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

Extracellular 5-HT in the anterior hypothalamus/preoptic area (AH/POA) and caudate nucleus of the freely moving cat was measured using in vivo brain microdialysis. Administration of 8-OH-DPAT, a 5-HT1A receptor agonist that decreases 5-HT neuronal activity, decreased extracellular 5-HT in both brain areas. Extracellular 5-HT levels were also examined in relationship to the sleep-wake cycle, because previous data from our laboratory have indicated that behavioral state is the primary determinant of 5-HT neuronal discharge. As with 5-HT neuronal discharge, extracellular 5-HT was increased during active behavioral states and decreased during somnolent periods. These first two sets of findings confirm the ability of the microdialysis technique to measure physiological fluctuations in extracellular 5-HT levels and support the hypothesis that neuronal discharge is a major determinant of extracellular 5-HT levels. Levels of the 5-HT metabolite 5-hydroxyindole acetic acid (5-HIAA) in the AH/POA were also responsive to changes in behavioral state and administration of 8-OH-DPAT, though fluctuations in extracellular 5-HIAA were less robust and temporally delayed. Finally, extracellular 5-HT and 5-HIAA were examined in the AH/POA during fever induced by systemic injection of the synthetic pyrogen muramyl dipeptide. Previous data from our laboratory have indicated that 5-HT neuronal activity is unaffected by this manipulation, though 5-HT has been implicated specifically in thermoregulation. Pyrogen-induced hypothermia produced no specific change in 5-HT efflux, because any changes noted could be accounted for by behavioral state changes. These data are consistent with the hypothesis that the brain serotonergic system is closely linked to the sleep-wake-arousal cycle. However, extracellular 5-HT may be involved in thermoregulatory processes as part of a global role in modulating neuronal activity in coordination with the behavioral state of the animal.
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PMID:Extracellular serotonin levels change with behavioral state but not with pyrogen-induced hyperthermia. 171 90

Changes in the body temperature (Tbo) of the unrestrained rat as well as the hyperphagic-like ingestion of food were simultaneously determined during the sustained elevation of neuropeptide Y1-36 (NPY) within the anterior hypothalamic preoptic area (AH/POA). A single guide tube was implanted stereotaxically in each rat for repeated perfusions by means of push-pull cannulae of either the CSF solvent vehicle or NPY. Following postoperative recovery, each site in the AH/POA was perfused for 6.0 min at a rate of 20 microliters/min over four successive intervals at a concentration of 100 ng/1.0 microliters or 250 ng/1.0 microliters, with an interval of 6.0 min intervening between perfusions. During repeated perfusions of NPY in the fully sated and normothermic rat, concentration-dependent eating, or a hypothermia or both responses occurred simultaneously. Mean cumulative intakes of food over 3.0 h were 12.1 +/- 1.4 and 21.5 +/- 2.7 g following the 100 and 250 ng concentrations of NPY, respectively. The mean maximal declines in Tbo were -0.92 +/- 0.21 and -1.1 +/- 0.28 degrees C, respectively after the lower and higher concentrations of the peptide. Push-pull perfusions of artificial CSF control vehicle at homologous anatomical sites in the AH/POA were without effect on feeding or the Tbo of the rats. These results demonstrate that repeated and sustained elevation of NPY in the AH/POA can cause a perturbation of the neuronal mechanisms underlying the normal "set-point" for body temperature as well as satiety.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypothermia and feeding induced simultaneously in rats by perfusion of neuropeptide Y in preoptic area. 176 96

The purpose of this study was to characterize the alpha 1- and alpha 2-noradrenergic receptor sub-types which could mediate the hypothermic response produced by norepinephrine (NE) and other alpha-noradrenergic agonists applied to the thermosensitive zone of the hypothalamus. An array of four guide tubes was implanted stereotaxically so that their tips rested just above the anterior hypothalamic, preoptic area (AH/POA) of the cat. Following post-operative recovery, a micro-injection of an agonist or antagonist of NE receptors or control CSF vehicle was given in a volume of 1.0-2.0 microliter in the AH/POA in each of the unrestrained cats. The alpha 1-noradrenergic receptor agonist, phenylephrine, but not methoxamine, applied to the AH/POA produced a dose-dependent hypothermia of up to 2.0 degrees C. When applied similarly, the alpha 2-noradrenergic agonist clonidine, as well as norepinephrine, which acts on both alpha 1- and alpha 2-noradrenergic receptors, also induced a decline in the cat's core temperature of up to 1.5 degrees C. The hypothermic response of clonidine was inhibited by pre-treatment of the AH/POA with a micro-injection of the selective alpha 2-noradrenergic blocking agent, yohimbine. However, yohimbine given similarly in the cat's AH/POA potentiated significantly both the phenylephrine and norepinephrine-induced hypothermia. The combined alpha 1-, alpha 2-noradrenergic receptor antagonist, phentolamine, also injected into AH/POA inhibited the thermolytic response evoked by both phenylephrine and norepinephrine, whereas it was virtually ineffective against the clonidine-induced hypothermia. These results, therefore, strongly suggest that both alpha 1- and alpha 2-noradrenergic receptors subserve the coordinated thermoregulatory mechanisms in AH/POA which are required for the functional dissipation of body heat and the consequent evocation of hypothermia.
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PMID:Hypothermia: role of alpha 1- and alpha 2-noradrenergic receptors in the hypothalamus of the cat. 303 98

The circumscribed effect of ethyl alcohol on the local efflux of serotonin (5-HT) within the thermosensitive region of the anterior hypothalamic, pre-optic area (AH/POA) of the unrestrained rat was examined in relation to core temperature. A single guide cannula for push-pull perfusion was implanted stereotaxically in the AH/POA within coronal planes AP 7.0-8.2. Following 3-4 push-pull perfusions with control artificial CSF of a site identified as reactive to 5-HT, ethanol in a concentration of 2.75 (471 mM) or 5.5 (942 mM) percent was perfused at the same locus over a 5-10 min interval. Successive samples of perfusate were assayed for their content of 5-HT by high performance liquid chromatography using electrochemical detection (HPLC-EC). Within a circumscribed region of the AH/POA of the rat maintained at an ambient temperature of 22 degrees C, ethanol induced either an immediate or delayed hypothermia of short latency or a transient decline followed by an immediate increase in core temperature. In each case, the shift in temperature depended on the anatomical site of push-pull perfusion. Overall, the fall in core temperature was accompanied by an inhibition in the efflux of 5-HT. However, the consequent rise in the rat's core temperature was associated with an enhanced release of 5-HT in the samples of perfusate collected from the AH/POA. These results suggest that serotonergic synapses within the AH/POA are apparently involved in the thermolytic effects of ethanol as well as in the thermogenesis following the interval of heat loss.
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PMID:Temperature-related release of serotonin from unrestrained rats' pre-optic area perfused with ethanol. 341 63

We have investigated the ability of three hyperthermic stimuli (PGE2, 5-HT and ACh) to elicit hyperthermia in the Helium-Cold (He-Cold) hypothermic hamster. Hamsters in these conditions are poikilothermic and will passively follow room temperature in a regulated cold room. Animals were injected centrally at AH/POA sites via an indwelling guide tube at body temperatures maintained between 9-12 degrees C. Active sites in the AH/POA were determined prior to the experiment by PGE2 injection. PGE2 injection at an effective AH/POA site immediately reversed the anesthetic induced hypothermia in warm air. Hamsters were induced into hypothermia by the He-Cold induction method and body temperatures were maintained in a 9 degrees C cold room. Colonic temperatures were monitored at 5 minute intervals by a YSI thermistor probe and telethermometer. Central injections of 5-HT (2 micrograms/microliter) and ACh (50 micrograms/microliter) at effective AH/POA sites evoked significant increases in colonic temperature in He-Cold hamsters. PGE2 injections were not different from saline control injections and did not elicit pronounced temperature changes in these animals. Specific blockade of the 5-HT and ACh temperature increases was demonstrated with specific antagonist injections. The results suggest that the central organization of heat-gain mechanisms in the AH/POA is the same as normothermic animals even at temperatures well below those previously investigated.
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PMID:Organization of central hyperthermic mechanisms in helium-cold hypothermic hamsters. 346 74

Guide cannulae for microinjection and push-pull perfusion in the unrestrained cat were implanted bilaterally in the anterior hypothalamic, preoptic area (AH/POA) and posterior hypothalamus (PH). Postoperatively, the region was first identified in AH/POA which was reactive to norepinephrine or in PH to excess Ca++ ions; in both cases a hypothermic response was produced. Then either an artificial CSF control vehicle or the Ca++ ion channel blocking agent, verapamil, was perfused for 30 min by means of push-pull cannulae at a rate of 25.0 microliters/min. Verapamil 0.4, 2.0 and 4.0 micrograms/microliter) induced a concentration-dependent hypothermia when perfused within AH/POA sites but hyperthermia when perfused in the caudal hypothalamus. An anatomical analysis of the sites of perfusion revealed that verapamil's thermolytic effect was localized within the classical thermosensitive region of the cat's diencephalon, a region ventral to the anterior commissure and dorsal to the optic chiasm. On the other hand, the loci in which verapamil evoked thermogenesis were localized to a region dorsal to the mammillary bodies and caudal to the descending columns of the fornix. It is suggested that verapamil interferes with Ca++ ion channels in the PH to shift the cat's "set-point" temperature. Conversely, however, verapamil apparently could act on catecholaminergic terminals in AH/POA to enhance the presynaptic release of norepinephrine which, in turn, stimulates the heat loss pathway to yield hypothermia.
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PMID:Neuroanatomical mapping of hypothalamic regions mediating verapamil hyper- and hypothermia in the cat. 376 34

Hamsters in deep experimentally induced hypothermia, at body temperatures between 7 degrees C and 11.5 degrees C, were microinjected with 5-HT and ACh at brain sites in the anterior-preoptic area of the hypothalamus (AH/POA). ACh or 5-HT was injected into an AH/POA site at different starting core temperatures in different groups of hypothermic hamsters. Colonic temperatures (Tc) were maintained, following He-Cold induction, in a temperature controlled environmental chamber and measured with a YSI thermister probe and YSI telethermometer. Injections of either 5-HT or ACh at Tc's between 7.0 degrees C and 9.0 degrees C elicited only modest increases in Tc i.e., 0.3 degrees C--0.6 degrees C, respectively. As Tc increased, however, to ranges between 9.1 degrees C--10.0 degrees C and in different animals to greater than 10 degrees C both ACh and 5-HT at the same sites elicited significant increases in Tc, 1.5 degrees C for 5-HT and 2.2 degrees C for ACh compared to saline injections. These data suggest that at the lowest Tc's we are observing a "cold block" of temperature sensitive sites in the AH/POA. Increasing the starting Tc beyond 9.0 degrees C however, evokes significant increases in heat-gain following AH/POA injection of either ACh or 5-HT. These data are consistent with Myers' observations concerning the organization of heat-gain mechanisms at AH/POA sites. In addition, they suggest that both the afferent limb of the heat-gain circuit (5-HT) and the efferent limb of the circuit (ACh) are functionally impaired when Tc is close to the physiological limit in the He-Cold hypothermic hamster.
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PMID:ACh and 5-HT stimulated thermogenesis at different core temperatures in the He-Cold hypothermic hamster. 386 62

Guide cannulae for push-pull perfusion were bilaterally implanted stereotaxically within the anterior hypothalamic, preoptic area (AH/POA) and posterior hypothalamus (PH) of the cat. Catecholamine-reactive sites were identified within AH/POA in which a microinjection of norepinephrine (NE) (5.0 micrograms) evoked a characteristic, transient hypothermia. Similarly the cation-reactive region within the PH was identified in which excess Ca2+ (25 mM) also evoked a hypothermic response. When verapamil was perfused at a rate of 25.0 microliters/min in a concentration of 0.4 or 2.0 micrograms/microliter within AH/POA at a NE-sensitive site, a concentration-dependent decline in the core temperature of the cat occurred. Conversely, verapamil perfused in the same manner with a Ca2+-reactive site caused an intense rise in the cat's body temperature which also was concentration dependent. These results show that the localized blockade of slow Ca2+ channels exerts direct, differential physiological effects within central nervous system tissue. In this case, verapamil mimics noradrenergic effects within the AH/POA; however, the hyperthermic response following Ca2+ channel blockade within tissue of the PH resembled that produced by ethyleneglycoltetraacetic acid or Na ions.
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PMID:Divergent action of verapamil perfused in two hypothalamic areas on body temperature of the cat. 403 99

The activity of norepinephrine (NE) within the thermosensitive region of the anterior hypothalamic, pre-optic area (AH/POA) of the rat was examined in relation to changes in core temperature produced by ethyl alcohol. Following stereotaxic implantation of push-pull guide tubes, a specific site in the AH/POA, reactive or non-reactive to NE, was labeled with 1.0 microliter of [3H]-NE. Alcohol in a concentration of 2.75% or 5.5% was then perfused locally at the same site by push-pull cannulae or administered peripherally in a dose of 2.0 g/kg. In control experiments, artificial CSF was perfused alone. The perfusion of alcohol enhanced or delayed the release of [3H]-NE in AH/POA or failed to alter the efflux of the catecholamine, with the specific response dependent principally on the: (1) anatomical site of hypothalamic perfusion, (2) concentration of alcohol, and (3) interval of perfusion itself. During the perfusion of alcohol within a very circumscribed region in the AH/POA, vasodilatation, as reflected by an increase in skin temperature, and a hypothermia of short latency, occurred. The change in core temperature was usually accompanied by a delay in the efflux of [3H]-NE. After the peripheral administration of 2.0 g/kg alcohol, an alteration in NE efflux from the AH/POA was also induced during the course of a hypothermic response accompanied by vasodilatation. These results suggest that alcohol exerts a direct central effect on nerve cells comprising the thermoregulatory mechanism located within the hypothalamus. Further, the well-known thermolytic effect of alcohol could be mediated in part by noradrenergic synapses within AH/POA, by means of their phasic release of NE.
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PMID:Release of norepinephrine from the rat's hypothalamus perfused with alcohol: relation to body temperature. 406 63

Hypothalamic loci of Sprague-Dawley rats were individually injected with cyclo (His-Pro) to determine the sites where that metabolite of thyrotropin-releasing hormone acts to produce hypothermia. There was almost always a positive hypothermic response in the preoptic-anterior hypothalamic area (POA/AHA); injection into the posterior or middle hypothalamic areas or into the hippocampus caused no significant decrease in core temperature. The fact that only injection into the POA/AHA evoked hypothermia suggests that this area is a major hypothalamic site of action of cyclo (His-Pro) in modulating thermoregulation in the rat.
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PMID:Cyclo (His-Pro): mapping hypothalamic sites for its hypothermic action. 717 86


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