Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Morphine and beta-endorphin inhibit the shaking response of pentobarbital-anesthetized rats to ice water. Stereotaxically guided administration of antibodies to cerebroside sulfate into the periaqueductal gray region, the most sensitive brain region in which to demonstrate inhibition of this response, antagonizes the effect of morphine and beta-endorphin. These results suggest that cerebroside sulfate may be an integral component of an opiate receptor in rat brain.
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PMID:Antibodies to cerebroside sulfate inhibit the effects of morphine and beta-endorphin. 624 89

Ethanol (2.0-5.0 g/kg, IP) caused a dose-related impairment of the aerial righting reflex of mice 60 min after injection. Ethanol (3.5 g/kg, IP) given simultaneously with neurotensin (30 micrograms, IC), bombesin (30 micrograms, IC) or beta-endorphin (20 micrograms, IC) caused a greater impairment of the reflex than ethanol alone. Simultaneous treatment with ethanol (4.0 g/kg, IP) and thyrotropin-releasing hormone (TRH, 3.0-30 micrograms, IC) caused less impairment of this measure than ethanol alone. None of the peptides altered the height of aerial righting when administered alone, or when administered with ethanol no peptide altered blood or brain ethanol content. Unexpectedly, TRH (20 and 40 mg/kg, IP) potentiated the action of ethanol by increasing punished licking in water-deprived rats, rather than antagonizing this acute action of ethanol. Like ethanol (1.0 and 2.0 g/kg, IP), beta-endorphin (100 micrograms, IC) suppressed ethanol-withdrawal tremor and audiogenic-seizure susceptibility in ethanol-dependent rats. beta-Endorphin (1 microgram) and bombesin (10 and 30 micrograms, IC) reduced only audiogenic-seizure susceptibility. TRH (10-100 micrograms, IC, or 1-40 mg/kg, IV) and neurotensin (10-100 micrograms, IC) had no effect on these ethanol-withdrawal signs. These findings suggest that centrally active peptides may play a role in certain acute and chronic actions of ethanol. Because TRH, neurotensin, bombesin and beta-endorphin do not alter all actions of ethanol in the same way, an interaction of ethanol with many functionally independent neuronal circuits is suggested.
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PMID:Modification of the actions of ethanol by centrally active peptides. 626 62

beta-Endorphin (5-80 microgram) or [D-Ala2,Met5]enkephalinamide (DALA) (5-40 microgram) was administered intracerebroventricularly to rats. With both opioid peptides, there was no direct relationship between log dose and mean number of wet-dog shakes (WDS) that occurred during the following 15 min. When the results were analyzed quantitatively, the dose of DALA that caused 50% of the rats to shake at least twice was 8.6 microgram (4.9-15 microgram). beta-Endorphin had such poor efficacy that an ED 50 could not be obtained. Morphine (1 and 5 mg/kg, s.c.) antagonized shaking caused by the optimal dose of DALA (20 microgram). Naloxone (0.1-10 mg/kg, s.c.) attenuated both DALA- and beta-endorphin-induced WDS in a dose-related manner. This latter result differentiates shaking associated with opioid peptides from that caused by thyrotropin releasing hormone (TRH), another endogenous stimulant of WDS in rats. There was no cross-tolerance between RX 336-M (7,8-dihydro-5',6'-dimethylcyclohex-5'-eno-1',2',8',14 codeinone), a novel shake inducing agent, and beta-endorphin. This finding again differentiates beta-endorphin-induced shaking from that caused by TRH and also from that associated with several exogenous stimulants of WDS.
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PMID:A quantitative analysis of the shaking behavior induced in rats by beta-endorphin and [D-Ala2, Met5]enkephalinamide. 627 33

The endogenous opiate-like peptides, beta-endorphin, methionine- and leucine-enkephalin have been investigated in unanaesthetized cats after intracerebroventricular injection. beta-Endorphin produced marked and prolonged psychomotor stimulation (restlessness, apprehension, looking around, vacant stare and impelling locomotion), accompanied by pupillary dilation and tremor which was prevented by nalorphine. In contrast to beta-endorphin, the enkephalins did not cause affective behavioural phenomena. However, the enkephalins evoked transient and inconsistent vomiting which was also prevented by nalorphine. It is apparent, therefore, that morphinomimetic brain peptides are involved in at least two functions in the central nervous system: beta-endorphin subserves the mediation of a long-lasting psychomotor stimulation, while the enkephalins mediate vomiting of a transient character.
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PMID:Differences in central effects of beta-endorphin and enkephalins: beta-endorphin. A potent psychomotor stimulant. 627 57

The effect on behavior of synthetic human beta-Endorphin injected into the cerebral ventricles of the cat was investigated in these experiments. beta-endorphin produced psychomotor excitation (i.e., restlessness, apprehension, flight and locomotion), accompanied by pupillary dilatation and tremor. Between periods of locomotion, the cat sat moving its head from side to side with eyes wide open and mydriasis, or stood stiffly with a vacant stare, pupils dilated and eyes wide open. During this time the cat did not react to objects moving in front of it. Behavioral changes produced by a single dose of beta-endorphin were dose-dependent and long-lasting. Pretreatment with intracerebroventricular nalorphine depressed or abolished the behavioral changes, mydriasis and tremor caused by beta-endorphin. It is concluded that beta-endorphin acts on central opiate receptors promoting psychomotor excitation.
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PMID:beta-Endorphin-induced psychomotor excitation in the cat. 628 17

The present study compares the potencies of D-Ala2-D-Leu5-enkephalin (DADL) and beta-endorphin (beta-EP) injection intrathecally and i.c.v. on the inhibition of tail-flick and ice water-induced shaking responses in pentobarbital-anesthetized rats. Peptides were injected stereotaxically into the third ventricle or into the spinal subarachnoid space. The tail-flick response was measured 10 or 20 min after the injection of DADL or beta-EP, respectively, after which the rats were immersed for 5 min in ice water and the number of shakes was counted. Intrathecal DADL and beta-EP were equipotent in inhibiting both the tail-flick and shaking responses. However, treatment with naloxone (2 mg/kg i.p.) shifted the dose-response curve for both responses to the right more for the beta-EP than for DADL. Unlike the equipotency intrathecally, DADL by i.c.v. injection was less potent than beta-EP in inhibiting both the tail-flick and shaking responses. Previous results in the unanesthetized rat had also shown that i.c.v. DADL was less potent than beta-EP in inhibiting the tail-flick response. Thus, the spinal cord is sensitive to both DADL and beta-EP, whereas the supraspinal area is more sensitive to beta-EP. Also, because the potency of i.c.v. beta-EP for inhibiting tail-flick but not shaking was substantially reduced in anesthetized compared to unanesthetized rats, the neuronal substrates involved in inhibition of shaking are different from those of inhibition of the tail-flick. The differential sensitivities to i.c.v. vs. intrathecal administration and the unequal responses to the antagonistic action of naloxone indicate that DADL and beta-EP produce their action through different opioid receptors.
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PMID:Inhibition of tail-flick and shaking responses by intrathecal and intraventricular D-Ala2-D-Leu5-enkephalin and beta-endorphin in anesthetized rats. 629 83

Effects of intracerebroventricular administration of beta-endorphin, thyrotropin-releasing hormone (TRH), cholecystokinin octapeptide (CCK-8), non-sulfated CCK-8 (CCK-8-NS) and caerulein on body shaking behavior were observed in rats. CCK-8 and its related peptides produced only a small increase in the number of body shakes, while TRH had the striking effect of stimulating body shakes, this increase being markedly suppressed by simultaneous administration of beta-endorphin. Moreover, the suppressive effect of beta-endorphin on TRH-induced body shakes was antagonized by simultaneous administration of caerulein and CCK-8. The body shakes induced by ice-water immersion were also reduced by beta-endorphin, this beta-endorphin effect being partly antagonized by caerulein and CCK-8.
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PMID:Effects of beta-endorphin, thyrotropin-releasing hormone and cholecystokinin on body shaking behavior in rats. 629 91

beta-Endorphin injected into the cerebral ventricles of unanesthetized cats produced dose-dependent and long-lasting restlessness, locomotion, stereotyped sideways movements of the head, vacant staring, apprehension and flight accompanied with mydriasis and tremor. The most impressive features of the psychomotor excitation were the locomotion and the sideways movements of the head. Intracerebroventricular nalorphine prevented the psychomotor excitation caused by intracerebroventricular beta-endorphin. Lithium chloride and lithium carbonate injected into the cerebral ventricles prevented and reversed the psychomotor excitation evoked by beta-endorphin similarly injected. In cats showing spontaneous locomotor activity, intracerebroventricular lithium chloride also suppressed this activity. It is suggested that beta-endorphin elicited psychomotor excitation by acting on central opiate receptors. However, the effect of lithium cannot be solely ascribed to an action on central opiate receptors and endogenous peptides. Since lithium affected the spontaneous as well as the beta-endorphin-induced locomotion, it may be supposed that the cation suppressed the ongoing input activity at central locomotion activity levels.
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PMID:Inhibition by lithium of beta-endorphin-induced psychomotor excitation in cats. 629 36

Naloxone in doses up to 2 mg/kg and beta-endorphin in doses up to 1 mg/kg had no suppressive effect on pressure-induced tremor or cortical EEG activity in the guinea pig. The lack of effect of either naloxone or beta-endorphin on the HPNS provides evidence that opiate receptor mechanisms are not significantly involved in this syndrome.
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PMID:Failure of naloxone or beta-endorphin to affect pressure-induced tremor in guinea pig. 631 Aug 41

The present study was undertaken to investigate whether beta-adrenoceptors are involved in regulation of yawning responses to oxytocin and alpha-melanocyte-stimulating hormone (alpha-MSH) in rats. Oxytocin administered intracerebroventricularly (ICV) at doses of 50 and 100 ng/rat elicited yawning. alpha-MSH (20 micrograms/rat, ICV) elicited not only yawning but also stretching and body shaking. RS-86 (2-ethyl-8-methyl-2,8-diazaspiro-(4,5)-decan-1,3-dion hydrobromide), a putative muscarinic M1 receptor agonist, administered ICV at a lower dose of 100 micrograms/rat and subcutaneously (SC) at doses of 0.25-2.5 mg/kg also elicited yawning. The yawning responses produced by these agents were markedly increased by intraperitoneal (IP) pretreatment with a beta-adrenoceptor antagonist, pindolol (20 mg/kg), which per se did not elicit yawning. The yawning induced by oxytocin (50 ng/rat, ICV) plus pindolol, but not that by alpha-MSH (20 micrograms/rat, ICV) or RS-86 (0.5 mg/kg, SC) plus pindolol, was inhibited by [d(CH2)5,Tyr(Me)2,Orn8]-vasotocin (100 ng/rat, ICV), an oxytocin receptor antagonist. The yawning induced by oxytocin, alpha-MSH, or RS-86 administered in combination with pindolol was inhibited by scopolamine (0.5 mg/kg, SC), a mucarinic receptor antagonist, without being affected by spiperone (0.5 mg/kg, SC), a dopamine D2 receptor antagonist. The results suggest that the yawning produced by the neuropeptides oxytocin and alpha-MSH is modulated by beta-adrenoceptor activity in an inhibitory manner as that produced by muscarinic M1 receptor agonists, and that it involves cholinergic, but not dopaminergic, activation.
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PMID:Involvement of beta-adrenoceptors in regulation of the yawning induced by neuropeptides, oxytocin and alpha-melanocyte-stimulating hormone, in rats. 761 71


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