Biomedical subjects

M Kavaliers

Publications and source records attributed to M Kavaliers.

At least 145 records · Page 8Linked to original sources

PubMed1986

Prolyl-leucyl-glycinamide (PLG): inhibition of offensive aggression in mice.

The effects on offensive aggression of the endogenous peptide-leucyl-glycinamide (PLG, MIF-1) and the exogenous opiate antagonist, naloxone, were examined in male mice. PLG (0.01-10 mg/Kg) reduced, in a dose-dependent manner, the incidence and intensity of offensive aggression in dominant resident mice. PLG was more potent than naloxone (1.0 mg/Kg). In a number of cases, PLG completely eliminated the display of offensive aggression towards intruder mice. These results raise the possibility that PLG may function as an "anti-aggressive" peptide whose actions may include antagonistic and/or modulatory influences on both opioid and non-opioid systems.

Aggression↗

PubMed1986

An octadecaneuropeptide (ODN) derived from diazepam binding inhibitor increases aggressive interactions in mice.

The effects of intracerebroventricular administrations of an octadecaneuropeptide (ODN) derived from the polypeptide, diazepam binding inhibitor (DBI), on offensive and defensive aggression were examined in male mice. During the initial period after administration (1-5 min) ODN inhibited social and agonistic behavior. At 30 min after treatment, ODN increased, in a dose-dependent manner, the incidence of and intensity of offensive aggression in dominant resident mice. ODN also increased the number of bites required to obtain defeat in subordinate mice during aggressive interactions, as well as reducing subsequent defeat-induced analgesia. These changes in offensive and defensive aggressive behavior that were induced by ODN were reduced by the benzodiazepine receptor antagonist Ro 15-1788. These results suggest that ODN has significant modulatory effects on aggression.

Aggression↗

PubMed1986

Magnetic field inhibition of morphine-induced analgesia and behavioral activity in mice: evidence for involvement of calcium ions.

An exposure for 60 min to a 0.5 Hz rotating magnetic field (1.5-90 G) significantly reduced the day-time analgesic (in CF-1 mice) and locomotory (in C-57BL mice) effects of morphine (10 mg/kg). Intracerebroventricular (i.c.v.) injections of a calcium chelator, EGTA, blocked these effects, while administration of the calcium ionophore, A23187, potentiated the inhibitory actions. In a parallel fashion, i.c.v. administration of Ca2+ reduced, in a dose-related manner, the analgesic and locomotory effects of morphine in control CF-1 and C57 mice. These latter inhibitory effects could also be blocked by EGTA and augmented by A23187, indicating that opiate effects on activity and nociception are both sensitive to antagonism by calcium. Taken together these results suggest that exposure to magnetic stimuli may alter morphine-induced responses in mice, in a manner compatible and consistent with effects on Ca2+ and possibly other divalent ions.

Analgesia↗

PubMed1986

Inhibitory influences of FMRFamide and PLG on stress-induced opioid analgesia and activity.

The effects of i.c.v. administration of the peptide FMRFamide (Phe-Met-Arg-Phe-NH2), as well as i.p. injections of PLG (Pro-Leu-Gly-NH2) and the opiate antagonist, naloxone, on immobilization-induced analgesia and locomotor activity were examined in CF-1 and C57BL strains of mice. Both naloxone (1.0 mg/kg) and FMRFamide (0.10-1.0 microgram) blocked the experimentally induced analgesia and activity, whereas PLG (0.10-10 mg/kg) suppressed only analgesia. These results indicate that FMRFamide (or FMRFamide-like neuropeptides) and PLG may function as differential antagonists of the behavioral and physiological consequences of endogenous opioid activation.

Animals↗

PubMed1986

Naloxone-reversible stress-induced feeding and analgesia in the slug Limax maximus.

Exposure to tail-pinch stress increased the thermal nociceptive thresholds and food intakes of the slug, Limax maximus. These stress-induced "analgesic" and feeding responses, which were similar to the behaviors observed after treatment with exogenous opiates, were blocked by the opiate antagonist, naloxone. These results indicate that exposure to stress increases endogenous opioid activity in slugs and induces various behavioral and physiological responses in a manner analogous to that reported in mammals.

Animals↗

PubMed1986

Stress-induced opioid analgesia and activity in mice: inhibitory influences of exposure to magnetic fields.

An exposure for 30 min to a 0.5 Hz rotating magnetic field (1.5-90 G) significantly reduced immobilization stress-induced, opioid analgesia and hyperactivity in CF-1 and C-57 BL strains of mice, respectively. The magnetic exposure also eliminated the day-night rhythm in stress-induced analgesia, with maximum inhibitory effects occurring in the dark period. Pre-treatment with naloxone (1.0 mg/kg) had comparable inhibitory effects on immobilization-induced analgesia and activity. These results suggest that exposure to magnetic stimuli can significantly influence stress-induced activation of endogenous opioid systems and their behavioral and physiological consequences.

Animals↗

PubMed1986

Environmental specificity of tolerance to morphine-induced analgesia in a terrestrial snail: generalization of the behavioral model of tolerance.

Terrestrial snails, Cepaea nemoralis, develop tolerance to morphine-induced analgesia, such that after 7-9 days of treatment with morphine (10 mg/kg) their response latencies to an aversive thermal stimuli (38.5 degrees C) are not significantly different from those of untreated control animals. In Experiment A snails were rendered tolerant to morphine using either of two pre-injection cues (light and dark background brightness or color) and then assessed for morphine-induced alterations in thermal nociceptive responses in both environments. In Experiment B snails were made tolerant to morphine in the presence of one of two different thermal cues (a stressful temperature of 35 degrees C that is normally avoided or an ambient temperature of 22 degrees C) and then tested for morphine-induced alterations in nociceptive responses in both environments. In the two experiments tolerance to morphine-induced analgesia was displayed when snails were exposed to the pre-injection environmental cue normally associated with the administration of morphine, but not when exposed to the alternative pre-injection cue. These results demonstrate that various environmental factors (background colors or brightness as well as temperature cues and potentially thermal stress), can function as environmental specific cues for the development of tolerance to morphine-induced analgesia in molluscs, in a manner consistent with a behavioral mechanism of tolerance. Thus, these results suggest that environmental specificity of tolerance involving either classical (Pavlovian) conditioning or habituation may be a general phenomenon having an early evolutionary development and broad phylogenetic continuity.

Analgesia↗

PubMed1986

Food hoarding and ingestion in the deer mouse, Peromyscus maniculatus: selective responses to mu and kappa opiate agonists.

The feeding behavior of the deer mouse, Peromyscus maniculatus, includes food hoarding as well as ingestion. Administration of the prototypical mu opiate agonist, morphine sulfate, 1-20 mg/kg, produced over three hours a significant dose-dependent stimulation of hoarding by free feeding deer mice. The specific kappa opiate agonist, U-50,488H, 0.10-10 mg/kg, markedly increased ingestion without having any augmentatory effects on hoarding. The mixed mu and kappa opiate agonist, ketocyclazocine hydrochloride, 1-10 mg/kg, as well as various combinations of morphine sulfate and U-50,488H, augmented both hoarding and ingestion. Food restriction for 24 hr caused a significant, naloxone (1.0 mg/kg) reversible, increase in food intake. Food deprivation also modified the hoarding and ingestion responses of the deer mice to the mu and kappa opiate agonists, reducing the relative amounts of food that were hoarded. These results indicate that mu and kappa opioid systems are differentially involved in the mediation of various aspects of feeding. This also suggests that environmental factors, such as food restriction, can modify the relative roles of mu and kappa opioid systems in the expression of feeding behavior.

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

PubMed1986

Mu- and kappa-opiate agonists modulate ingestive behaviors in the slug, Limax maximus.

Administration of the prototypical mu opiate agonist, morphine sulphate, 1-10 mg/kg, produced over three hours a significant dose-dependent increase in the ingestive responses of free-feeding slugs, Limax maximus, although lower doses, 0.10 mg/kg, attenuated feeding. The mixed mu and kappa opiate agonist, ketocyclazocine hydrochloride, in the dose range 1.0-10 mg/kg, also induced significant increases in food consumption. With both of these opiates there was a latency of about 0.5 hr before initiation of feeding. The more specific kappa opioid agonist, U-50,488H, given over the dose range 0.10-1.0 mg/kg, produced a more potent increase in three hour food consumption by Limax, whereas a dose of 10 mg/kg produced a significant increase in ingestive responses for 3-4 hr after a 1-2 hr period of inactivity. The prototypic mu opiate antagonist, naloxone hydrochloride (1.0 mg/kg) blocked the feeding effects of morphine and ketocyclazocine and reduced the effects of U-50,488H. The delta antagonist, ICI 154,129, in a dose of 10 mg/kg, reduced the effects of morphine as well as decreasing food intake of free-feeding slugs. These results indicate that activation of differential opiate receptors in invertebrates has similar effects on feeding behavior as occur in mammals, suggesting early evolutionary development of opioid involvement in the control of feeding.

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

PubMed1986

FMRFamide: an endogenous peptide with marked inhibitory effects on opioid-induced feeding behavior.

The peptide FMRFamide (Phe-Met-Arg-Phe-NH2), which displays a broad phylogenetic distribution, is considered to have important regulatory influences on basic functions in invertebrates. Extensive FMRFamide-like immunoreactive neuropeptides have also been demonstrated in the mammalian central nervous system, suggesting a possible physiological role for these peptides in mammals. There is evidence that FMRFamide, and/or related neuropeptides, may modulate opioid-mediated responses. Intracerebroventricular (ICV) administrations of FMRFamide inhibit in a dose-dependent manner (0.01-10 micrograms) mu- (morphine) and kappa- (U-50,488H) opiate-induced feeding in the laboratory mouse. In deer mice, FMRFamide inhibits the display of exogenous opiate-induced components of natural feeding behavior, such as food hoarding and food ingestion. In addition, ICV administrations of FMRFamide also antagonize endogenous opioid-mediated, stress-induced feeding in mice. These observations suggest that FMRFamide, or FMRFamide-like peptides present in the mammalian brain, may have important roles in the control of opioid-mediated feeding.

Animals↗

PubMed1985

Differential opiate influences on food hoarding and intake in the deer mouse, Peromyscus maniculatus.

The feeding behavior of the deer mouse, Peromyscus maniculatus, includes food hoarding as well as ingestion. In this animal the mu opiate agonist, morphine, and the kappa opiate agonist, U-50, 488H, selectively stimulate food hoarding and ingestion, respectively. This suggests that mu and kappa opiate systems may differentially mediate primary components of natural feeding behavior.

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

PubMed1985

Exposure to nuclear magnetic resonance imaging procedure attenuates morphine-induced analgesia in mice.

Adult male mice exposed to a Nuclear Magnetic Resonance Imaging (NMRI) procedure during the mid-dark period and injected with morphine (10 mg/kg) failed to exhibit the normal nocturnally enhanced morphine analgesia response to a thermal stimulus that was displayed by mice exposed to a sham imaging procedure and treated with morphine (p less than .01). When tested during the mid-light period, animals exposed to the NMRI procedure and given morphine displayed attenuated analgesia levels relative to sham exposed mice (p less than .01) treated with morphine. However, the morphine induced analgesia was not totally abolished since the imaged mice still exhibited analgesia relative to saline treated mice (p less than .01). These results suggest that the magnetic and/or radio-frequency fields associated with the NMRI procedure alter both day- and night-time responses to morphine. These results may reflect magnetic field induced alterations in neuronal calcium binding and/or alterations in nocturnal pineal gland activity.

Analgesia↗

PubMed1985

Tolerance to morphine-induced analgesia in mice: magnetic fields function as environmental specific cues and reduce tolerance development.

Mice receiving daily injection of morphine (10 mg/kg) developed tolerance to morphine-induced analgesia, such that after 5-7 days of treatment their thermal response (paw licking) latencies in the hot plate test were indistinguishable from those of control animals. Exposure to a rotating magnetic field for thirty minutes before the daily morphine administrations significantly reduced the development of tolerance. These magnetic exposures also significantly increased over 7-10 days the basal nociceptive thresholds and paw licking response latencies of saline treated mice. Control and sham exposed mice that were fully tolerant to the analgesic effects of morphine failed to show any tolerance to morphine-induced analgesia when exposed to the magnetic stimuli prior to injection. Likewise, the partial tolerance to morphine shown by mice exposed to the rotating magnetic field pre-injection environmental cues was eliminated when control or sham pre-injection cues lacking the magnetic stimuli were provided. In all cases tolerance to morphine-induced analgesia was evident in the subsequent re-test with the original cues. These results indicate that magnetic field exposure can reduce the development of tolerance to the analgesic effects of morphine. They also show that magnetic stimuli function as significant environmental cues for the development of tolerance to morphine-induced analgesia. This suggests that magnetic stimuli affect both the associative (classical conditioning) and non-associative (physiological, pharmacological) mechanisms involved in the development of opiate tolerance.

Analgesia↗

PubMed1985

Nocturnal feeding in the mouse--opiate and pineal influences.

Mice displayed daily rhythms in their basal and morphine-induced food intake, consuming significantly greater amounts of food at night. Non-invasive inhibition of the activity of the pineal gland by either exposure to a bright pulse of light or treatment with the L-amino-acid decarboxylase inhibitor, benserazide, reduced the elevated night-time food intakes. These effects on feeding were most evident on the first night the activity of the pineal was reduced. On subsequent nights light pulses had a diminished effect on basal and morphine-induced food intake. These results suggest that although the enhanced nocturnal food intake of mice may be modulated by pineal and opioid sensitive mechanisms, pineal activity is not essential for the expression of opioid-mediated feeding.

Animals↗

PubMed1985

The influence of opiate agonists on day-night feeding rhythms in young and old mice.

Daily rhythms of feeding behavior and responses to ketocyclazocine, morphine and naloxone were measured in young (1-2 months) and old (24-30 months) male CF-1 mice. All of the mice consumed more food at night than in the day-time, though this nocturnal peak was markedly reduced in the old animals, who consumed more in the day. The young mice also displayed a significant nocturnal enhancement in ketocyclazocine- and morphine-stimulated feeding. This day-night rhythm in ingestive responses was absent in the old mice. In comparison to the young mice, the opiate-stimulated food consumptions of the old animals were reduced at all times. Additionally, the old animals failed to show any day-night variations in the suppressive effects of naloxone on deprivation-induced food intake that were displayed by the young animals.

Aging↗

PubMed1985

The effects of aging on day-night rhythms of kappa opiate-mediated feeding in the mouse.

Day-night rhythms in feeding behavior and response to the specific kappa opioid agonist U-50,488H (0.10-10. mg/kg) were measured in young (1-2 months), mature (8-12 months) and old (24-30 months) male CF-1 mice. All the mice consumed more food at night than in the day-time, though this nocturnal peak was markedly reduced in old and mature animals. Young mice also displayed a significant, dose-related, nocturnal enhancement in U-50,488H-stimulated feeding. This day-night rhythm was reduced in mature animals and absent in old mice. In old mice, U-50,488H significantly stimulated feeding only after the high dose of 10 mg/kg. Additionally, old animals did not show the dose-dependent latency to initiation of feeding after administration which was observed in young mice and to a lesser extent in mature animals.

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

PubMed1985

The effects of opioid and FMRF-amide peptides on thermal behavior in the snail.

Administration of methionine-enkephalin, beta-endorphin or, as previously shown, the opiate agonist, morphine sulfate (0.10-10.0 micrograms per snail), resulted in significant dose-dependent increases in the latency of thermal (40 degrees C hot plate) avoidance behavior of the terrestrial snail, Cepaea nemoralis. The analgesic effects could be blocked by the opiate antagonist, naloxone, as well as by the non-opioid peptides, FMRF-amide and YGG-FMRF-amide. When administered by themselves the FMRF-amide peptides had significant bimodal effects either decreasing (0.10 and 10.0 micrograms) or increasing (1.0 micrograms) the latency of the response to the thermal stimulus. These results indicate that opioid and FMRE-amide peptides may be involved in the determination of thermal behavior in the snail. They also suggest that FMRF-amide peptides may function as endogenous modulators of opioid activity.

Animals↗

PubMed1985

Exposure to rotating magnetic fields alters morphine-induced behavioral responses in two strains of mice.

An exposure for 60 min to a 0.5 Hz rotating magnetic field (1.5-90 G) significantly reduced the day-time analgesic and locomotory effects of morphine (10 mg/kg) in CF-1 and C-57BL strains of mice, respectively. Exposure to lower intensity 60 Hz magnetic fields (0.-1.0 G) had no effect on analgesia induced by morphine. The reduction in responsiveness to morphine after exposure to the greater intensity rotating field was not evident 24 hr later. No changes were seen in the latencies of basal thermal responses or levels of activity of saline-treated mice exposed to the magnetic stimuli.

Animals↗