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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possible analgesic effects of i.c.v. administration of several aminoglycoside antibiotics were evaluated in mice using hot plate and tail flick tests. Neomycin (10-80 micrograms/mouse), gentamicin (40-160 micrograms/mouse) and kanamycin (80-320 micrograms/mouse) produced dose-dependent increases in the latencies to forepaw licking and jumping in hot plate test. These drugs also produced dose-dependent increases in the percentage of animals showing analgesia in tail flick test. The order of potency of these aminoglycoside antibiotics in both tests was neomycin greater than gentamicin greater than kanamycin, which is exactly the same order that these drugs show as N-type calcium channel blockers. Bearing in mind this fact and the well known analgesic activity of several drugs which decrease neuronal calcium availability, we suggest that the mechanism of aminoglycoside-induced antinociception may be related to the capacity of these antibiotics to block N-type calcium channels and decrease neuronal calcium availability.
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PMID:Analgesic effects of centrally administered aminoglycoside antibiotics in mice. 186 86

There is substantial evidence that magnetic fields can reduce opiate-induced analgesia, with alterations in calcium channel function and/or calcium ion flux being implicated in the mediation of these inhibitory effects. The present experiments were designed to examine the effects of protein kinase C (PKC), a calcium/diacylglycerol/phospholipid-dependent protein kinase, on opiate-induced analgesia and its involvement in mediating the inhibitory effects of exposure to magnetic fields. We observed that morphine-induced antinociception, or 'analgesia', in the land snail, Cepaea nemoralis, as measured by the enhanced latency of response to a thermal (38.5 degrees C) stimulus, was reduced in dose-related manner by the PKC activator, SC-9. Exposure of snails for 2 h to a low intensity (1.0 gauss rms) 60-Hz magnetic field also reduced morphine-induced analgesia. The inhibitory effects of the 60-Hz magnetic field on morphine-induced analgesia were significantly reduced by the PKC inhibitors, H-7 and H-9, and significantly enhanced by the PKC activator, SC-9. The non-specific protein kinase inhibitor, HA-1004, and the preferential calmodulin inhibitor, W-7, had no significant effects on either morphine-induced analgesia or the inhibitory actions of exposure to the magnetic fields. These results suggest that: (1) PKC has antagonistic effects on opiate-mediated analgesia in the snail, Cepaea, and (2) that the inhibitory effects of magnetic fields on opiate-induced analgesia involve alterations in PKC.
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PMID:Evidence for the involvement of protein kinase C in the modulation of morphine-induced 'analgesia' and the inhibitory effects of exposure to 60-Hz magnetic fields in the snail, Cepaea nemoralis. 193 19

1. Diltiazem, verapamil and nifedipine produced a dose-dependent analgesic response in mice. 2. A fixed oral dose of acetylsalicylic acid increased this analgesic response. 3. Analgesia was maintained when mice were treated chronically with calcium channel blockers alone or when combined with aspirin.
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PMID:Effect of diltiazem, nifedipine and verapamil on the antinociceptive action of acetylsalicylic acid in mice. 205 Feb 80

1. The analgesic effects of diltiazem and verapamil, both per se and together with morphine, were studied using subcutaneous (s.c.) and intracerebroventricular (i.c.v.) administrations, in the hot-plate test in mice. 2. The i.c.v. injection of verapamil (15-120 micrograms/mouse) and diltiazem (60-120 micrograms/mouse) induced dose-dependent analgesic effects. 3. The i.c.v. administration of verapamil (30-120 micrograms/mouse) and diltiazem (60-120 micrograms/mouse) significantly enhanced, in a dose-dependent way, the analgesic effects of morphine and produced a parallel displacement to the left of the morphine log dose-response line. 4. When these calcium channel blockers were administered subcutaneously at doses of 40 and 80 mg/kg, they exerted no analgesic actions, but dose-dependently potentiated the analgesic effects of morphine, producing a parallel shift to the left of the morphine log dose-response line. 5. These results suggest that inhibition of calcium entry through calcium channels induced by verapamil and diltiazem may play a role in analgesia development.
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PMID:Analgesic effects of diltiazem and verapamil after central and peripheral administration in the hot-plate test. 227 85

An investigation was made of the analgesic effects of the subcutaneous coadministration of fentanyl, an opioid mu-agonist (15 micrograms/kg), clonidine, an alpha 2-agonist (100 micrograms/kg), and verapamil, a calcium channel blocker (10 mg/kg) in rats. Nociceptive sensitivity was assessed with hot-plate and tail-flick techniques. None of the three drugs alone was associated with appreciable analgesic effects in the doses used. The simultaneous administration of the three drugs resulted in marked analgesia superior to that of all binary combinations of these drugs. Two-way analysis of variance showed statistically significant differences in hot-plate and tail-flick latencies after drug treatments (P less than 0.001). The significant differences in the area under the time-response curve values (P less than 0.001) might indicate not only an increased analgesic effect, but also a prolongation of antinociception. These results suggest the existence of hitherto unreported interactions between drugs involved in the production of analgesia.
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PMID:Enhancement of fentanyl analgesia by clonidine plus verapamil in rats. 230 80

Acute morphine treatment has been shown to cause a uniform calcium depletion in various brain regions and to evoke hypermotility in mice. On the other hand, it has been reported previously that calcium channel blockers reduce the behavioral stimulation induced by different methods in mice, and it is known that these drugs increase the morphine analgesia and reduce the abstinence syndrome. The effect of calcium channel blockers, nifedipine and diltiazem, on the morphine- and amphetamine-induced hypermotility were evaluated. Mice activity was measured with photocell motility meters. The results show that neither nifedipine nor diltiazem decrease significantly the motility in control and amphetamine-treated mice; however, when they were administered to morphine-treated mice the hypermotility was significantly reduced. The mechanism responsible for this interference is still unknown.
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PMID:Calcium channel blockers: effect on morphine-induced hypermotility. 234 68

The change in the nociceptive reactions of rats was characterized after stressful acoustic (115 dB) stimulation. Acoustic loading for five minutes resulted in considerable analgesia in the hot-plate test, whereas a significant analgesic response was not observed in the tail-flick test. The analgesic reaction after acoustic stimulation was resistant to naloxone pretreatment and was also found in morphine-tolerant rats, but the acute thermoregulatory and analgesic effects of morphine were greatly potentiated by simultaneous acoustic loading. Substance P or cholecystokinin treatment likewise failed to prevent the analgesic effect of auditory stimulation. No tolerance developed to the analgesic effect on repeated stressing. Diltiazem, a slow calcium channel blocker, facilitated the analgesia. The data suggest a stress-induced analgesia with obviously non-opiate properties, although an indirect involvement of opiate effects could not be excluded.
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PMID:Non-opiate analgesia following stressful acoustic stimulation. 241 94

The effects of the calcium channel antagonists diltiazem, nifedipine and verapamil and the calcium channel agonist, BAY K 8644, on offensive and defensive aggression and defeat-induced opioid analgesia were examined in male mice in resident-intruder interactions. The calcium channel antagonists decreased and the agonist increased the aggressive behaviors displayed by the mice. In addition, the calcium channel antagonists augmented, while the agonist attenuated defeat-induced analgesia displayed by the intruder mice. These results suggest that calcium channel antagonists have inhibitory influences on aggressive behavior and may facilitate endogenous opioid activity.
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PMID:Aggression and defeat-induced opioid analgesia displayed by mice are modified by calcium channel antagonists and agonists. 243 3

The effects of the calcium channel antagonists diltiazem, nifedipine and the calcium channel agonist, BAY K 8644, on immobilization-induced opioid analgesia and locomotor activity were examined in CF-1 and C57BL strains of mice, respectively. The calcium channel antagonists enhanced the experimenatlly induced analgesia and activity, whereas the agonist reduced these responses. In addition, the calcium channel antagonists augmented, while the agonist attenuated, the analgesic effects of the specific mu and delta opioid agonists, DAGO and [D-Pen2,D-Pen5]-enkephalin (DPDPE), respectively. These results indicate that calcium channel antagonists have facilitatory and/or modulatory effects on the behavioral and physiological consequences of endogenous mu and delta opioid activity.
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PMID:Stimulatory influences of calcium channel antagonists on stress-induced opioid analgesia and locomotor activity. 243 74

Determinations were made of the effects of the calcium channel blockers, nifedipine and verapamil, on the antagonistic effects of FMRFamide (Phe-Met-Arg-Phe-NH2) and naloxone on morphine- and immobilization-induced opioid analgesia in mice. Intraperitoneal (i.p.) administrations of the calcium channel antagonists significantly reduced the inhibitory effects of intracerebroventricular (i.c.v.) FMRFamide, but had no effects on i.p. or i.c.v. naloxone-mediated inhibition of either morphine- or immobilization-induced analgesia. These results suggest that the antagonistic effects of FMRFamide, (or other endogenous FMRFamide-like peptides) on both opiate- and opioid-mediated analgesia in mice may involve alterations in the functioning of calcium channels.
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PMID:Calcium channel blockers inhibit the antagonistic effects of Phe-Met-Arg-Phe-amide (FMRFamide) on morphine- and stress-induced analgesia in mice. 244 May 27


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