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)

Neuromedin N (NN) is a hexapeptide recently isolated from porcine spinal cord that shares a four-amino acid homology with the C-terminus of the biologically active tridecapeptide neurotensin (NT). Microinjection with NT into the ventral tegmental area or nucleus accumbens of rats has been shown to increase locomotor activity and dopamine (DA) metabolism in some limbic areas or to inhibit the motor stimulant effect of intra-accumbens administration of DA, respectively. In this study the effects of microinjected NN were compared with those of NT. After injection into the ventral tegmental area, NN was shown to be more potent than NT at increasing spontaneous motor activity and to produce an increase in DA metabolism in the nucleus accumbens, prefrontal cortex, diagonal band of Broca and septum. However, when injected into the nucleus accumbens, NN was markedly less potent than NT at inhibiting DA-induced behavioral hyperactivity. In addition to DA-related effects, i.c.v. injection with NT causes hypothermia, and i.c.v. administration with NN was without effect on colonic temperature. These data demonstrate that NN has a behavioral profile distinct from that of NT.
 ...
PMID:Neuromedin N mimics the actions of neurotensin in the ventral tegmental area but not in the nucleus accumbens. 375 55

The effects of intraventricular neurotensin (NT) at doses of 0.1, 1.0, and 10.0 micrograms on blood pressure (BP), heart rate (HR), heat production (M), heat loss (H), and colonic temperature (T co1) were investigated in conscious rats in a direct calorimeter at 18 and 28 degrees C. At 18 degrees C, a 10.0 micrograms of NT significantly increased BP for several minutes after injection with prolonged bradycardia. The larger two doses (1.0 and 10.0 micrograms) significantly reduced M and T co1. In sinoaortic denervated rats, a 1.0 microgram of NT elevated BP and decreased HR. The decrease in HR was significantly smaller than that in nerve intact rats, which indicates the occurrence of baroreflex with intraventricular NT. The changes in M and T co1 in the denervated rats were, however, not statistically different from the intact rats. The baroreflexive suppression of metabolism seems to play a minimum role in the NT-induced hypothermia. H slightly increased for several minutes after central NT (1.0 and 10.0 micrograms) and significantly decreased thereafter. Thermal conductance significantly increased for a longer period of time after NT injection. At 28 degrees C, 1.0 microgram of NT increased H and M. It is concluded that central NT produced hypothermia by reducing M and enhancing H in the cool environment, but not at 28 degrees C.
 ...
PMID:Effects of intraventricular neurotensin on blood pressure and heat balance in rats. 404 36

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

To investigate the mechanisms responsible for the thermolytic action of neurotensin (NT), cannulae for intracerebroventricular (ICV) injection were implanted stereotaxically in Sprague-Dawley rats. Postoperatively, body temperature in the unrestrained rat was monitored continuously by a colonic thermistor probe. NT in a dose of 1.5-4.5 micrograms or CSF carrier vehicle was infused bilaterally in the cerebral ventricle (ICV) in a volume of 7.5 microliters. With the rats kept at an ambient temperature of 22 degrees C, NT given ICV produced a dose-dependent fall in core temperature of greater than 0.8 degree C. Pre-treatment of the animal's cerebral ventricle with amine receptor antagonists, phentolamine (20.0 micrograms), butaclamol (10.0 micrograms), methysergide (20.0 micrograms) or atropine (25.0 micrograms), all similarly infused ICV, failed to alter the hypothermia induced by NT. However, the calcium chelating agent, EGTA, given ICV in a dose of 4.0-8.0 micrograms blocked the thermolytic effect of NT on body temperature in a concentration-dependent manner. These results suggest that the central thermolytic action of NT is not mediated by catecholamine or other aminergic pathways which are implicated in the central mechanisms of thermoregulation. Rather, the peptide may act on a cellular process involving calcium activity in the hypothalamus, presumably to impair the maintenance of the animal's "set-point" for body temperature.
 ...
PMID:Evaluation of neurotensin's thermolytic action by ICV infusion with receptor antagonists and a Ca++ chelator. 619 77

Polypeptides are endogenous agents, involved in the regulation of many physiologic functions and the pathogenesis of several diseases. Polypeptide antagonists form a group of new chemical entities which may provide valid therapeutic agents. Some polypeptides (angiotensin, kinins) are released through the action of proteolytic enzymes (renin, kallikreins) and act as hormones or autacoids; others (substance P, neurotensin) are synthetized by nervous cells to serve as neurotransmitters or neuromodulators. The main homeostatic role of the renin-angiotensin system is to uphold high systemic arterial blood pressure. Overproduction of renin and insufficient checking of renin secretion are among the most common causes of arterial hypertension. Several forms of arterial hypertension (neurovascular, idiopathic) benefit from a reduction in renin-angiotensin system activity. This is achieved either through decreasing renin secretion, by inhibiting conversion of angiotensin I into angiotensin II, or through blocking the peripheral actions (at the receptor sites) of angiotensin II. Renin secretion is very significantly reduced by beta-blocking agents (propranolol); conversion of angiotensin I into angiotensin II is inhibited by teprotide, captopril and their derivatives; peripheral actions of angiotensin II are blocked by saralasin. Bradykinin and related agents produce vasodilation, increase vascular permeability and stimulate pain fibers. Kinins thus reproduce the cardinal features of inflammation and are held to be mediators of the inflammatory reaction. The substance P neuropeptide is found in the brain and bowel; it may act as a transmitter of the sensation of pain at the spinal cord and central nervous system sites. Among other effects outside of the brain, substance P is a potent vasodilator and inhibits renin secretion. Neurotensin is a neuropeptide which produces hypothermia, muscular relaxation and analgesia. Outside of the brain, this peptide is involved in the regulation of gastric secretion, intestinal motility and insulin and glucagon secretion. The vasoactive intestinal peptide, found in certain cholinergic nerve endings, is a large peptide which inhibits gastric secretion, intestinal motility and vascular tone.
 ...
PMID:[Polypeptides and antagonists]. 620 6

Neurotensin is a putative peptide neurotransmitter in the mammalian brain. The light microscopic localization of the neurotensin receptor has been carried out by the autoradiographic localization of [3H]neurotensin binding sites in slide-mounted tissue sections. Large variations in receptor distribution were found, even in small areas. In many regions, the distribution of the receptor paralleled that of the immunoreactive neurotensin found in other studies. The results suggest sites of neurotensin's action in producing various physiological effects such as hypothermia and analgesia.
 ...
PMID:Neurotensin receptor localization by light microscopic autoradiography in rat brain. 626 Feb 80

The effects of the three peptides neurotensin, beta-endorphin, and bombesin on ethanol-induced behaviors were studied in mice. Intracisternal administration of these peptides to mice prolonged the duration of sleep induced by ethanol (5.2 g/kg). Neurotensin and beta-endorphin also enhanced ethanol-induced hypothermia. None of the peptides, when administered alone, produced sleep. However, all three compounds impaired the aerial righting reflex and induced sleep when followed by an IP dose of ethanol (3.5 g/kg), which alone did not induce sleep. These results, taken together with previous findings, suggest that neuropeptides may be involved in the complex mechanisms of action of ethanol on the CNS.
 ...
PMID:The effects of neurotensin, beta-endorphin, and bombesin on ethanol-induced behaviors in mice. 630 2

The effects of intraventricular administration of neurotensin (0.9, 3.75 and 15.0 micrograms) on hyperactivity and stereotypy induced by either amphetamine (1 mg/kg), nomifensine (20 mg/kg), apomorphine (0.5 mg/kg) or N-n-propylnorapomorphine (0.5 mg/kg) were examined. Results indicate that for each drug treatment, the effects of neurotensin were identical: hyperactivity was significantly reduced while stereotypy remained unaffected. Results also revealed that neurotensin significantly increased the hypothermia induced by apomorphine and N-n-propylnorapomorphine. Possible mechanisms which could underly neurotensin's selective inhibitory action on hyperactivity produced by both pre and post synaptic dopaminergic stimulation are discussed.
 ...
PMID:Neurotensin affects hyperactivity but not stereotypy induced by pre and post synaptic dopaminergic stimulation. 632 65

Previous studies have shown that the opioid antagonist naloxone does not alter neurotensin (NT)-induced antinociception. In the present studies, tolerance to morphine in mice significantly attenuated NT-induced antinociception, but not NT-induced hypothermia. In addition, centrally administered NT inhibited naloxone-precipitated jumping in morphine-dependent mice. These results indicate complex interactions between NT-induced antinociception and opioid systems.
 ...
PMID:The effects of chronic morphine treatment on neurotensin-induced antinociception. 641 25


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>