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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Previous work from our laboratory has shown that cannabis induces aggressive behaviour in rats that have been deprived of rapid eye movement (REM) sleep. It was suggested that this effect was related to brain catecholamines, with dopamine playing an agonist role and noradrenaline an inhibitory one. The present paper describes new experiments dealing with this subject. 2. Previous REM sleep-deprivation enhanced both delta9-tetrahydrocannabinol (THC)-induced hypothermia and nomifensine effects on aggressive behaviour. 3. A marihuana extract decreased brain dopamine turnover in REM sleep-deprived rats, an effect not observed in non-deprived rats. Noradrenaline metabolism was not altered. 4. Fighting behaviour was elicited in REM sleep-deprived rats treated with 4 different dopamine-beta-hydroxylase inhibitors. 5. Apomorphine, nomifensine and delta9-THC administered to non-deprived rats pretreated with bis(4-methyl-1-homopiperanzinyl-thiocarbonyl) disulphide (Fla-63), induced fighting behaviour. 6. Nomifensine and apomorphine induced fighting in non-deprived rats pretreated with delta9-THC. 7. Clonidine inhibited the fighting elicited in REM sleep-deprived rats by either delta9-THC or Fla-63 pretreatment. 8. The data are discussed in terms of the influence of REM sleep-deprivation (or the stress associated with deprivation) on the response to dopaminergic drugs and cannabis. Taken together they emphasize the participation of brain dopamine and noradrenaline systems in the aggressive behaviour studied.
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PMID:Cannabis, catecholamines, rapid eye movement sleep and aggressive behaviour. 20 20

Rats pretreated daily with delta9-tetrahydrocannabinol (delta9-THC, 8 mg/kg) during 14 days showed tolerance to THC-induced hypothermia and depression of CAR acquisition in a shuttle-box. The noncontingent exposure of THC also produced tolerance to spontaneous (unlearned) behaviors as measured in a open-field test. The data suggest no essential role for learned tolerance in the sense that animals have to to learn to perform under the influence of THC for several of these behaviors.
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PMID:delta9-Tetrahydrocannabinol: tolerance after noncontingent exposure in rats. 63 25

The acute, reciprocal dose-response interactions between delta9-tetrahydrocannabinol (delta9-THC; 2.5, 5.0 and 10.0 mg/kg; IG) and each of three stimulants - d-amphetamine (dA; 1, 2 and 4 mg/kg; IP), cocaine (COC; 10, 20 and 30 mg/kg; IP), and nicotine (NIC; 0.25, 0.5 and 1.0 mg/kg; IP) were studied for their effects on performance of a conditioned avoidance response (CAR), photocell activity, heart rate, body temperature, and rotarod performance. delta9-THC impaired CAR and rotarod performance, depressed photocell activity, and decreased heart rate and body temperature. None of the three stimulants influenced CAR performance, but dA and COC increased the number of intertrial responses, and this latter effect was partially antagonized by delta9-THC. dA and COC, but not NIC, stimulated photocell activity. delta9-THC completely blocked this effect of dA, whereas there was mutual antagonism between delta9-THC and COC on this measure and NIC markedly potentiated the depression caused by delta9-THC. dA and COC tended to offset the impairment of rotarod performance caused by delta9-THC, whereas NIC augmented it. The bradycardia and hypothermia caused by delta9-THC tended to be augmented by these stimulants, especially NIC. The interactions were also studied after subacute treatment for six days with delta9-THC and/or each of the three stimulants. There was evidence for tolerance to the effects of delta9-THC on all measures and this tolerance generally resulted in less interactive effects between delta9-THC and the stimulants. Little or no tolerance was seen for the effects of the three stimulants or their interaction with delta9-THC. The time course of radioactivity derived from 14C-delta9-THC and each of the radiolabelled stimulants was determined in plasma and brain. Only minor interactive effects were found and, in general, they could not account for the functional interactions.
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PMID:Interactions of delta9-tetrahydrocannabinol with d-amphetamine, cocaine, and nicotine in rats. 65 37

delta9-Tetrahydrocannabinol, 11-OH-delta9-tetrahydrocannabinol and 9-nor-9beta-OH-hexahydrocannabinol produced hypothermia and increased catecholamine synthesis in mouse brain. The potencies of the effects of these compounds were correlated. Cannabinol and cannabidiol were inactive in both tests.
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PMID:The effects of cannabinoids on body temperature and brain catecholamine synthesis. 66 8

delta9-Tetrahydrocannabinol (THC; 2.5, 5.0, 10.0 mg/kg, PO) impaired avoidance and rotarod performance, and caused bradycardia and hypothermia. Phencyclidine (PCP; 1.25, 2.5, 5.0 mg/kg, IP) impaired avoidance and rotarod performance and caused a marked increase in photocell activity. When combined, the depressant properties of each drug were enhanced and the stimulation of photocell activity cg/kg THC and its interactions with PCP followed subacute treatment for six days, whereas many of the effects of PCP were enhanced after subacute treatment with a dose of 2.5 mg/kg. Open-field behavior was affected by each drug alone and in combination in a similar way as photocell activity, but the depression caused by their interaction was greater; both drugs caused an increase in urination. Response rates on an FR-10 schedule of food reinforcement were decreased by 2.5 mg/kg PCP, but not by 5.0 mg/kg THC; the combination caused greater response suppression than either drug alone. The functional interactions between THC and PCP were not related to changes in the concentrations of 14C or 3H in plasma or brain derived from 14C-delta9-THC and 3H-PCP, respectively.
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PMID:Interactions between delta9-tetrahydrocannabinol and phencyclidine hydrochloride in rats. 85 Jun 86

The preoptic region (POR) is a primary central site for thermoregulation. Bilateral lesions of POR disrupt thermoregulation, and in rats, produce a characteristic syndrome including hyperthermia. delta9-Tetrahydrocannabinol (delta9-THC), a potent hypothermic agent, appears to mediate this effect via some central mechanism. The studies reported here suggest that delta9-THC induces hypothermia at a site other than POR. Male Sprague-Dawley rats were divided into 2 groups, one with subsequently confirmed bilateral POR lesions and a sham operated group. The lesioned animals developed hyperthemia (+2.1degrees +/- 0.1degreesC, p less than 0.01) within 2 hr after surgery when compared to the sham operated controls. delta9-THC was administered intraperitoneally (5 and 10 mg/kg). Rectal temperature was recorded at 30 min intervals for 2.5 hr. Both lesioned and nonlesioned rats exhibited hypothermia within 30 min of delta9-THC administration. The hypothermic response to 5 and 10 mg/kg delta9-THC in the lesioned animals was significantly greater (p less than 0.05) and showed a trend toward longer duration than the hypothermia induced in the sham operated controls. These data demonstrate that delta9-THC is able to induce a hypothermic response in rats whose body temperatures were elevated by POR ablation. Although delta9-THC does not appear to act primarily at POR to induce hypothermia, it is evident than an intact POR plays a role in modifying the duration and magnitude of delta9-THC induced hypothermia.
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PMID:Hypothermia induced by delta9-tetrahydrocannabinol in rats with electrolytic lesions of preoptic region. 99 43

delta 9-Tetrahydrocannabinol (delta 9-THC) has been reported to attenuate both reserpine-induced serotonin depletion and reserpine-induced hypothermia. We have observed that delta 9-THC preincubation led to a dose-responsive increase in the amount of 3H-reserpine bound to a crude mitochondrial fraction of rat forebrain. The experiments reported here further characterize this phenomenon. Preincubation with delta 9-THC produced a shift in the localization of 3H-reserpine from the incubation medium and the microsomal supernatant (decrease of 66%) to the crude mitochondrial (CM) pellet (increase of 154%). The CM pellet was subfractionated both by differential centrifugation after osmotic shock and by layering on a five-step discontinuous sucrose gradient and centrifuging at 80,000 x g. Osmotic shock with 0.032 M sucrose and centrifugation revealed that the delta 9-THC-induced increase in 3H-reserpine was contained in both the synaptic vesicle fraction (247%) and the fraction containing myelin, ruptured synaptosomes and mitochondria (324%). Separating the CM fraction into five component parts showed that delta 9-THC increased the 3H-reserpine bound by about 275% in the three fractions containing myelin, membrane fragments or mitochondria. Even more dramatic increases (greater than 1000%) were observed in the two fractions containing cholinergic and non-cholinergic nerve endings. In addition, we have determined that many other drugs which are believed to have membrane mediated mechanisms have no effect on the amount of 3H-reserpine bound to the crude mitochondrial fraction. Although other possibilities exist, these data support the hypothesis that delta 9-THC retards the action of reserpine by altering the normal distribution of reserpine in various membrane components of the rat brain.
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PMID:In vitro alteration of the subcellular distribution of 3H-reserpine in the rat forebrain by delta 9-tetrahydrocannabinol. 100 13

Experiment 1. The acute effects of delta9-THC (1.25, 2.50, 5.00, and 10.00 mg/kg) and delta8-THC (1.25, 2.50, 5.00, and 10.00 mg/kg) was an approximately equipotent, dose related depression of water intake in water-deprived rats. Animals given hashish, inhaled as smoke, showed a depression of water consumption comparable to rats given the highest dose of either of the synthetic THCs. Water intake after chevril smoke was similar to that seen after vehicle injections. Experiment 2. A dose related depression of water-and-food intake, and reduction of body weight with a gradual recovery was found in rats, maintained on a Limited Time of drinking schedule (LT, 2 hr) and subchronically (21 days) treated with delta9-THC (1.25, 2.50, or 5.00 mg/kg). From the 22nd day all animals were given the vehicle only for 10 days. There were no indications of withdrawal effects due to the drug termination. Reinstating the drug after the 10 day drug free period suggested an increased sensitivity to THC as compared to the 21st injection. Experiment 3. In non-deprived rats delta9-THC caused similar effect as in Exp. 2, although to less extent. From both experiments it is concluded that there is an inhibition or even loss of body weight and that food intake seems more severely depressed than water intake. The temperature recordings suggest that the predominant consequence of lower, behaviorally, effective doses of THC on rectal temperature of rats is hyperthermia rather than hypothermia. Initially this effect was most pronounced for the lowest dose (1.25 mg/kg) but with repeated injections the two higher doses (2.50 and 5.00 mg/kg) showed hyperthermia to the same extent as the lowest dose. Hypothermia was seen after a high dose of delta8-THC (20.00 mg/kg) but after 3 daily injections this effect was gone.
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PMID:Acute and subchronic influences of tetrahydrocannabinols on water and food intake, body weight, and temperature in rats. 118 35

Pharmacological effects (catalepsy, hypothermia, pentobarbital-induced sleep prolongation, anticonvulsant and analgesic effects) of delta 8- and delta 9-tetrahydrocannabinols, and their 11-hydroxy-metabolites were evaluated and compared in mice. delta 9-Tetrahydrocannabinol and 11-hydroxy-delta 9-tetrahydrocannabinol exhibited somewhat greater effects than did delta 8-tetrahydrocannabinol and 11-hydroxy-delta 8-tetrahydrocannabinol, respectively, in all pharmacological indices tested. Greater effects of 11-hydroxy-metabolites than those of tetrahydrocannabinols were also demonstrated.
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PMID:Comparison of pharmacological effects of tetrahydrocannabinols and their 11-hydroxy-metabolites in mice. 217 83

delta 8-Tetrahydrocannabinol (THC)- and 8 beta, 9 beta-epoxyhexahydrocannabinol (EHHC)-tolerant mice were tolerant to the hypothermia produced by morphine while 8 alpha, 9 alpha-EHHC-tolerant mice were not. Morphine-tolerant mice acquired partial tolerance to the hypothermic effect of 8 alpha,9 alpha-EHHC, but not to the effect of delta 8-THC and 8 beta,9 beta-EHHC. Cataleptogenic effects of all cannabinoids were enhanced in morphine-tolerant mice as compared to non-tolerant animals. It seems that morphine-tolerant mice exhibited hypersensitivity to the cataleptogenic effect of the cannabinoids without potentiation of the hypothermia. These results suggest that the morphine-tolerant mouse may acquire 'latent' cross-tolerance to the hypothermic effect of the cannabinoids.
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PMID:Change in hypothermia and catalepsy induced by cannabinoids or morphine in mice tolerant to these substances. 366 37


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