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D H Malin

Publications and source records attributed to D H Malin.

At least 37 records · Page 2Linked to original sources
PubMed1992

Analog of neuropeptide FF attenuates morphine tolerance.

Previous studies suggest that neuropeptide FF (NPFF) plays a role in opiate dependence and subsequent abstinence syndrome. Endogenous NPFF also appears to play a role in opiate tolerance since third ventricle injection of IgG from NPFF antiserum selectively restores morphine sensitivity in morphine-tolerant rats. The NPFF analog, desamino YFLFQPQRamide (daY8Ra) has previously antagonized behavioral effects of NPFF and has attenuated morphine dependence. The present study assessed whether daY8Ra could similarly attenuate morphine tolerance. Third ventricle (i.c.v.) injection of daY8Ra restored the analgesic response to i.c.v. morphine in morphine-tolerant rats (radiant heat tail flick test). Saline injection failed to produce this effect. In opiate-naive rats, however, the same treatment with daY8Ra did not affect the analgesic response to i.c.v. morphine. Thus, daY8Ra appears to selectively restore morphine sensitivity in opiate-tolerant animals. These results further support the hypothesis that endogenous NPFF contributes to opiate tolerance.

Amino Acid Sequence↗
PubMed1992

Galanin attenuates retention of one-trial reward learning.

Galanin is a neuropeptide that coexists with acetylcholine in the septohippocampal pathway. Galanin appears to have a negative modulating influence on cholinergic transmission, suggesting that it might interfere with memory formation on a one-trial discriminative reward learning task. The apparatus was a starburst maze with five radiating alleys, one an ascending baited alley. The subjects were 38 two to three month old Sprague-Dawley rats cannulated in the body of the lateral ventricles and deprived to 80% of initial weight. Ten rats were infused i.c.v. over six mins. with 8 micrograms galanin in 24 microliters saline and 10 with saline alone. Twenty mins. after completion of infusion, each rat was placed in the maze and observed under "blind" conditions for number of errors (blind alleys entered) and latency to reach reward. Each rat's speed score was 100 sec./latency. One day later, each rat was retested in the maze. Each rat's retention scores were its decrease in errors and increase in speed between the single training trial and the retention trial. Galanin infused rats showed significantly less retention by both measures. In a second experiment, either the same dose of galanin or saline alone was infused 20 mins. before the retention trial. There was no significant effect, suggesting that galanin may interfere with memory formation rather than memory retrieval or task performance.

Animals↗
PubMed1992

Rodent model of nicotine abstinence syndrome.

Few animals models are currently in use for the recognized clinical problem of nicotine dependence and abstinence. This study introduces a rapid and convenient model using the rat. Sixteen male rats were rendered nicotine dependent by 7 days of continuous subcutaneous infusion of either 3 mg/kg/day (n = 8) or 9 mg/kg/day (n = 8) nicotine tartrate salt; 8 control rats were infused with saline alone. Rats were observed for 15 min before, during, and after the drug infusion period using a tally sheet modified from a standard checklist of opiate abstinence signs. There were few signs observed in any group at baseline and at the end of the infusion period. However, nicotine-infused rats showed a significant, dose-related increase over the control group at 16 h after the end of infusion, largely subsiding by 40 h. The most frequently observed signs during withdrawals included: teeth-chattering/chews, writhes/gasps, ptosis, tremors/shakes, and yawns. A significant drop in locomotor activity and increase in weight gain following termination of nicotine infusion provided additional evidence of an abstinence syndrome. This syndrome was alleviated by SC administration of 0.4 mg/kg nicotine tartrate.

Animals↗
PubMed1991

IgG from neuropeptide FF antiserum reverses morphine tolerance in the rat.

Previous studies suggest that neuropeptide FF (NPFF) plays a role in opiate dependence and subsequent abstinence syndrome. The present study assessed the role of NPFF in opiate tolerance. Third ventricular injection of IgG from NPFF antiserum restored the analgesic response to i.c.v. morphine in morphine-tolerant rats (radiant heat tail flick test). IgG from control serum failed to produce this effect. In opiate-naive rats, however, the same treatment with IgG from NPFF antiserum did not affect the analgesic response to i.c.v. morphine. Thus, immunoneutralization of NPFF appears to selectively restore morphine sensitivity in opiate-tolerant animals. These results support the hypothesis that endogenous NPFF contributes to opiate tolerance.

Amino Acid Sequence↗
PubMed1990

Augmented analgesic effects of L-tryptophan combined with low current transcranial electrostimulation.

The analgesic effects of low current transcranial electrostimulation are both naloxone and pCPA-reversible, suggesting that they may be mediated in part by endogenous opioid and serotonergic activity. The present experiments indicate that pretreatment with the serotonin precursor L-tryptophan results in an increased analgesic effect of electrostimulation as measured by the 50 degrees C wet tail flick test in the rat. Rats receiving both L-tryptophan and electrostimulation displayed significantly more analgesia than rats receiving electrostimulation and injection vehicle alone, rats receiving drug and sham stimulation or rats receiving vehicle and sham stimulation.

Analgesia↗
PubMed1989

Augmented analgesic effects of enkephalinase inhibitors combined with transcranial electrostimulation.

The analgesic effects of very low current transcranial electrostimulation are naloxone-reversible and thus presumably mediated by endogenous opioid activity. The present experiments indicate that blocking enkephalinase activity by i.c.v. thiorphan or i.p. acetorphan results in an increased analgesic effect of electrostimulation as measured by the 50 degrees C wet tail flick test. In the case of each drug, rats receiving both drug and electrostimulation displayed significantly more analgesia than rats receiving electrostimulation and injection vehicle alone, rats receiving drug and sham stimulation or rats receiving vehicle and sham stimulation.

Analgesia↗
PubMed1989

Low current electrostimulation produces naloxone-reversible analgesia in rats.

A new form of transcranial electrostimulation (TE) has been shown to induce analgesia in rats, as measured by the wet tail flick test. Charge-balanced rectangular current pulses of very low amplitude were delivered bilaterally into low impedance regions of the rat pinnae. The resultant analgesia was studied as a function of systematic variations in stimulus frequency, amplitude and duration. The optimal current for inducing analgesia was found to be 10 microA, well below the startle threshold, and several orders of magnitude below effective stimulus current levels required for other treatment modalities. The optimal stimulation duration was 30 min, during which time a slow onset of analgesia was noted. Significant analgesia persisted for at least 200 min after stimulation ended, and no evidence was found of tolerance developing in the course of 5 daily stimulation sessions. Consistent with findings for other forms of electrostimulation, the analgesic effect of TE was abolished by subcutaneous injection of 3 mg/kg naloxone, suggesting that the mechanism of TE analgesia has an endogenous opioid component.

Animals↗
PubMed1988

Auricular microelectrostimulation: naloxone-reversible attenuation of opiate abstinence syndrome.

This study evaluated the effects in rats of very low amplitude (10 mu amp) charge-balanced 10-Hz stimulation delivered bilaterally to low impedance points on the outer ear. This microelectrostimulation markedly and significantly reduced the number of opiate abstinence signs observed following a week of continuous morphine infusion. This effect was prevented by subcutaneous injection of 3 mg/kg naloxone, suggesting that stimulation of endogenous opioid activity plays a major role in the actions of auricular microelectrostimulation.

Animals↗
PubMed1987

Cerebrospinal fluid from morphine-dependent rats precipitates opiate abstinence syndrome.

Cerebrospinal fluid (CSF) was withdrawn from opiate-dependent rats following six hours of abstinence. It was infused into the third ventricle of opiate-dependent rats, precipitating immediate abstinence signs. The effect was similar to that of infusing the opiate antagonist naloxone, suggesting that opiate-dependent organisms may secrete an endogenous opiate antagonist substance. CSF withdrawn from non-dependent rats failed to precipitate an abstinence syndrome in morphine-dependent recipients. Conversely, CSF withdrawn from opiate-dependent rats following six hours of abstinence failed to precipitate an abstinence syndrome in non-dependent recipients. The active factor in the CSF is probably a peptide since it is filterable through a 10,000 MW filter and its activity is destroyed by three different proteolytic enzymes.

Animals↗
PubMed1986

Clonidine reverses the behavioral and respiratory effects of continuous naloxone infusion.

Opiate naive rats received 24 hours of continuous subcutaneous infusion of 0.67 mg/kg/hr naloxone via osmotic minipump. As in previous studies, this induced an opiate-abstinence-like syndrome of significantly increased oxygen consumption and behavioral signs (wet-dog shakes, abdominal writhes, etc.). Clonidine, which selectively reduces central noradrenergic activity, has been shown to reverse opiate abstinence syndrome. Subcutaneous injection of 0.033 and 0.01 mg/kg clonidine totally reversed the abstinence-like behaviors and respiratory activity induced by naloxone infusion. This constitutes an additional point of similarity between opiate abstinence syndrome and the "endorphin blockade syndrome" or withdrawal from endogenous opioids resulting from chronic naloxone treatment. It is consistent with the hypothesis that hyperactivity of central noradrenergic mechanisms may contribute to both phenomena.

Animals↗
PubMed1985

Continuous infusion of naloxone: effects on behavior and oxygen consumption.

Twenty-eight hours of endorphin receptor blockade by subcutaneous naloxone infusion produced behavioral and respiratory symptoms resembling opiate abstinence syndrome. Rats were implanted subcutaneously with two Alzet osmotic minipumps delivering 0.7 mg/kg per hour naloxone or with two control minipumps containing distilled water only. They were observed for 10 minutes under blind conditions at 16 and 28 hours post-implantation. The naloxone-infused rats showed significantly more wet dog shakes, abdominal writhes and overall abstinence-like symptoms than did the control rats. These symptoms decreased after 28 hours despite continued naloxone infusion. Acute administration of naloxone failed to produce abstinence-like symptoms, even when combined with the trauma of carrying two implanted water-filled minipumps for 28 hours. In another experiment, naloxone-infused rats showed a highly significant 53.4% elevation of O2 consumption over water-infused control rats in a pure O2 atmosphere at 28 hours after implantation. This difference disappeared at 48 hours post-implantation. In contrast to the effect of naloxone infusion, acute administration of three different doses of naloxone failed to significantly increase O2 consumption.

Animals↗
PubMed1982

Behavioral alterations produced by chronic naloxone injections.

Repeated blockade of the endorphin receptors eventually induces symptoms resembling an opiate abstinence syndrome, despite the complete absence of opiate narcotics. Rats were injected with 0.6 mg/kg naloxone or with injection vehicle alone twice a day for six days. They were observed twice a day for four subsequent days. Body shakes, head shakes, scratches and total symptoms were significantly elevated in the naloxone treated group over controls. Symptoms were completely reversed by a small dose of morphine but not by naloxone. In a second experiment, rats were injected for ten days with the same dosage of naloxone. The abstinence-like syndrome began after six days of naloxone and continued for several days after cessation of injections. Total symptoms, body shakes, scratches and aggression were significantly elevated over controls and were reversed by morphine but not by naloxone.

Animals↗
PubMed1976

Stimulus specific effect of scotophobin on mouse plasma corticoids.

Scotophobin is a peptide previously extracted from brains of rodents shocked in the dark compartment of a white/dark apparatus and identified as the behaviorally active dark avoidance-inducing factor. This study attempted to ascertain whether a stable synthetic analog of scotophobin induced no adrenocortical stress reaction, a generalized, unconditioned stress reaction, or a stress reaction selectively triggered by the dark compartment of the apparatus. Twenty eight mice were injected IP with the synthetic substance and 28 with placebo. A day later half of each group was placed in the dark compartment and the other half in the light compartment. Fifteen min afterward, the animals were bled, and serum samples were obtained. Plasma corticoid levels were determined by radioassay. Only the animals injected with scotophobin analog and exposed to the dark box had elevated levels. The interaction effect between drug treatment and light or dark environment was highly significant.

Adrenal Cortex↗