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Biomedical subjects

M Kavaliers

Publications and source records attributed to M Kavaliers.

At least 163 records · Page 9Linked to original sources

Magnetic fields inhibit opioid-induced feeding in the slug, Limax maximus.

Exposure to rotating and elevated magnetic fields significantly reduced over three hours the ingestive effects of the opiate agonist, morphine (10 mg/kg), in free-feeding slugs, Limax maximus. Magnetic field exposure also inhibited the opioid-mediated increased ingestive responses of slugs that had been food-deprived for 24 hr. These results suggest that magnetic stimuli inhibit opiate-mediated behavioral and physiological functions in invertebrates in a similar manner as observed in vertebrates.

Animals↗

FMRFamide, a putative endogenous opiate antagonist: evidence from suppression of defeat-induced analgesia and feeding in mice.

Social conflict and defeat in mice leads to an activation of endogenous opiate systems. The effects of intracerebroventricular administration of the peptide FMRFamide (Phe-Met-Arg-Phe-NH2) and the opiate antagonist naloxone, on aggressive encounters, defeat-induced analgesia and defeat-induced feeding were examined in male mice. Both substances reduced the number of bites required to cause defeat in subordinate mice during aggressive encounters, as well as suppressing the subsequent defeat-induced analgesia. Administration of FMRFamide or naloxone also reduced defeat-induced feeding. These results indicate that FMRFamide (or FMRFamide-like neuropeptides) may function as endogenous opioid antagonists.

Analgesia↗

PLG and FMRFamide--endogenous peptides with marked inhibitory effects on opioid-induced feeding.

Social conflict and defeat in mice leads to an activation of endogenous opiate systems and the display of marked feeding behavior. Intraperitoneal administrations of prolyl-leucyl-glycinamide (PLG 0.01-10 mg/kg) leads to a dose-dependent inhibition of defeat-induced feeding that is analogous to that obtained after treatment with either the endogenous peptide FMRFamide (Phe-Met-Arg-Phe-NH2), or the prototypic opiate antagonist, naloxone. These results suggest that PLG, and FMRFamide, or related small peptides may function as endogenous antagonists of opioid-induced feeding.

Animals↗

Magnetic fields as environmental specific cues for morphine-induced analgesia: interactions with tolerance development.

It has been previously demonstrated that weak fluctuating magnetic fields can act as environmental specific cues for the development of tolerance to morphine-induced analgesia in mice. During the course of this tolerance development the basal nociceptive response of the animals preexposed to magnetic fields are also increased. The magnetic field-induced increase in the basal nociceptive response can be blocked by the opiate antagonist, naloxone, suggesting an opioid-mediated stress effect of the magnetic stimuli. It is suggested that part of the actions of the magnetic stimuli as environmental specific stimuli may arise through their actions as stressors during the tolerance acquisition phase, as well as from their effects on opioid systems.

Animals↗

Opioid systems and feeding in the slug, Limax maximus: similarities to and implications for mammalian feeding.

Substantial evidence is accumulating to implicate opioid systems in the regulation of behavioral and physiological functions in invertebrates in a manner analogous to that observed in vertebrates. This communication reviews opiate involvement in the mediation of the ingestive behaviors of the terrestrial slug, Limax maximus. The similarities to and implications for opioid modulation of mammalian feeding are considered.

Animals↗

Inhibitory influences of FMRFamide on morphine- and deprivation-induced feeding.

Intracerebroventricular administration of 0.01-1.0 microgram of the peptide FMRFamide (Phe-Met-Arg-Phe-NH2) to mice reduced morphine-induced feeding. Administration of FMRFamide also inhibited feeding induced by a 24-hour period of food deprivation. These results suggest that FMRFamide or FMRFamide-like neuropeptides play an important role in the control of opioid-mediated feeding.

Animals↗

Evidence for the activation of the endogenous opiate system in hamsters infected with human blood flukes, Schistosoma mansoni.

Nociceptive thresholds were investigated in golden hamsters infected with the human blood fluke, Schistosoma mansoni. Increases in thermal thresholds suggestive of analgesia were evident by 20-25 days of infection. These increased further during a 40-42 day period. The altered responses were suppressed by the opioid antagonist naloxone. Non-invasive inhibition of the activity of the pineal gland by exposure to light also reduced nocturnal analgesia in schistosome infected animals. Naloxone antagonism and pineal inhibition of morphine- induced analgesia was obtained similarly in control, uninfected animals. Taken together, these findings suggest strongly that infection with S. mansoni results in a chronic activation of the endogenous opiate system.

Analgesia↗

Ionizing radiation induces opioid-mediated analgesia in male mice.

The effects of exposure to ionizing radiation on the nociceptive thresholds of CF-1 mice were examined. Significant increases in thermal response latencies, indicative of analgesia were observed after exposure to either high or low doses of radiation. However, the onset of analgesia occurred significantly more rapidly after treatment with the high doses. Administration of the opiate antagonist, naloxone, blocked and reversed the analgesic effects of both the high and low dose of radiation. These findings support the hypothesis that exposure to ionizing radiation results in opioid-mediated analgesia.

Animals↗

Social conflict activates opioid analgesic and ingestive behaviors in male mice.

The activation of endogenous opioid mechanisms and their subsequent effects on rodent behavior and physiology has usually been characterized following artificial stress. In this study the more naturalistic stress arising from social conflict between male mice was used to investigate the involvement of opioid systems in post-conflict analgesic and ingestive behaviors. Both the aggressive encounters and the subsequent defeat experience resulted in marked analgesia and the induction of ingestive behaviors. Feeding and drinking responses were analogous to those observed after administrations of either the endogenous opioid peptide, beta-endorphin, or the exogenous opioid agonist morphine. The ingestive behaviors following defeat or central opiate administration were blocked by the opiate antagonist naloxone. The present results support the hypothesis of a direct activation of the endogenous opiate system following social conflict.

Aggression↗

The presence of an opioid system mediating behavioral thermoregulation in the terrestrial snail, Cepaea nemoralis.

Administration of the opiate agonist, morphine sulfate (0.1-10 micrograms per snail) resulted in a significant dose- and time-dependent increase in the temperatures selected by the terrestrial snail, Cepaea nemoralis, in a thermal gradient. These thermoregulatory effects could be blocked and reversed by naloxone hydrochloride, with the opiate antagonist by itself (1 and 10 micrograms) causing a significant decrease in preferred temperatures. After 6-10 days of daily administration of morphine, Cepaea displayed tolerance, the effects of morphine decreasing and thermal preferences becoming similar to those of saline-treated individuals. These results suggest that an opioid system is involved in the control of thermoregulation in snails, in a manner that is similar to that shown by vertebrates.

Animals↗

Opioid-induced feeding in the slug, Limax maximus.

Administration of the opioid agonist, morphine (1 and 10 mg X kg-1), resulted in significant, dose-dependent increases in the ingestive responses of food-deprived slugs, Limax maximus, and in the initiation of feeding in satiated animals. These effects could be blocked by the opiate antagonist, naloxone (1 mg kg-1), with naloxone by itself causing a significant decrease in the feeding of food-deprived slugs. These results suggest that opiates are involved in the control of the feeding behavior of Limax.

Animals↗

Opiates influence behavioral thermoregulation in the curly-tailed lizard, Leiocephalus carinatus.

Low doses of the opioid agonist, morphine (1-3 mg kg-1), significantly increased the behaviorally selected body temperatures of the curly-tailed lizard, Leiocephalus carinatus. A higher dose of morphine (10 mg kg-1) resulted in an initial behavioral hyperthermia that was followed by a significant decrease in preferred temperatures and a subsequent behavioral hypothermia which declined to control levels within 3-4 hr. These effects could be blocked and reversed by the opiate antagonist, naloxone, with naloxone (1 and 10 mg kg-1) by itself causing significant dose-dependent decreases in preferred temperatures. These morphine and naloxone induced changes occurred regardless of initial body temperatures. These results suggest that opiates are involved in the control of behavioral thermoregulation in lizards.

Animals↗

Magnetic fields abolish the enhanced nocturnal analgesic response to morphine in mice.

Mice given morphine displayed diel rhythms in the latency of their behavioral response to placement on a hot plate, there being a several fold increase in their nocturnal reaction times. Exposure to a rotating magnetic field eliminated the day-night analgesia rhythms, reducing over 5-10 days the enhanced nocturnal latencies to those found during the day. The attenuation returned to normal nocturnal levels several days after removal of the rotating magnetic field and could be subsequently re-established by reapplication of the magnetic field condition. It is suggested that these changes in analgesia may reflect alterations in the activity of the pineal gland during exposure to magnetic fields.

Analgesia↗

Aging and daily rhythms of analgesia in mice: effects of natural illumination and twilight.

Day-night rhythms in aversive thresholds and morphine-induced analgesia were assessed in young (1-3 months) and old (22-30 months) male mice exposed to natural summer (43 degrees N lat.) lighting using a hot-plate technique. In both age groups peak aversive thresholds and morphine-induced analgesia were present at night, with significantly reduced response times in the day. Response times increased during the course of the day with maximum increases in aversive thresholds and analgesia occurring during the decreasing light levels of dusk. Maximum decreases in the nocturnal response times occurred during the increasing light levels of dawn. The old mice displayed significantly lower nocturnal aversive thresholds and morphine-induced analgesia, as well as less pronounced patterns of change in response times during the dawn and dusk twilight lighting transitions. No significant effects of age were evident during the day-time.

Aging↗

Age and day-night changes in clonidine-induced analgesia in mice.

Administrations of clonidine hydrochloride (0.1, 1.0 mg/kg) to young, mature, and old mice influenced their response time on a thermally aversive surface (50 degrees C) in an age-dependent manner. This analgesic effect was of short duration. During daytime measurement periods, young and mature mice showed significantly greater analgesic responses than did the old animals. Although all animals were able to perform the appropriate paw-licking response, the old mice displayed tremors and locomotor disturbances after receiving clonidine. These effects were not seen in the younger groups. Both the young and mature animals showed a substantial enhancement of their analgesic responses after receiving clonidine at night, whereas a significant but much reduced nighttime increase in antinociceptive effect was seen in old animals. Yohimbine, but not prazosin, inhibited clonidine-induced analgesia in young animals. Old mice given combinations of clonidine and these adrenergic antagonists showed elevations in response times, accompanied by severe behavioural changes.

Age Factors↗

Daily rhythms of analgesia in mice: effects of age and photoperiod.

Daily rhythms in response to aversive thermal stimulation and the analgesic effectiveness of morphine were assessed by the hot-plate method with young (1-2 months), mature (8-12 months) and old (20-30 months) mice exposed to various light-dark conditions (LD 12:12; 16:8; 8:16 h). The patterns of response after saline or morphine varied with the specific light-dark conditions examined, but routinely, there were increases in response latency from the early portions of the light phase to later time, and a further enhancement of the time to respond with onset of the dark phase. The dark-phase response declined abruptly with the start of the light-phase. Significant age-related declines were observed in the elevated, dark-phase morphine-analgesic and basal aversive responses, with no consistent effects of age evident in the light-phase.

Aging↗

Reduced nocturnal morphine analgesia in mice following a geomagnetic disturbance.

Latency to respond to an aversive thermal stimulus and the degree of analgesia induced by morphine were examined in mice injected with either isotonic saline or morphine sulfate (10 mg/kg) during midscotophase of a 12:12 h LD cycle. When mean response latencies were compared to the degree of geomagnetic disturbance (Ap index) present on test days, it was found that during the geomagnetic storm on December 17th, 1982, a significant reduction (P less than 0.01) in response latency was evident in both saline- and morphine-treated mice. The reduction in response latencies was greater, and lasted longer in the morphine-treated animals. It is suggested that the pineal gland may mediate this biomagnetic effect.

Analgesia↗

Ageing, opioid analgesia and the pineal gland.

The effects of ageing on day-night rhythms of analgesia was examined with young (1-2 months), mature (8-12 months) and old (20-30 months) mice. Significant age-related declines were observed both in the absolute levels and diel rhythms of morphine analgesia, with the most pronounced changes occurring at night. Administration of the pineal hormone, melatonin, augmented day-time levels of analgesia in all age classes and reversed the age-related decline in nocturnal morphine analgesia in old mice. Inhibition of pineal function in young mice by either exposure to light pulses or treatment with benserazide mimicked the effects of ageing on nocturnal morphine analgesia. These findings suggest that the pineal gland and melatonin are involved in modulating diel rhythms of analgesia and have an influential role on age-related changes in opioid responses.

Aging↗