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)

Acute exposure of adult male albino rats to higher ambient temperature (40 degrees C) for 2 h significantly increased body temperature (BT). Administration of either bicuculline (1 mg/kg, i.p.), a GABA antagonist, or physostigmine (0.1 mg/kg, i.p.), an inhibitor of acetylcholinesterase, significantly increased BT of normal and heat-exposed rats. Treatment with muscimol (1 mg/kg, i.p.), a GABA agonist, produced hypothermia in normal rats and prevented an increase in BT of heat-exposed rats. The dopamine agonist, L-dopa (100 mg/kg, p.o.) along with carbidopa (10 mg/kg, p.o.) reduced BT of normal rats. Further, the bicuculline-or physostigmine-induced enhancement of BT in normal and heat-exposed rats was potentiated when both drugs were administered concomitantly. But this potentiating effect remained unaltered when dopamine antagonist haloperidol (1 mg/kg, i.p.) was administered along with bicuculline and physostigmine. Treatment with atropine (5 mg/kg, i.p.), a cholinergic antagonist, abolished the hyperthermic effect of bicuculline but potentiated the hypothermic effect of muscimol either at 28 degrees C or at 40 degrees C. Bicuculline-induced hyperthermia was attenuated at normal or higher temperature by pretreatment with L-dopa + carbidopa. The administration of L-dopa + carbidopa either abolished or reduced the hyperthermic effect of physostigmine at room temperature or at higher ambient temperature. These results suggest that (a) GABAergic, cholinergic and dopaminergic systems are involved in thermoregulation, (b) exposure to high environmental temperature may inhibit central GABAergic activity which activates the cholinergic system without affecting the dopaminergic system and raises BT, (c) central dopaminergic and GABAergic systems act independently through the modulation of cholinergic activity in the regulation of BT under normal ambient temperature.
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PMID:Does GABA act through dopaminergic/cholinergic interaction in the regulation of higher environmental temperature-induced change in body temperature? 223 64

1. Intraperitoneal (i.p.) injection of diazepam (1.5-6 mg/kg) decreased the core body temperature (BT) of the rats. The effect was dose-dependent. 2. The hypothermia produced by diazepam (6 mg/kg, i.p.) was decreased in animals pretreated with high doses of bicuculline (BIC, 3 mg/kg, i.p.), while low doses of BIC (1.5 mg/kg, i.p.) potentiated the hypothermia. 3. Picrotoxin (PIC, 1 and 2 mg/kg, i.p.) pretreatment also decreased the hypothermic effect of diazepam. 4. Pretreatment of animals with atropine (AT, 10 mg/kg, i.p.) or propranolol (PRO, 10 mg/kg, i.p.) potentiated the hypothermic response of diazepam. Phenoxybenzamine (PHEN, 0.5 mg/kg, i.p.), methergoline (METH, 0.5 mg/kg, i.p.) or pimozide (PIM, 0.5 mg/kg, i.p.) did not change the diazepam hypothermia. 5. Single administration of BIC, PIC, PRO, PIM or METH also induced hypothermia. 6. One can postulate that diazepam hypothermia may be induced through GABAA receptor sites. However, further studies will clarify this hypothesis.
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PMID:Involvement of GABAA receptor sites in diazepam hypothermia. 257 24

GABA, delta-aminovaleric acid (DAVA) and sodium valproate (VPA) decrease core temperature in conscious rats. Bicuculline increases GABA-induced hypothermia, does not modify DAVA (250 mg/kg) and VPA (100 and 400 mg/kg) hypothermia and antagonizes initial hypothermia by DAVA (1000 mg/kg) and VPA (200 mg/kg) and late hypothermia by DAVA (500 mg/kg) and VPA (200 mg/kg). Picrotoxin increases late hypothermia by GABA (250 mg/kg) and VPA (400 mg/kg), but decreases initial hypothermia by VPA (200 mg/kg). Pentylenetetrazol increases variably GABA-induced hypothermia, inhibits early early hypothermia by DAVA and increases hypothermia induced by VPA (400 mg/kg). We conclude that GABA and GABA-agonists (DAVA and VPA) may induce hypothermia partly mediated by activation of bicuculline-insensitive GABA-receptors.
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PMID:Involvement of bicuculline-insensitive receptors in the hypothermic effect of GABA and its agonists. 299 72

In acute ethanol studies aminooxyacetic acid (AOAA) alone produced marked hypothermia although a test dose of ethanol was able to produce a further drop in body temperature in AOAA treated mice. Even though tolerance to ethanol-induced hypothermia was present in ethanol-dependent mice, AOAA administration was able to produce a further decrease in body temperature. Bicuculline potentiated ethanol-induced hypothermia in the acute studies but the tolerance to hypothermia which had developed in ethanol-dependent mice prevented the bicuculline-induced potentiation of ethanol hypothermia. AOAA markedly potentiated acute ethanol-induced motor incoordination whereas bicuculline had no effect. Although partial tolerance had developed to ethanol-induced motor incoordination in dependent mice, AOAA potentiated, whereas a lower dose of bicuculline antagonized, motor incoordination. In the acute studies ethanol had a biphasic effect on AOAA-induced GABA accumulation in the hypothalamus and corpus striatum: low doses prevented and a slightly higher dose was without effect on GABA accumulation. Ethanol-dependent mice were unable to respond to an AOAA-induced increase in GABA accumulation although basal levels of GABA were unaffected by chronic ethanol ingestion. The results show that brain GABA or GABA-mediated central mechanisms may be involved in the mediation of ethanol-induced motor incoordination but not hypothermia.
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PMID:GABA mediation of the central effects of acute and chronic ethanol in mice. 403 3

Exposure (2 h) of male albino rats to higher environmental temperature (HET, 40 degrees C) significantly increased the body temperature (BT). Administration of bicuculline (1 mg/kg, i.p.), physostigmine (0.2 mg/kg, i.p.), or their combination significantly raised the BT of normal rats (kept at 28 degrees C) or of HET-exposed rats. Atropine (5 mg/kg, i.p.) abolished the hyperthermic effect of bicuculline in normal and HET-exposed rats. The BT of normal and HET-exposed rat was increased with morphine (1 mg/kg, i.p.) and was reduced with naloxone (1 mg/kg, i.p.). Bicuculline or physostigmine-induced rise in BT of HET-exposed rats was potentiated following cotreatment of physostigmine with morphine. Atropine-induced hypothermia was abolished due to the cotreatment of atropine with morphine with physostigmine but was attenuated with atropine. In normal rats (kept at 28 degrees C), only atropine attenuated (morphine + bicuculline)-induced hyperthermia. L-Dopa + carbidopa or haloperidol did not significantly affect the BT of rats under similar conditions. These results suggest that short-term (2 h) exposure to HET activates the opioidergic neuron, which activates cholinergic activity through the inhibition of GABAergic system and, thus, enhances the BT.
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PMID:Higher environmental temperature-induced increase of body temperature: involvement of central opioidergic-GABAergic interaction. 750 82

Sympathetic nerve activity to brown adipose tissue (BAT) regulates adipocyte metabolism of its stored lipid fuel and thus the thermogenesis in BAT. To determine if the discharge of neurons in the rostral raphe pallidus (RPa) can influence BAT thermogenesis, changes in sympathetic nerve activity to BAT were recorded after microinjection (60 nl) of the GABAA receptor antagonist bicuculline (500 microM) into the RPa in chloralose-urethan-anesthetized, ventilated rats. Bicuculline caused a large, rapid rise in the sympathetic nerve activity to BAT (which had also increased during acute hypothermia) from very low, normothermic control levels to maximum values (mean: 1,949 +/- 604% control; n = 13) after 4-6 min. The sympathetic nerve discharge to BAT had a mean burst frequency (3. 5 +/- 0.3 Hz) that was significantly less than the heart rate (7.3 +/- 0.2 beats/min), and it was not inhibited during baroreceptor reflex activation. Bicuculline-stimulated increases in the sympathetic nerve activity to BAT and cold-evoked increases in neuronal fos expression were localized to the RPa at the level of the caudal half of the facial nucleus. This dramatic increase in sympathetic nerve activity to BAT after disinhibition of neurons in rostral RPa is consistent with a major role for RPa neurons, perhaps as sympathetic premotoneurons for BAT, in medullary control of BAT thermogenesis.
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PMID:GABA-mediated inhibition of raphe pallidus neurons regulates sympathetic outflow to brown adipose tissue. 995 Sep 4

1. In order to ascertain whether both GABA(A) and GABA(B), or only GABA(B) receptors, directly modulate thermoregulation in conscious rabbits, GABA(A)/GABA(B) agonist and antagonist agents were injected intracerebroventricularly in conscious rabbits while monitoring changes in rectal temperature (RT), gross motor behaviour (GMB) and electrocorticogram (ECoG) power spectra (ps) from sensorimotor cortices. 2. GABA (48 micromol), nipecotic acid (50 nmol), THIP (60 nmol), muscimol (18 nmol) and baclofen (8 nmol) induced hypothermia (-deltaRTmax values of 1.70+/-0.1, 1.4+/-0.2, 1.0+/-0.4, 1.1+/-0.2 and 1.6+/-0.3 degrees C, respectively), accompanied by inhibition of GMB and ECoG synchronization. THIP increased ps at delta frequency band (1.1-3.3 Hz), while GABA, nipecotic acid, muscimol and baclofen did the same at both delta and (4.6-6.5 Hz) frequency bands. ECoG ps changes were concomitant or even preceded hypothermia. 3. Bicuculline (1.8 nmol) induced hyperthermia (deltaRTmax 1.2+/-0.5 degrees C) and slight excitation of GMB, while CGP35348 (1.2 micromol) did not affect RT nor GMB. Both compounds did not affect ECoG ps. 4. Bicuculline potentiated muscimol-induced hypothermia, inhibition of GMB and synchronization of ECoG, while CGP35348 fully antagonized these effects. 5. In conclusion, the present results, while confirming the prevailing role of GABA(B), also outline a direct involvement of GABA(A) receptors in the central mechanisms of thermoregulation. Ascending inhibition towards discrete cortical areas controlling muscular activity and thermogenesis may result from GABA receptor activation in neurones proximal to the ventricles, thus contributing to hypothermia, although hypothermia-induced reduction of neuronal activity of these cortical areas cannot be ruled out.
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PMID:Changes in rectal temperature and ECoG spectral power of sensorimotor cortex elicited in conscious rabbits by i.c.v. injection of GABA, GABA(A) and GABA(B) agonists and antagonists. 1466 29