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)

Dopamine, when injected into the anterior hypothalamus of the rabbit, induced a slight hyperthermia due to an upward shift of the threshold central temperature for induction of cold thermogenesis, panting and vasodilation. A slightly reduced thermosensitivity of the controller regulating vasodilation may also contribute to the hyperthermic effect of dopamine. Intrahypothalamic injections of the dopamine agonist, apomorphine, induced a similar effect to that of dopamine, with the exception that the thermosensitivity of the controller regulating vasodilation was not changed. Intraperitoneal injections of a dopamine antagonist, haloperidol, induced a marked hypothermia, due to a downward shift of the threshold central temperature for induction of cold thermogenesis, panting and vasodilation. A slightly reduced thermosensitivity of the controller regulating vasodilation was also observed. Intrahypothalamic injections of haloperidol did not induce an antagonist effect to dopamine, but rather tended to induce hyperthermia. Thermoregulatory responses, occurring after administration of dopamine or apomorphine, partially resembled those seen after administration of neurotensin or prostaglandins.
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PMID:The role of dopaminergic pathways in thermoregulation in the rabbit. 292 77

Oxytocin (OXY) administered intracisternally to adult male mice produced a significant dose-related (1-4 micrograms) increase in colonic temperatures at an ambient temperature of 25 degrees C. The maximal rise in temperature occurred 30 min after administration of the peptide. The interactive effects on colonic temperature of central OXY with equimolar amounts of neurotensin, bombesin or beta-endorphin or of 2 2 mg/kg of chlorpromazine were investigated. OXY significantly antagonized the hypothermia produced by all of these substances. Pretreatment of mice with haloperidol or naloxone failed to prevent OXY-induced hyperthermia. The hyperthermic action of OXY and the interactive effects of OXY with other peptides on thermoregulation may be physiologically significant during parturition and lactation.
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PMID:Interactive effects of intracisternal oxytocin and other centrally active substances on colonic temperatures of mice. 294 25

Neurotensin (NT) differentially altered ethanol-induced anesthesia as measured by duration of loss of righting response or by blood ethanol levels producing loss of righting response in mice (LS and SS) which were selectively bred for differences in response to ethanol. At doses of 5-500 ng i.c.v., NT increased ethanol sensitivity in SS mice, but not in LS mice, as measured by blood ethanol concentrations at loss of righting response. At higher doses, 0.5-10 micrograms i.c.v., NT enhanced the sensitivity of both SS and LS mice to ethanol-induced anesthesia. The hypothermic effect of ethanol determined at loss of righting response was not altered in either LS or SS mice at low doses of NT, but at higher doses NT enhanced ethanol-induced hypothermia in both lines of mice. The altered anesthetic sensitivity was specific for ethanol in that NT did not alter pentobarbital-induced sleep time in either LS or SS mice and halothane anesthesia was altered slightly only in LS mice. NT analogues, N-acetyl-NT8-13, and [D-Trp11]-NT but not NT1-8 enhanced the anesthetic action of ethanol in SS mice. Bombesin, cholecystokinin sulfate, substance P, [D-Trp8, D-Cys14]-somatostatin and corticotropin releasing hormone (CRF) were not effective in enhancing ethanol-induced anesthesia in LS or SS mice. CRF appeared to decrease ethanol sensitivity in LS but not in SS mice. Beta-Endorphin (beta-END) markedly increased the ethanol sensitivity of SS and to a lesser extent of LS mice at relatively high doses, e.g. 0.5-1.0 micrograms i.c.v. The results of the present study indicate that differences in brain sensitivity of LS and SS mice to ethanol may be mediated by genetic differences in NT systems. Likewise, NT, and probably beta-endorphin, may interact with other neurochemical processes that are involved in the mechanism of ethanol-induced anesthesia and that differ genetically in LS and SS mice.
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PMID:Neurotensin selectively alters ethanol-induced anesthesia in LS/Ibg and SS/Ibg lines of mice. 294 96

Neurotensin-producing perikarya and fibers have been identified in the ventral tegmental area of the rat, and recent microinjection studies indicate that neurotensin may function in the ventral tegmental area to regulate body temperature. In this study, the hypothermic response produced by intraventral tegmental injection of neurotensin was shown to be dose-dependent, with a threshold dose between 0.25 and 0.75 micrograms. When fluphenazine, a dopamine receptor antagonist, was microinjected into various forebrain nuclei simultaneous with neurotensin infusion into the ventral tegmental area, it was found to block neurotensin hypothermia. In contrast, injection with fluphenazine into the nucleus accumbens, lateral septum or preoptic area did not alter the hypothermic response. Furthermore, injection with atropine, phentolamine or diphenhydramine into the diagonal band of Broca did not block neurotensin hypothermia. Neurotensin was also injected directly into the preoptic region and shown to produce hypothermia. However, concurrent infusion of fluphenazine with neurotensin into the preoptic region did not attenuate neurotensin hypothermia. These data are consistent with the postulate that neurotensin acts in the ventral tegmental area to enhance dopamine release in the diagonal band of Broca, thereby producing hypothermia. However, neurotensin-induced hypothermia occurring after injection into the preoptic area does not appear to involve dopamine systems.
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PMID:Microinjection of neurotensin into the ventral tegmental area produces hypothermia: evaluation of dopaminergic mediation. 298 60

Mice inoculated with many temperature-sensitive (ts) vesicular stomatitis virus (VSV) mutants incur a less aggressive disease than mice infected with wild-type VSV. The normal body temperature of mice, 38 degrees C, is not a permissive temperature for replication of the temperature-sensitive VSV mutants in cell culture. To determine whether the body temperature of mice caused the alteration in disease states, a neuropeptide that induces hypothermia in rodents was injected into mice before their infection with a temperature-sensitive VSV mutant. Only 1.0 ng of the neuropeptide neurotensin, injected intracerebroventricularly, was required to lower the core temperatures of mice an average of 2.5 degrees C. A single injection of neurotensin before infection with tsG31 VSV (complementation group III) dramatically altered the course of disease. Without neurotensin only 3% of the mice infected with tsG31 VSV died, but when neurotensin was administered 24 h before the inoculation of the tsG31 VSV, 80% of the mice died. The course of disease in mice produced by infection with another temperature-sensitive VSV mutant, tsG11 VSV (complementation group I), also was altered when neurotensin was injected before inoculation of the virus. Instead of 3% of the mice dying as in a normal infection with tsG11 VSV, treatment with neurotensin before inoculation produced a rapidly fatal disease, killing 90% of the mice.
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PMID:Neuropeptide-induced hypothermia and the course of central nervous system disease mediated by temperature-sensitive mutants of vesicular stomatitis virus. 299 82

In addition to short-acting analgesic actions by itself and modulation of analgesic responses induced by endogenous opioids and neurotensin, central administration of thyrotropin-releasing hormone (TRH) potentiates footshock analgesia. The present study evaluated the effects of TRH upon the neurohormonally-mediated though nonopioid analgesia induced by swims in rats. Intracerebroventricular TRH (10 and 50 micrograms) dose-dependently potentiated swim (21, 15, 2 degrees C baths) analgesia on the tail-flick test, an effect which was not due to the hypothermic or basal pain threshold changes. Intravenous (8 mg/kg) TRH potentiated swim (21 degrees C) analgesia; the 600:1 difference in potency between routes strongly suggests central sites of neuromodulatory action. Intracerebroventricular diketopiperazine (50 micrograms), a TRH metabolite, and RX77368 (50 micrograms), a TRH analogue, also potentiated swim (21 degrees C) analgesia, effects also independent of hypothermia and basal reactivity to pain. Finally, given the excitatory interaction between TRH and acetylcholine as well as the cholinergic involvement in swim analgesia, intracerebroventricular TRH potentiated pilocarpine (10 mg/kg, IP) analgesia.
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PMID:Neuromodulatory effects of TRH upon swim and cholinergic analgesia. 310 67

The intracerebroventricular administration of neuromedin N (from 50 ng to 5 micrograms) elicited a dose- and time-dependent hypothermia in mice. Two aminopeptidase inhibitors, bestatin (50 micrograms) and puromycin (50 micrograms), the endopeptidase 24.11 inhibitor, thiorphan (10 micrograms), and the angiotensin-converting enzyme inhibitor, captopril (50 micrograms), were tested for their ability to potentiate the neuromedin N-induced hypothermia. Only bestatin significantly increased the response to the peptide. In addition, thiorphan, though devoid of effect on the neuromedin N-induced hypothermia when given alone, further potentiated the response elicited by neuromedin N and bestatin. The combinations of puromycin/thiorphan and bestatin/captopril did not potentiate the neuromedin N-induced hypothermia.
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PMID:Hypothermic effect of neuromedin N in mice and its potentiation by peptidase inhibitors. 341 19

Intracerebrally-administered neurotensin produces a marked hypothermia in a variety of mammals. In this study, prior adaptation to a cold environment was found to significantly antagonize the hypothermia produced by intracisternally-administered neurotensin in mice. This antagonism required both previous exposure to cold ambient temperatures and cold exposure immediately prior to, or simultaneously with, neurotensin administration. The antagonism of neurotensin-induced hypothermia by prior cold-adaptation was blocked by indomethacin, but not by acetylsalicylic acid, suggesting that brain prostaglandin synthesis may be essential for this newly-discovered phenomenon.
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PMID:Adaptation to cold antagonizes neurotensin-induced hypothermia in mice. 369 37

In previous reports, we have demonstrated that intracisternal (IC) administration of neurotensin (NT), an endogenous tridecapeptide, produces significant antinociception in a variety of analgesic tests, including the hot-plate test. In addition, many of the central nervous system effects of NT (i.e., hypothermia, gastric cytoprotection) appear to be mediated by brain dopamine (DA) systems. In this study, we evaluated the effect of selected DA agonists and antagonists on NT-induced antinociception in the hot-plate test with mice. Doses, route of administration, and pretreatment interval were determined from the available literature to significantly affect the incidence of DA-dependent behaviors. Pretreatment with chlorpromazine but not haloperidol significantly potentiated NT-induced antinociception. This potentiating effect of chlorpromazine appears not to be due to any intrinsic antinociceptive activity of this agent, chlorpromazine had no significant effect on hot-plate latencies when administered alone. The involvement of DA on NT-induced antinociception was further substantiated by the findings that pretreatment with several DA receptor agonists, including methylphenidate, apomorphine, and d-amphetamine, significantly antagonized the antinociceptive response to IC NT. None of these agents significantly altered the animal's response to the hot-plate when administered alone. The data furnished in the present report suggest that central DA circuits may be involved in the expression of NT-induced antinociception.
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PMID:Effect of dopamine agonists and antagonists on neurotensin-induced antinociception. 370 80

Neurotensin (NT) and carbachol both caused hypothermia when injected into the periaqueductal grey area (PAG) of rat brain. Atropine prevented carbachol- but not NT-induced hypothermia. NT-induced hypothermia was unaffected by various neurotransmitter agonists and antagonists in the PAG. Both NT antibodies and thyrotrophin releasing hormone prevented carbachol hypothermia. It is concluded that the hypothermic action of carbachol in the PAG is mediated via endogenous NT.
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PMID:The hypothermic action of carbachol in the rat brain periaqueductal grey area may involve neurotensin. 374 53


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