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)

The binding of a radiolabeled bomebesin analogue to rat brain membranes was studied. [125I-Tyr4]Bombesin bound with high affinity (KD = 3 nM) to a single class of non-interacting sites. Binding was specific, saturable (3.8 pmol of sites/g of wet tissue), and reversible. Regional and subcellular distribution studies showed that the density of sites was 7-fold greater in the hippocampus than the medulla/pons and greater in synaptosomal fractions than in mitochondrial or nuclear fractions. The abilities of numerous bombesin analogues to induce hypothermia and to inhibit [125I-Tyr4]bombesin-binding activity correlate well. Numerous amino acid residues near the CONH2-terminal are required for high-affinity binding and biological potency.
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PMID:Bomebesin: specific binding to rat brain membranes. 28 86

Bombesin infusion into the preoptic area (POA) has previously been shown to induce hypothermia in rats that are food deprived or made hypoglycemic with insulin. The present study evaluated the potency and receptor specificity of this response. Bombesin was microinfused into the POA of food-deprived rats (n = 7) and insulin-pretreated rats (n = 7) at doses of 0, 5, 12, 25, and 50 ng/0.5 microliters. Changes in core body temperature (rectal) were assessed at 1 h. Hypothermia was observed under both conditions with doses as low as 5 ng (3.1 pM) as compared to vehicle (0 ng). In a separate study, infusion of the reduced peptide bond analog (Psi13,14 Leu14)bombesin (2.5 micrograms) prior to bombesin injection (25 ng) was found to prevent the hypothermic response observed in the bombesin control condition. These data suggest that bombesin is a potent hypothermic agent that interacts with gastrin-releasing peptide receptors localized within the POA region to impact thermoregulation.
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PMID:Bombesin-induced hypothermia: a dose-response and receptor antagonist study. 133 86

Effects of bombesin on brown adipose tissue (BAT) thyroxine (T4) 5'-deiodinase (5'D) activity and rectal temperature were examined in male mice. Immediately following an intracerebroventricular (ICV) or intravenous (IV) injection of bombesin (0.1-100 ng/animal) or vehicle (20 mM bacitracin dissolved in 0.9% saline), the mice were placed in a room at 4 degrees C or 22 degrees C for 30, 60, 120 or 240 min. The ICV injection of bombesin dose-dependently lessened cold-induced increase in BAT 5'D activity and increased hypothermia determined at 120 min of cold exposure, whereas the IV injection of bombesin was without effect. Bombesin (ICV)-induced hypothermia preceded the inhibition of BAT 5'D activity by at least 30 min at 4 degrees C. BAT 5'D activity was not affected by ICV injection of bombesin in mice kept at 22 degrees C, although the rectal temperature was significantly decreased. Bombesin thus appears to prevent cold-induced increase in T4 5'D activity in mouse BAT by its central effect. Bombesin-induced excessive hypothermia itself and/or the decrease in sympathetic tone of BAT by bombesin might decrease cold-induced increase in BAT 5'D activity.
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PMID:Impairment of cold-induced increase in thyroxine 5'-deiodinase activity in mouse brown adipose tissue by the intracerebroventricular administration of bombesin. 162 Jun 49

The relative roles of lateral hypothalamic cell bodies and fibers of passage were assessed in the development of lesion-induced hyperthermia and bombesin-induced hypothermia. Electrolytic lesions or discrete fiber transections were combined with intracisternal bombesin injection to show that each of these two thermoregulatory effects involves fibers crossing the borders of the lateral hypothalamus; however, the two effects primarily involve fibers crossing different borders. Thus, the hyperthermia and the abolition of bombesin-induced hypothermia which follow lateral hypothalamic damage appear to result from disruption of separate thermoregulatory pathways.
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PMID:Destruction of different fiber tracts underlies development of lateral hypothalamic lesion-induced hyperthermia and loss of bombesin-induced hypothermia. 176 Jul 39

Previous research has shown that microinfusion of bombesin into the preoptic area (POA) decreases core body temperature in rats that are food-deprived or made hypoglycemic with insulin. The present study employed 2-deoxy-D-glucose, a competitive inhibitor of glycolysis, to further investigate the importance of a reduction in glucose utilization in the production of bombesin-induced hypothermia. Rats (n = 7) were pretreated with 2-DG (0, 25, 50, 100, 200 mg/kg; IP) followed by bombesin (100 ng/1.0 microliters) microinfusions into the POA. The highest dose of 2-DG (200 mg) was also tested in the absence of bombesin as a control. Pretreatment with 2-DG resulted in a dose-related reduction in Tb following bombesin. Injections of 2-DG alone did not significantly alter Tb. The results provide additional evidence that the production of bombesin-induced hypothermia in fasted rats is linked to a reduction in glucose utilization.
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PMID:Bombesin produces hypothermia in rats pretreated with 2-deoxy-D-glucose. 204 13

Bombesin-like peptides are widely distributed in the mammalian central nervous system and participate in the regulation of a variety of autonomic functions. Central injection of bombesin produces hypothermia at normal ambient temperatures, but only if the rat has been food-deprived or made hypoglycemic with insulin. Two experiments were conducted to reevaluate the impact of bombesin microinfusion into the hypothalamic paraventricular nucleus (PVN) on core body temperature and feeding behavior. In Experiment 1, bombesin (0.05 and 0.1 microgram/1.0 microliter) produced hypothermia, but not hypophagia, in rats (n = 5) pretreated with insulin (10 U/kg; IM). Since a similar response was observed in rats with injection sites adjacent to the PVN, a smaller injection volume was evaluated in Experiment 2. Hypothermia, but not hypophagia, was observed in rats (n = 5) pretreated with insulin following bombesin (0.025 and 0.05 micrograms/0.5 microliter). Bombesin did not produce hypothermia in rats with injection sites outside of the PVN. These findings suggest that the PVN is a sensitive site for bombesin-induced hypothermia.
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PMID:Microinfusion of bombesin into the hypothalamic paraventricular nucleus produces hypothermia in the insulin-pretreated rat. 221 15

The tetradecapeptide bombesin is a potent agent in producing hypothermia when injected centrally. Bombesin-induced hypothermia at normal ambient temperature occurs under conditions of food deprivation or insulin-induced hypoglycemia. This experiment examined the effect of refeeding on the duration of bombesin-induced hypothermia. Rats (n = 7) received microinfusions of bombesin (0.1 microgram/1.0 microliter) into the preoptic area under separate conditions of food deprivation (18 h) and insulin pretreatment (10 U/kg, IM). Core body temperature was evaluated over a period of 4 h with or without food available during testing. Hypothermia was observed under all conditions during the first 2 h. Food-deprived and insulin-pretreated rats not permitted access to food remained hypothermic until at least 4 h following bombesin. These results are discussed in terms of the possible role of glucose availability in the production and duration of bombesin-induced hypothermia.
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PMID:Refeeding attenuates bombesin-induced hypothermia in the rat. 228 66

This report describes the influence of bombesin on the gross behavior of goldfish, frogs, mice, rats, guinea pigs, rabbits, chicks, pigeons and monkeys. Goldfish, frogs, chicks and pigeons were overtly unaffected by bombesin given centrally and/or peripherally. Mice, rats, guinea pigs, rabbits and monkeys responded quickly to intracerebroventricular (i.c.v.) and/or intrathecal (i.th.) administration of bombesin by displaying a range of behaviors suggestive of altered skin sensation. In mice, bombesin was essentially equipotent as a scratch inducer by i.c.v. and i.th. routes (A50 = 0.010-0.019 microgram) but 6800 times less potent i.p. In rats, bombesin-induced grooming and scratching behaviors were shown to be qualitatively different from those associated with ACTH-(1-24) and thyrotropin releasing hormone. Spantide and [D-Arg1, D-Pro2, D-Trp7,9, Leu11]substance P (both at 0.20, 0.50 and 0.80 microgram i.c.v.), two proposed bombesin receptor antagonists, did not markedly influence bombesin-induced scratching or hypothermia in rats.
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PMID:Effects of bombesin on behavior. 240 26

Three separate experiments were conducted to characterize the effects of bombesin on core body temperature in food-deprived rats and further evaluate the role of food deprivation in this response. Previous research has demonstrated that naloxone reverses bombesin-induced hypothermia in cold-exposed rats. The present study was unable to demonstrate a similar reversal under conditions of food deprivation following naloxone. In a second experiment, cold exposure (11 degrees C) was shown to potentiate bombesin-induced hypothermia in food-deprived rats. Taken together, these data support the notion that bombesin-induced hypothermia in food-deprived and cold-exposed rats represent the activation or disruption of different thermoregulatory mechanism(s). The final experiment evaluated the effects of bombesin microinfusion into the preoptic area of the anterior hypothalamus on core body temperature. Animals were tested under conditions of food satiation, food deprivation, and insulin pretreatment. Bombesin produced hypothermia in food-deprived and insulin-treated rats. No hypothermia was observed in food-satiated rats. Our finding supports the notion that factors associated with the fasting state are important for the production of hypothermia by bombesin in food-deprived rats.
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PMID:Bombesin-induced hypothermia in food-deprived rats. 262 11

Previous studies have shown that central injection of bombesin produces hypothermia in food-deprived, but not food satiated rats at normal ambient temperatures. The present study evaluated the effects of bombesin on core body temperature (Tb) and feeding behavior in rats pretreated with insulin. Administration of bombesin (0.25, 0.5, and 1.0 microgram) into the lateral cerebral ventricle produced hypothermia in rats injected with insulin (10 U/kg; i.m.). No significant change in core temperature was observed in control rats following bombesin. Insulin treatments significantly stimulated feeding behavior and the highest dose of bombesin significantly reduced feeding behavior. The results demonstrate bombesin-induced hypothermia under metabolic conditions similar to acute starvation. These findings are consistent with the hypothesis that bombesin-induced hypothermia in food-deprived rats is directly related to the fasting state.
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PMID:Bombesin produces hypothermia in insulin treated rats. 266 43


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