions with stress and the adrenal system. 895 30

Complex interactions exist between the hypothalamic-pituitary-adrenal (HPA) axis and the serotonergic system, and it has been suggested that these interactions may be fundamental to the pathophysiology and treatment of depressive illnesses. It has previously been found that chronic administration of corticosterone leads to adrenal suppression and an attenuation of somatodendritic 5-HT1A receptor function. Adrenalectomy (ADX) has been shown to cause an increase in postsynaptic 5-HT1A receptor numbers and possibly function. However, other reports have suggested that ADX does not alter somatodendritic 5-HT1A receptor mRNA or binding, though little is known of the effect of ADX on the function of somatodendritic 5-HT1A receptors. This study investigated the effect of markedly reducing corticosterone levels by ADX on 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT)-induced hypothermia in mice, an in vivo model of somatodendritic 5-HT1A receptor function. The degree of 8-OH-DPAT-induced hypothermia did not differ between control, sham, and ADX animals 14 days post operatively. Although repeated administration of corticosterone attenuates somatodendritic 5-HT1A receptor function, these data demonstrate that lowering of corticosteroid levels by ADX have no effect. This suggests that the effects of repeated corticosterone administration is not mediated by a secondary adrenal suppression. The difference in the effects of ADX on somatodendritic as opposed to postsynaptic 5-HT1A receptors may reflect the differential expression of corticosteroid receptor subtypes at postsynaptic and somatodendritic sites.
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PMID:Effects of adrenalectomy on 8-OH-DPAT induced hypothermia in mice. 1010 85

Corticosteroid modulation of serotonergic function may play a central role in mood disorders. 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) produces a hypothermia in mice that serves as an in-vivo model of somatodendritic 5-HT1A autoreceptor function. Daily injections (s.c.) of 50 mg/kg of corticosterone (CORT) for 3 days attenuates 8-OH-DPAT hypothermia tested 24 h later. This study sought to further clarify the nature of the CORT-mediated attenuation of somatodendritic 5-HT1A receptor function. Mice underwent various CORT manipulations prior to an 8-OH-DPAT challenge. Neither 14-day bilateral adrenalectomy (ADX), nor CORT 50 mg/kg/day, administered continuously by osmotic minipump over 72 h had any effect on the 8-OH-DPAT hypothermic response. In contrast, daily injections of CORT over three consecutive days caused a significant attenuation in 8-OH-DPAT hypothermia when tested 24 h later. However, administration of an additional dose of CORT 2 h prior to the 8-OH-DPAT challenge occluded this CORT-mediated attenuation in a dose-dependent fashion. The findings demonstrate that CORT modulates somatodendritic 5-HT1A receptor function in a complex manner. Attenuation is seen only after intermittent administration of CORT. In addition, the degree of attenuation depends on CORT concentrations at the time of testing. These findings may have implications regarding mechanisms of adaptation to stress.
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PMID:Corticosterone modulation of somatodendritic 5-HT1A receptor function in mice. 1223 33