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)

Pronounced resting tremor was produced in unanesthetized cats by injecting morphine (25-110 mug) into the caudate nucleus. The effects of morphine were antagonized by intracaudate (i.c.) injections of nalorphine (81-263 mug). Tremor activity was also inhibited by i.c. injections of dopamine (61-145 mug), Ca2+ (24-40 mug), scopolamine (88-121 mug) and hemicholinium-3 (HC-3; 73-129 mug) while serotonin (125 mug) was ineffective. Tremor inhibition by HC-3 was reversed by i.c. doses of acetylcholine (15-30 mug) which were subthreshold for tremor production in the absence of morphine. Morphine (55-110 mug) further increased the intensity of ongoing tremor activity induced by physostigmine (111 mug i.c.) I.c. injections of nalorphine antagonized the motor effects of morphine without affecting physostigmime tremor. Tremor production by morphine is attributed to a reduction in dopamine function which allows cholinergic activity in the caudate nucleus to predominate.
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PMID:Tremor production by intracaudate injections of morphine. 114 25

We have previously demonstrated that scratching was significantly increased in a rat model of polyarthritis and that this could be reversed by morphine and electrical stimulation of pain-modulating brain areas. We therefore proposed that scratching might represent a parameter of chronic pain. In this study, we examined the spontaneous behaviour of rats in a model of peripheral neuropathy induced by loosely tying 4 ligatures around the right common sciatic nerve. In half of the animals (N = 7), the ligatures were made with resorbable sutures and, in the other half (N = 7), with non-resorbable sutures of the same size. Postoperatively, scratching was significantly increased at the ligated side. This increase was already observed on the first postoperative day, and maximal effects were reached on the 3rd day. We also observed a qualitative change in the scratching behaviour; postoperatively, scratching was often a vibratory-like shaking of the hind paw in the air. The time course of the increased scratching was time-locked with the development of allodynia to thermal stimulation. No differences were found either in the time course of the increased scratching behaviour or in the time course of the thermal allodynia between the rats ligated with resorbable and with non-resorbable sutures. However, a difference in the walking pattern, as measured by the sciatic functional index (SFI), was observed between the two groups: whereas the SFI normalized after 4 weeks in rats ligated with resorbable sutures, it remained disturbed until the end of the 16-week observation period in the rats ligated with non-resorbable sutures. Morphine 1, 2 and 5 mg/kg dose-dependently reduced the increased scratching behaviour. This was not due to a general depressant effect on the rats' behaviour. This finding is discussed in light of the debate on opioid sensitivity of neuropathic pain. The present results add new evidence that scratching is a possible sign of chronic pain in the animal.
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PMID:A time course analysis of the changes in spontaneous and evoked behaviour in a rat model of neuropathic pain. 132 48

The cause of postanesthesia shaking (PS) is unknown. PS develops spontaneously and unpredictably in up to 67% of patients emerging from general anesthesia, and it continues for minutes to hours when not treated with medications or radiant heat lamps. The purposes of this study were to (1) examine whether butorphanol tartrate (Stadol; Anaquest, Madison, WI/Bristol-Meyers Squibb, Evansville, IN), meperidine (Demerol; Winthrop, NY, NY), and morphine are differentially effective in suppressing PS, (2) compare PS suppression by sex, and (3) determine time to PS development. PS, measured on a 0 to 3 visual scale, developed in 120 of 533 patients (23%). Medication treatment was initiated for 66 of 120 patients by PACU nurses following standard policies and procedures for intravenous doses of 1 mg butorphanol (n = 12), 15 to 30 mg meperidine (n = 18; n = 23), or 2 to 4 mg morphine (n = 13). Treatment effect was measured in units on a 0 to 2 visual scale. By t test, butorphanol is more effective within 2 minutes than meperidine for suppressing shaking alone (P less than .02) or shaking among patients also complaining of pain (P less than .02). Morphine does not relieve shaking. The chi 2 test indicates women suppress PS more rapidly than men (P less than .01), and PS develops within 5 minutes of PACU arrival (P less than .001). Findings suggest that butorphanol is an alternative PS treatment to meperidine, since it relieves shaking within 2 to 5 minutes without producing nausea, vomiting, or recurrence of shaking.
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PMID:Butorphanol tartrate (Stadol) relieves postanesthesia shaking more effectively than meperidine (Demerol) or morphine. 157

Administration of 5% formalin into the rat or guinea pig hind paw evokes two spontaneous responses: flinching/shaking and licking/biting of the injected paw. The temporal and behavioral characteristics of these objective endpoints are described. Additionally, several practical suggestions aimed at standardizing this test for the evaluation of analgesics are presented. The early/acute and late/tonic (0-10 and 20-35 min post-formalin, respectively) phases of flinching were used to quantitate antinociception in the rat. PD 117302, the kappa selective agonist, was three times more potent than morphine against tonic flinching after SC administration. Formalin may therefore be a noxious stimulus of choice in the evaluation of kappa agonists. Morphine was only twice as potent against tonic flinching as against acute flinching or the tail-dip reflex to water (50 degrees C). In contrast, PD 117302 was 27 times less potent on early phase and was inactive in the tail-dip test. Thus, while morphine is essentially equipotent across tests, PD 117302 shows a spectrum of activity with impressive potency and efficacy being obtained against tonic pain. Kappa receptors may therefore be prominently involved in tonic pain states. Aspirin given orally was not consistently antinociceptive in either phase of the formalin test. Spinal transection completely abolished late phase responding but only partly attenuated flinching in the early phase. This suggests that the relative involvement of spinal (as opposed to supraspinal) processing of noxious inputs may, at least in part, be a function of stimulus intensity and underlie the differences in antinociceptive potency observed in this work.
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PMID:Standardization of the rat paw formalin test for the evaluation of analgesics. 188 2

The relationship between wet-dog shaking (WDS) and afterdischarge (AD) elicited by dorsal hippocampal stimulation was investigated. The number of the WDS during a 150-s observation period was 9.6 +/- 2.0 (mean +/- SEM) and no WDS was seen during the non-seizure period. The effects of morphine and neuroleptics on WDS and AD were also investigated. Morphine significantly inhibited the number of WDS elicited by hippocampal stimulation. Naloxone significantly antagonized the inhibitory effect of morphine. Haloperidol and chlorpromazine significantly and dose-dependently inhibited the number of WDS at very small doses. The inhibitory effect of chlorpromazine on WDS was not antagonized by pretreatment with naloxone. The present results suggest that central dopaminergic mechanisms may be important in WDS elicited by hippocampal stimulation. The effect of morphine on WDS is probably mediated via an opioid receptor having a modulating effect on central dopaminergic mechanisms.
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PMID:Effects of morphine and neuroleptics on wet-dog shaking behavior elicited by hippocampal stimulation in rats. 286 Jun 86

In untreated rats, the intraperitoneal injection of putrescine evoked a typical wet-dog shake response, that was maximal at a dose of 300 mg/kg and at room temperature (22 degrees) (number of shakes: 84.00 +/- 17.90/hr). In a hot environment (30 degrees) the number of shakes was markedly reduced (26.90 +/- 5.19/hr). The putrescine-induced shaking behaviour was unaffected by atropine, bicuculline, chlorpheniramine, cimetidine, methysergide, naloxone and noradrenaline, but was markedly antagonized by morphine. Naloxone pretreatment nullified the antagonistic activity of morphine. Histological studies showed marked alterations in brain vascular permeability, which was increased by putrescine. Morphine completely prevented this putrescine-induced vascular effect. These results suggest a correlation between WDS produced by putrescine and increase in brain vascular permeability. Furthermore they show that morphine can affect brain vascular permeability.
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PMID:Shaking behaviour induced by putrescine in naive rats: a pharmacological and histological study. 289 67

Male Sprague-Dawley rats maintained under controlled lighting and temperature conditions were used in this experiment. Morphine dependency was induced by giving increasing doses of morphine by intraperitoneal injection (IP group) or by the ingestion of morphine through drinking water (PO group). Animals were injected with 10, 20, 30 and 50 mg/kg morphine sulfate at days 1, 2, 3 and 4, respectively. Another group of animals received increasing concentrations of morphine through drinking water from 0.1, 0.2, 0.3 to 0.4 mg/ml at 48 h intervals. Morphine dependent animals were given naloxone by the intraperitoneal route to precipitate withdrawal. Glucose (3 g/kg or 10 g/kg) was given 10 min prior to the administration of naloxone to the respective groups. Another two groups of animals were made diabetic by the administration of streptozotocin. In one group, animals received increasing concentrations of 10, 20, 30 and 50 mg/kg morphine sulfate by the IP route at days 1, 2, 3 and 4, while the other group was not treated with morphine but was assessed for withdrawal signs to serve as the control. Withdrawal signs were assessed by observing the presence of diarrhea, tremor, piloerection, hunchbacked posture, teeth chattering, salivation, erection, restless activity, territorial exploring, irritability to handling, vocalization and jumping. Results obtained indicate that glucose administration at 10 g/kg abolished most of the withdrawal signs, and we were unable to induce the same degree of morphine dependency in diabetic animals as compared to the non-diabetic groups. It was concluded from this study that hyperglycemia could suppress morphine withdrawal signs.
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PMID:Hyperglycemic suppression of morphine withdrawal signs in the rat. 314 67

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

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

Formalin which was said to produce prolonged pain and inflammation was injected subcutaneously into the back of guinea pigs, and minor tremor pain response (MTP-response) was measured using the MT-pick up, integrator and digital volt meter. The MTP-response curve showed a biphasic pattern. Immediately after injection, the MTP-response curve showed a significant peak which lasted for about 2 min (the first phase) and subsequently dipped rapidly, and after 5 min, it began to rise slowly again and had a peak at 30 min (the second phase). Morphine (6 mg/kg, s.c.) inhibited completely the first and second phases. Levallorphan (1.2 mg/kg), however, reversed the inhibitory effect of morphine at the first phase, but not at the second phase. Aspirin (200 mg/kg, i.p.), aminopyrine (100 mg/kg, s.c.) and pentazocine (5 mg-10 mg/kg, s.c.) inhibited significantly the formalin-induced MTP-response at both phases. Pyridinol carbamate (200 mg/kg, i.p.) and hydrocortisone (25 mg/kg, i.p.) had no effect on the MTP-response at the first phase, but inhibited it at the second phase. There was a parallelism between the time course of the vascular permeability induced by formalin and that of the second phase of MTP-response. From these results, it is suggested that the first phase of MTP-response is derived from the direct effect of formalin on free nerve endings, while the second phase is derived from the inflammation. Since two kinds of pain features were differentiated in this method, the relationships with so-called "immediate pain" and "delayed pain" were discussed. Furthermore, this method can be utilized to assess pain and the action of analgesics objectively and quantitatively.
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PMID:[Formalin-induced minor tremor response as an indicator of pain]. 651 Aug 42


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