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

The central administration of neurotensin, an endogenous hypothalamic tridecapeptide, produces a marked dose-related decrease in body temperature of mice and rats at an ambient temperature of 25 degrees C. This effect is even more pronounced when mice are placed at 4 degrees C to increase the rate of decline of body temperature. Other sequelae observed after central administration of neurotensin are decreases in locomotor activity in rats and a marked dose-related enhancement in pentobarbital-induced mortality, sedation and hypothermia. This latter effect was shown to be due to a significant reduction in the metabolic degradation of the barbiturate. None of the above-mentioned effects are observed after peripheral neurotensin administration, suggesting that this peptide does not readily cross the blood-brain barrier. Neurotensin appears to be one of a growing list of neuropeptides that can affect CNS function.
 ...
PMID:Neurotensin: central nervous system effects of a hypothalamic peptide. 40 65

The influence of pertussis toxin (PTX) on thermic responses elicited by morphine and neurotensin was evaluated in unrestrained rats kept at 22 degrees C. High doses of morphine (9-36 micrograms/rat i.c.v.) lowered body temperature and low doses (1.25, 2.5 micrograms/rat i.c.v.) produced hyperthermia. The hyperthermic effect was more resistant than the hypothermic effect to naloxone antagonism. Neurotensin (50, 100 micrograms/rat i.c.v.) induced marked hypothermia followed by hyperthermia. I.c.v. injection of PTX (1 microgram), six days before morphine (18 micrograms/rat i.c.v.), replaced the opiate hypothermia by consistent hyperthermia and reduced by 60% the hyperthermia elicited by morphine (2.5 micrograms/rat i.c.v.). The toxin also affected the thermic responses induced by neurotensin (50 micrograms/rat i.c.v.) administered six days after PTX (1 microgram/rat i.c.v.). The initial hypothermia was enhanced by 173% and the late hyperthermia was fully antagonized. It thus appears that PTX-sensitive G-proteins play different roles in the molecular events underlying the thermoregulatory responses to morphine and neurotensin.
 ...
PMID:Influence of pertussis toxin on thermic responses to morphine and neurotensin in rats. 145 36

Neurotensin (NT), injected centrally, markedly enhances sensitivity to ethanol-induced anesthesia in SS but not in LS mice (4). Since LS and SS mice were bred selectively for differential sensitivity to ethanol, these findings suggest that neurotensinergic neuronal processes mediate some of ethanol's actions and that LS and SS mice might differ genetically in neurotensinergic systems. Indeed, in biochemical studies it was shown that LS and SS mice differ in NT-like immunoreactivity in specific brain regions, i.e., hypothalamus, and in NT receptor densities (Bmax) in frontal cortex and striatum. In other experiments LS and SS mice differed in behavioral responses to centrally administered NT. Intracerebroventricular (ICV) administration of NT produced dose-dependent changes in motor activity, hypothermia, and analgesia in both LS and SS mice. SS mice appeared to be more sensitive than LS to NT-induced analgesia but not hypothermia. Neurotensin increased or decreased locomotor activity in both SS and LS mice following intraventral tegmental area or ICV administration, respectively. The results indicate that LS and SS mice, which were selectively bred for differences in ethanol sensitivity, differ genetically in NT concentrations, receptor densities in specific brain regions, and in some receptor-mediated behavioral responses to NT.
 ...
PMID:Comparison of neurotensin levels, receptors and actions in LS/Ibg and SS/Ibg mice. 254 8

Ethanol, i.p., produced a greater dose-dependent hypothermia in long sleep (LS) than in short sleep (SS) mice with significant decreases in rectal temperature observed only at doses greater than 3 g/kg, i.p. Likewise, at doses of 1 to 2 g/kg ethanol, i.p., these lines of mice differ markedly in locomotor activity. Neurotensin (NT), intracerebroventricular (I.C.V.), induced a similar hypothermia in both SS and LS mice at doses greater than 0.02 microgram. Doses of ethanol (1.0 g/kg) or NT (0.005 microgram, i.c.v.) that failed to cause hypothermia when administered separately produced a pronounced hypothermia when administered together. Potentiation of NT and ethanol-induced hypothermia was greater in SS than in LS mice. Sensitivity to NT-induced hypothermia was greater following i.c.v. administration than by infusion into the nucleus accumbens (NA) or the ventral tegmental area (VTA). Neurotensin, i.c.v. or intra-NA, markedly inhibited ethanol-induced increase in locomotor activity in both SS and LS mice; however, NT, intra-VTA, did not alter the effects of ethanol on locomotor activity. The results suggest that NT and ethanol act in a synergistic manner on specific neuronal processes mediating thermoregulation and spontaneous motor activity.
 ...
PMID:Neurotensin and ethanol interactions on hypothermia and locomotor activity in LS and SS mice. 264 82

The effects of microinjections of thyrotropin-releasing hormone (TRH), neurotensin and ICI 174864 into the nucleus accumbens, nucleus caudatus, septum and mesencephalic periaqueductal grey were studied on ethanol-induced narcosis in the rat. Levels of narcosis were assessed by alterations in ethanol-induced hypothermia and sleep time. Ethanol produces a 2 degree C fall in body temperature over the first hour which then recovered over the next 2 h. Sedation was produced to the extent that the righting reflex was lost for between 80 and 90 min. In the nucleus caudatus all 3 peptides were ineffective at altering narcosis. In the periaqueductal grey, septum and accumbens, TRH (5 micrograms) and ICI 174864 (1 microgram) microinjections significantly reduced the sleep time by between 50 and 70%. ICI 174864 was approximately 10 times more potent that TRH at reducing the sleep time. In addition, both these peptides significantly accelerated the recovery from the ethanol-induced hypothermia in the periaqueductal grey, septum and accumbens. ICI 174864 prevented the ethanol-induced fall in body temperature. Neurotensin (5 micrograms) significantly increased the sleep time by up to 50% and potentiated the ethanol-induced hypothermia. These results suggest that the administration of TRH or the blockade of delta-opioid receptors, resulting in an inhibition of endogenous enkephalin transmission, may significantly inhibit ethanol narcosis in the rat. Opposing this, the application of neurotensin appears to potentiate ethanol narcosis. These results also indicate that endogenous enkephalin release plays an important role in ethanol narcosis.
 ...
PMID:The effect of neurotensin, TRH and the delta-opioid receptor antagonist ICI 174864 on alcohol-induced narcosis in rats. 282 97

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.
 ...
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.
 ...
PMID:Microinjection of neurotensin into the ventral tegmental area produces hypothermia: evaluation of dopaminergic mediation. 298 60

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.
 ...
PMID:The hypothermic action of carbachol in the rat brain periaqueductal grey area may involve neurotensin. 374 53

Neurotensin is an endogenous neuropeptide that fulfills some of the criteria for a neurotransmitter in the mammalian central nervous system. It exists in high concentrations in the ventral tegmental area and adjacent midline nuclei of the ventromedial mesencephalon, and recent microinjection studies have demonstrated that neurotensin can act in this brain region to produce both a decrease in colonic temperature, and an increase in spontaneous motor activity. In this study it was found that hypothermia was most successfully evoked following neurotensin injection along the midline of the ventral mesencephalon, corresponding to the nucleus linearis centralis. In contrast, behavioral hyperactivity was produced with greatest consistency in the ventral tegmental area, corresponding to the nucleus paranigralis and nucleus parabrachialis pigmentosus. However, in its caudal aspect, the nucleus paranigralis was found unresponsive to neurotensin. Behavioral hyperactivity was also observed after neurotensin injection along the midline into the nucleus interfascicularis. Only injections made into the nucleus linearis rostralis produced hypothermia and hyperactivity in the same rat. This distribution of neurotensin-responsive nuclei corresponded to the distribution of neurotensin containing perikarya and fibers. With the exception of the nucleus interfascicularis, neurotensin-containing neurons were distributed throughout the rostral portion of the ventromedial mesencephalon, the nucleus parabrachialis pigmentosus containing the greatest density. However, in the caudal portion, neurotensin neurons were found almost exclusively in the nucleus linearis centralis. Neurotensin-containing fibers were of greatest density in the nucleus interfascicularis and the nucleus linearis centralis. Considering the known capacity of neurotensin to activate dopamine neurons in the ventromedial mesencephalon, and the partial mediolateral topographical distribution of dopaminergic projections from this region to the limbic forebrain, it is possible that neurotensin may be activating two distinct populations of dopamine neurons to produce hypothermia and behavioral hyperactivity.
 ...
PMID:Neurotensin in the ventromedial mesencephalon of the rat: anatomical and functional considerations. 608 29

In this study we have examined the interactions of bombesin (1 microgram ICV), neurotensin (1 microgram ICV), TRH (10 micrograms ICV), somatostatin (10 micrograms ICV), PGE2 (10 micrograms ICV) and naloxone (10 mg/kg SC) on thermoregulation in the rat at room temperature (20 +/- 1 degree C). Given alone, bombesin, neurotensin, somatostatin and naloxone all produced hypothermia (bombesin greater than neurotensin greater than somatostatin congruent to naloxone). PGE2 was hyperthermic, and TRH had no effect. Bombesin and PGE2 neutralized one another's effects. Neurotensin had no effect on PGE2-induced hyperthermia. Naloxone enhanced the hypothermic effect of bombesin and somatostatin enhanced the rate of onset of hypothermia after bombesin. TRH had no effect on bombesin-induced hypothermia. TRH, somatostatin and naloxone had no effect on neurotensin-induced hypothermia. TRH antagonized the hypothermia due to naloxone and somatostatin.
 ...
PMID:Neuropeptides and thermoregulation: the interactions of bombesin, neurotensin, TRH, somatostatin, naloxone and prostaglandins. 612 11


1 2 3 4 5 Next >>