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Biomedical subjects

M Kavaliers

Publications and source records attributed to M Kavaliers.

At least 109 records · Page 6Linked to original sources
PubMed1990

Exposure to mosquitoes, Aedes togoi (Theo.), induces and augments opioid-mediated analgesia in mice.

Mosquitoes and other biting flies are natural aversive stimuli commonly encountered by wild and domestic animals and by humans. We observed that male mice exposed for 30 min to a low density of female mosquitoes (Aedes togoi) displayed significant increases in nociceptive responses which were indicative of the induction of analgesia. This analgesia was blocked by the prototypic opiate antagonist naloxone (1.0 mg/kg). Exposure to a novel stimulus had no significant effect on nociception, whereas 30 min of restraint stress induced a naloxone-reversible analgesia qualitatively similar to that observed after exposure to mosquitoes. Confinement in a small chamber for 30 min also had a significant analgesic effect whose amplitude and duration were markedly potentiated by concurrent exposure to mosquitoes. These results show that exposure to mosquitoes, and likely other biting flies, both induces an opioid-mediated analgesia and augments the analgesic effects of other stressful stimuli.

Aedes↗
PubMed1990

Sex differences in the inhibitory effects of the NMDA antagonist, MK-801, on morphine and stress-induced analgesia.

We examined the effects of intraperitoneal administrations of the noncompetitive NMDA receptor antagonist, (+) MK-801, its inactive enantiomer, (-) MK-801, and the prototypic opiate antagonist, naloxone, on restraint- and morphine-induced analgesia in male and female deer mice, Peromyscus maniculatus. Both restraint (30 min) and morphine (1.0 mg/kg) induced significant analgesic responses with male mice displaying significantly greater levels of opioid-induced analgesia than female animals. These analgesic responses were completely blocked by, naloxone (1.0 mg/kg), significantly reduced by (+) MK-801 (0.25 mg/kg) and unaffected by (-) MK-801 (0.25 mg/kg) pretreatments. There were significant male-female differences in the inhibitory effects of (+) MK-801; the higher levels of morphine- and restraint-induced analgesia of the males were completely blocked, while the lower level analgesic responses of the females were significantly reduced, but not blocked, by (+) MK-801. These observations provide further evidence that NMDA receptors are involved in the mediation of endogenous and exogenous opioid analgesia and show that there are significant male-female differences in the inhibitory effects of (+) MK-801 on opioid-mediated analgesia.

Analgesia↗
PubMed1989

Effects of magnetic resonance imaging (MRI) on the formation of mouse dentin and bone.

The effects of magnetic resonance imaging (MRI) on dentin and bone formation in mice were examined using standard autoradiographic and liquid scintillation procedures. It was observed that exposure to a standard 23.2 min clinical multislice MRI (0.15T) procedure caused a significant increase in the synthesis of the collagenous matrix of dentin in the incisors of mice. There were no significant effects on alveolar and tibial bone matrix synthesis. These results suggest that the magnetic fields associated with MRI can affect the activity of cells and/or tissues that are involved in rapid synthetic activity.

Animals↗
PubMed1989

Day-night rhythms of shoaling behavior in goldfish: opioid and pineal involvement.

Intracerebroventricular (ICV) administration of the opioid peptide, beta-endorphin (5.0 pg/g) to goldfish, Carassius auratus, significantly increased the cohesiveness and duration of shoaling ('bout' length) in shoals of five fish, as well as decreasing the latency of shoal formation in response to an external disturbance, while a higher dose of beta-endorphin (15 pg/g) decreased shoaling. There were day-night rhythms in shoaling and in the extent of the facilitatory effects of beta-endorphin (5.0 pg/g) on shoaling behavior, the fish displaying significantly greater shoaling responses in the day than during the night. The facilitatory effects of the low dose of beta-endorphin were blocked by systemic administration of naloxone (1.0 mg/kg), while ICV administrations of naloxone (1.0 pg/g) decreased daytime shoaling behavior. Removal of the pineal gland disrupted the day-night rhythm of shoaling, reducing daytime levels of shoaling. In addition, pinealectomy reduced the stimulatory effects of beta-endorphin (5.0 pg/g) on shoaling, and attenuated the day-night rhythms in the effects on beta-endorphin on shoaling. These results suggest that both opioid systems and the pineal gland influence shoaling behavior and the expression of its day-night rhythm in goldfish.

Animals↗
PubMed1989

Population differences in benzodiazepine sensitive male scent-induced analgesia in the deer mouse, Peromyscus maniculatus.

We compared opioid and nonopioid involvement in the mediation of scent-induced analgesia in two populations of deer mice, Peromyscus maniculatus; P. m. artemisiae from a mainland region and P. m. angustus from a small marine island. Exposure to bedding taken from the soiled home cage of an isolated (dominant aggressive) male resident elicited a significant increase in the nociceptive responses of male deer mice from mixed sex pairs, with the island population of mice displaying significantly greater analgesic responses than the mainland animals. In the mainland population of mice, the large amplitude analgesia induced by the scent of a conspecific was insensitive to the opiate antagonist, naloxone, but could be blocked by either the benzodiazepine antagonist, Ro 15-1788, or agonist, diazepam. Exposure to the scent of individuals from the island population elicited a lower amplitude analgesia that was sensitive to both the opiate and benzodiazepine manipulations. In the island population, both the lower amplitude analgesia induced by the scent of a conspecific and the higher amplitude analgesic elicited by the scent of a mainland animal was blocked by naloxone and only partially reduced by the benzodiazepine manipulations. Bedding treated with the peppermint also induced analgesia, with the island mice displaying a markedly greater analgesic response than the mainland animals. In both populations of deer mice the peppermint-induced analgesia was blocked by naloxone and insensitive to the benzodiazepine manipulations. These findings are considered in terms of their possible ecological significance and relations to the differences in agonistic and social behaviors between island and mainland populations of deer mice and other small rodents.

Analgesia↗
PubMed1989

The effects of naloxone on body rotation-induced analgesia and anorexia in male mice.

The effects of body rotation in a horizontal plane and the opiate antagonist, naloxone, on the nociceptive responses and the feeding behavior of male mice were examined. In the first experiment the mice were rotated (70 rpm, schedule of 15 sec on; 5 sec off) for 60 minutes or exposed to sham rotation for the same duration. Midway through the rotation or sham procedure the mice were either injected with naloxone (1 mg/kg) or isotonic saline. At the end of the 60-minute treatment period the animals were placed on a warm surface (47.5 degrees C) and their latency to show a foot-licking response was measured. The rotation procedure produced a significant (p less than 0.01) increase in response latency in the saline-injected mice and the naloxone injections blocked this analgesic effect. This finding provides evidence for opioid involvement in the rotation-induced analgesia. In Experiment 2 mice on a food restriction schedule were rotated (70 rpm, 15 sec on; 5 sec off) or sham exposed for 60 minutes. Midway through this treatment period the mice were either injected with naloxone (1 mg/kg) or isotonic saline. Following the treatment period the mice were given access to food for 2 hours. The rotation procedure produced a significant (p less than 0.01) reduction in feeding (anorexia) in the first 30 minutes of food access for the saline-injected mice. Injections of naloxone significantly (p less than 0.05) enhanced the rotation-induced anorexia. These experiments demonstrate that rotation-induced analgesia in mice is blocked by the opiate antagonist, naloxone, whereas rotation-induced anorexia is not.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗
PubMed1989

Beta-funaltrexamine disrupts the day-night rhythm of nociception in mice.

Determinations were made of the effects of beta-funaltrexamine (beta-FNA), an irreversible mu-opioid receptor antagonist, on the day-night rhythm of nociception in male mice. Peripheral administration of beta-FNA (20 and 40 mg/kg) disrupted the day-night rhythm of foot-licking response to aversive thermal (50 degrees C) stimulation. The peak nocturnal response latency was attenuated and the marked increases and decreases in response latency present at the light-dark and dark-light transitions, respectively, were suppressed. These results suggest that mu opioids are associated with the generation and expression of the day-night rhythm of this particular measure of nociception in mice.

Animals↗
PubMed1988

Analgesic effects of the putative FSH-suppressing gonadal steroid, 3 alpha-hydroxy-4-pregnen-20-one: possible modes of action.

The effects of intracerebroventricular (i.c.v.) administrations of the putative follicle stimulating hormone (FSH) suppressing gonadal steroid, 3 alpha-hydroxy-4-pregnen-20-one (3A4P) on the nociceptive responses of male mice were examined. This allylic steroid elicited significant, dose-dependent (0.001-1.0 micrograms) analgesic responses for 90-150 min after injection. These analgesic effects of 3A4P were stereospecific, the stereoisomer, 3 beta-hydroxy-4-pregnen-20-one (3B4P) failing to affect the nociceptive responses. The analgesic effects of 3A4P were blocked by peripheral administrations of the GABA antagonists, bicuculline and picrotoxin, and reduced by the benzodiazepine antagonist, Ro 15-1788. The exogenous opiate antagonist, naloxone, and the putative endogenous opioid antagonist, Tyr-MIF-1 (Pro-Leu-Gly-amide), also reduced 3A4P-induced analgesia, while i.c.v. administration of 3A4P (0.001 and 0.01 micrograms) itself attenuated the analgesic effects arising from peripheral administrations of opiate receptor agonist, morphine. In addition, the calcium channel antagonists, nifedipine and verapamil, enhanced 3A4P-induced analgesia but had no evident effects on the actions of 3B4P. These results suggest that the central analgesic effects of the FSH-suppressing steroid, 3A4P, arise via benzodiazepine--GABA--opiate mechanisms and calcium channels. These findings also suggest possible central modes of action whereby 3A4P may elicit selective suppression of FSH.

20-alpha-Dihydroprogesterone↗
PubMed1988

Exposure to time varying magnetic fields associated with magnetic resonance imaging reduces fentanyl-induced analgesia in mice.

The effects of exposure to clinical magnetic resonance imaging (MRI) on analgesia induced by the mu opiate agonist, fentanyl, was examined in mice. During the dark period, adult male mice were exposed for 23.2 min to the time-varying (0.6 T/sec) magnetic field (TVMF) component of the MRI procedure. Following this exposure, the analgesic potency of fentanyl citrate (0.1 mg/kg) was determined at 5, 10, 15, and 30 min post-injection, using a thermal test stimulus (hot-plate 50 degrees C). Exposure to the magnetic-field gradients attenuated the fentanyl-induced analgesia in a manner comparable to that previously observed with morphine. These results indicate that the time-varying magnetic fields associated with MRI have significant inhibitory effects on the analgesic effects of specific mu-opiate-directed ligands.

Analgesia↗
PubMed1988

Inhibitory influences of the adrenal steroid, 3 alpha, 5 alpha-tetrahydrodeoxycorticosterone [correction of tetrahydroxycorticosterone] on aggression and defeat-induced analgesia in mice.

The effects of intraperitoneal administrations of the deoxycorticosterone metabolite, 5 alpha-pregnane-, 21 diol-20-one (3 alpha, 5 alpha-tetrahydrodeoxycorticosterone; alpha-THDOC) on the responses to aggression and defeat-induced analgesia were examined in subordinate intruder male mice in "resident-intruder" pairings. alpha-THDOC reduced in a dose-dependent mannter (1-20 mg/kg) the number of bites and time to obtain defeat in subordinate mice during the agonistic encounters, as well as attenuating defeat-induced analgesia. These inhibitory effects of alpha-THDOC were separate from its sedative actions at 20-30 mg/kg. In addition, the stereo-isomer, 3 beta-pregnane-3 alpha, 21 diol-20-one (20 mg/kg) had no significant effects on the agonistic encounters and defeat, indicating that the inhibitory effects of alpha-THDOC on agonistic interactions are stereospecific. Pretreatment with the benzodiazepine antagonist Ro 15-1788 (5 and 10 mg/kg) attenuated the inhibitory effects of alpha-THDOC on defeat-induced analgesia. Ro 15-1788 (5, 10 mg/kg) by itself, however, had minimal effects on these agonistic interactions and subsequent defeat-induced analgesia. These results indicate that the naturally occurring steroid, alpha-THDOC, has significant effects on responses to aggression and defeat-induced analgesia.

Aggression↗
PubMed1988

Magnetic fields inhibit opioid-mediated 'analgesic' behaviours of the terrestrial snail, Cepaea nemoralis.

1. The terrestrial snail, Cepaea nemoralis, when placed on a warmed surface (40 degrees C) displays a thermal avoidance behaviour that entails an elevation of the anterior portion of the fully extended foot. The latency of this nociceptive response was increased by the prototypical mu and specific kappa opiate agonists, morphine and U-50, 488H, respectively, in a manner indicative of anti-nociception and the induction of 'analgesia'. Pretreatment with the prototypical opiate antagonist, naloxone, blocked the morphine- and reduced the U-50, 488H-induced analgesia. Naloxone had no effects on the thermal response latencies of saline treated animals. 2. Exposure to either cold (7 degrees C) or warm (38 degrees C) temperature stress increased the nociceptive thresholds of Cepaea in a manner indicative of the induction of 'stress-induced analgesia'. The warm stress-induced analgesia was opioid mediated, being blocked by naloxone, whereas, the cold stress-induced analgesia was insensitive to naloxone. 3. Exposure for 15-30 min to 0.5 Hz weak rotating magnetic fields (1.5-8.0 G) significantly reduced the analgesic effects of the mu and kappa opiate agonists in a manner similar to that observed with naloxone. The magnetic stimuli also inhibited the endogenous opioid mediated warm stress-induced analgesia and significantly reduced the cold stress-induced analgesia. The magnetic stimuli had no evident effects on the nociceptive responses of saline-treated animals. The dihydropyridine (DHP) and non-DHP calcium channel antagonists diltiazem, verapamil. and nifedipine differentially and significantly reduced, while the DHP calcium channel agonist, BAY K8644, significantly enhanced the inhibitory effects of the magnetic fields on morphine-induced analgesia.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1988

Brief exposure to a natural predator, the short-tailed weasel, induces benzodiazepine-sensitive analgesia in white-footed mice.

Exposure to a natural predator, the short-tailed weasel, Mustela erminea, elicited significant increases in the nociceptive responses of wild male white-footed mice, Peromyscus leucopus. A short (30 sec), ecologically relevant, nonvisual exposure to a weasel elicited a relatively brief (15 min) analgesia that was insensitive to the opiate antagonist, naloxone (1.0 mg/kg), and was blocked by either pre- or post-exposure injections of the benzodiazepine antagonist, Ro15-1788 (10 mg/kg), or agonist, diazepam (4.0 mg/kg). A 5 min exposure to the weasel elicited an analgesic response of longer duration (15-30 min) that was sensitive to both naloxone and the benzodiazepine agonist and antagonist. A 15 min exposure to the weasel induced a higher amplitude analgesia that was of relatively long duration (45 min), blocked by naloxone, and insensitive to the benzodiazepine manipulations. Exposures of 5 and 15 min to a nonpredator, the European rabbit, Oryctolagus cuniculus, elicited low amplitude, naloxone-reversible analgesic responses that were unaffected by the benzodiazepine manipulations. Thirty-sec exposures to the rabbit had no significant effects on the nociceptive response of the rabbit. These results indicate that a brief, ecologically appropriate, exposure to a predator elicits a benzodiazepine-mediated analgesia while a more prolonged exposure to a predator induces opioid-mediated analgesia. These results show that the opioid and nonopioid distinction between the effects of long- and short-term laboratory stresses is also evident with a natural, ecologically relevant, stressor.

Analgesia↗
PubMed1988

Novelty-induced opioid analgesia in the terrestrial snail, Cepaea nemoralis.

Exposure for 1-15 min to the surface of either a non-functional (22 degrees C) hot-plate or a polypropylene tube increased the thermal (38.5 degrees C) nociceptive thresholds of the terrestrial snail, Cepaea nemoralis. This "analgesic response," which was evident 10-15 sec after exposure to the new stimuli and lasted for 15-30 min, was blocked by the opiate antagonist naloxone. The analgesic response was not observed in snails previously made familiar with the test situation. Snails exposed to a functional (36.5 degrees C) stressful hot-plate surface to which they were aversive also displayed a naloxone-reversible analgesia. However, the level and duration of analgesia was markedly greater than that observed following exposure to the novel non-physically stressful stimuli and was not inhibited by prior familiarization with the stimuli. These observations demonstrate that novelty per se can activate endogenous opioid system(s) and induce an analgesic response in a snail. They also suggest a phylogenetic continuity in responses to novel stimuli and environmental conditions.

Animals↗
PubMed1988

Male scent-induced analgesia in the deer mouse, Peromyscus maniculatus: involvement of benzodiazepine systems.

Exposure to bedding taken from the soiled home cage of an isolated male resident elicited a significant increase in the nociceptive responses of male deer mice, Peromyscus maniculatus artemisiae, from mixed sex pairs. The analgesia induced by exposure to the male scent was insensitive to the opiate antagonist, naloxone, and was blocked by either pre- or post-olfactory exposure injections of the benzodiazepine antagonist, Ro 15-1788, or agonist, diazepam. This non-opioid analgesia was of brief duration (15-30 min) and rapid onset, being evident after 1 min of exposure to the olfactory cues. Bedding treated with the novel odor of peppermint also induced analgesia in the deer mice. This analgesia was opioid mediated, being blocked by naloxone and insensitive to the benzodiazepine manipulations. Exposure to either fresh bedding, or the soiled bedding of another mixed sex pair of deer mice, had no significant effect on nociception. These results indicate that exposure of male deer mice to the olfactory cues associated with a potentially threatening individual (dominant/aggressive isolated male) elicits an analgesic response that involves alterations in the activity of benzodiazepine systems.

Aggression↗
PubMed1988

Effects of opiate agonists and antagonists on aggressive encounters and subsequent opioid-induced analgesia, activity and feeding responses in male mice.

The effects of peripheral administration of the mu, kappa and sigma opiate agonists, levorphanol (1.0 mg/kg), U-50,488 (1.0 and 10.0 mg/kg), (+/-) SKF-10,047 (10.0 and 30.0 mg/kg), respectively, as well as the delta opiate antagonists, ICI-154,129 (10.0 mg/kg), and the prototypic antagonist, naloxone (1.0 mg/kg), on the agonistic behaviors and subsequent analgesic, locomotory and ingestive responses of subordinate mice were examined in a "resident-intruder" paradigm. The latter behaviors were examined in both defeated and nondefeated mice that had received an equivalent level of aggression. The mu and delta opiate antagonists decreased, while the mu, kappa, and sigma opiate agonists selectively increased aggressive behavior (number of bouts of aggressive interactions, number of bites to defeat, time to defeat). Both naloxone and the delta antagonist suppressed defeat- and aggression-induced activity and feeding, while only naloxone blocked the analgesic response. Levorphanol enhanced, U-50,488 had variable dose related effects, and SKF-10,047 decreased the defeat and aggressive-induced responses. These results indicate that various opioid systems and opiate receptors are differentially involved in the mediation of various components of the agonistic encounters and in the expression of the consequences of social conflict and defeat-induced opioid activation.

Aggression↗
PubMed1988

Evolutionary and comparative aspects of nociception.

The ability to detect and respond to aversive environmental stimuli is a basic feature of animals that is expressed in the term 'nociception.' Nociception and nociceptive responses provide an index of the sensitivity of individuals to aversive physical stimuli. Measurements of alterations in nociceptive responses (antinociception and analgesia) are commonly used to monitor the behavioral and physiological status of animals following experimental manipulation that usually, but not always, involve exposure to either noxious, stressful or potentially stressful physical and/or biological stimuli. This review briefly considers: i) the phylogenetic development of nociceptive responses and behaviors ii) evolutionary and comparative patterns of the neuromodulation of nociceptive behaviors by opioid peptides and other nonopioid peptidal regulatory mechanisms; iii) the effects of various biological variables, including; age, development, sex, and temporal factors (biological rhythms) on nociception in rodents.

Animals↗
PubMed1988

Body-rotation induced analgesia in male mice: effects of duration and type of rotation procedure.

The effects of body-rotation in a horizontal plane on the nociceptive responses of male mice were examined. In the first experiment the mice were rotated (70 rpm, schedule of 15 sec on; 5 sec off) for 30 minutes or exposed to sham rotation. The animals were then placed on a warm surface (47.5 degrees C) and their latency to show a foot-licking response was measured. Immediately after the preceding rotation procedure a trend toward a significant increase in response latencies, indicative of analgesia, was observed (p = 0.057). However, if tested 30 minutes after the end of the rotation period, no analgesia could be demonstrated (p greater than 0.50). In Experiment 2 mice were rotated (15 sec on; 5 sec off) or sham rotated for durations of 60 or 90 minutes. Response latencies were significantly elevated (p less than 0.01) after both rotation durations, but not differentially so (p greater than 0.20). In the last experiment the effects of 60 minutes of the intermittent rotation procedure (15 sec on; 5 sec off) were compared to those of 60 minutes of continuous rotation. Both types of rotation resulted in the induction of analgesia and the intermittent procedure produced a significantly greater degree of analgesia than the continuous rotation (p less than 0.05). These experiments demonstrate that 60 to 90 minutes of body-rotation can produce a significant "stress-induced" analgesia in mice and that an intermittent schedule of rotation is more effective than a continuous rotation exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗