Phenytoin reversal and prevention of morphine-induced catalepsy in the rat

Cookson, S. L.; Mann, J. Douglas

doi:10.1016/0091-3057(80)90160-4

Cited by 3 publications

(4 citation statements)

References 18 publications

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“…Morphine‐induced immobility (opiate catalepsy) was significantly higher on Day 1 relative to Day 28, suggestive of motor tolerance. The exact mechanism underlying opiate‐induced catalepsy is not known although it can be significantly prevented or reversed by phenytoin (antiepileptic) and naloxone (opioid receptor antagonist) (Cookson and Mann, 1980), and the development of tolerance to morphine‐induced catalepsy can be delayed by lesioning the ventral tegmental area (VTA) (Hand and Franklin, 1985).…”

Section: Discussionmentioning

confidence: 99%

Cocaine‐ and morphine‐induced synaptic plasticity in the nucleus accumbens

Alcantara

Lim

Floyd

et al. 2010

Synapse

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The critical brain areas and molecular mechanisms involved in drug abuse and dependence have been extensively studied. Drug-induced persistent behaviors such as sensitization, tolerance or relapse, however, far outlast any previously reported mechanisms. A challenge in the field of addiction, therefore, has been to identify drug-induced changes in brain circuitry that may subserve long-lasting changes in behavior. The present study examined behavioral changes and electron microscopic evidence of altered synaptic connectivity within the nucleus accumbens (NAc) following repeated administration of cocaine or morphine. The unbiased quantitative stereological physical disector method was used to estimate the number of synapses per neuron. Increases in synapse to neuron ratio were found in the NAc shell of cocaine-treated (49.1%) and morphine-treated (55.1%) rats and in the NAc core of cocaine-treated animals (49.1%). This study provides direct ultrastructural evidence of drug-induced synaptic plasticity and identifies synaptic remodeling as a potential neural substrate underlying drug-induced behavioral sensitization.

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Section: Discussionmentioning

confidence: 99%

Cocaine‐ and morphine‐induced synaptic plasticity in the nucleus accumbens

Alcantara

Lim

Floyd

et al. 2010

Synapse

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“…Earlier findings suggested that at least some forms of morphine-induced activation were seizuredependent, for example, phenytoin pretreatment was reported to eliminate opiate-induced feline mania (Fertziger et al, 1974). Phenytoin also has been shown to reduce morphine-induced catalepsy in rats (Cookson and Mann, 1978). It may be concluded that the responses induced by morphine must be evaluated carefully within and across species and testing situations.…”

Section: Discussionmentioning

confidence: 99%

Facilitation of opiate-and enkephalin-induced motor activity in the mouse by phenytoin sodium and carbamazepine

Katz

Schmaltz

1979

Psychopharmacology

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In the first experiment, adult male Swiss-Webster mice were systemically injected with a standard dose of morphine. Compared to the influence of vehicle, the motor activity of morphine-injected mice was increased. Neither phenytoin sodium nor carbamazepine alone facilitated motor activity, but pretreatment with both drugs further facilitated the increased motor activity produced by morphine. In a second experiment, mice were injected centrally with a long-acting analog of leu-enkephalin. It also increased motor activity in comparison with vehicle. Again, both phenytoin sodium and carbamazepine further facilitated this response. Both experiments suggest a facilitatory interaction between some aspects of these anticonvulsants and opiate-induced motor activity.

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“…The effects of the same drugs upon activation produced by central administration of a long-lasting enkephalin analog (o-ala'-leu-enkephalinamide) were investigated, with similar results. These findings confirm a behavioral interaction between opiate and anticonvulsant drugs, although it may be selective for certain classes of anticonvulsant compounds.Previous studies (Cookson and Mann, 1978; Katz and Schmaltz, 1979) have proposed the existence of behavioral interactions between endogenous and exogenous opiates and anticonvulsant drugs, with anticonvulsants facilitating behavioral activation to opiates. It may be inferred that some property of opiates, possibly related to seizures, normally inhibits at least certain classes of behavior and this additionally supported electroencephalographically (e.g.…”

mentioning

confidence: 99%

“…Previous studies (Cookson and Mann, 1978; Katz and Schmaltz, 1979) have proposed the existence of behavioral interactions between endogenous and exogenous opiates and anticonvulsant drugs, with anticonvulsants facilitating behavioral activation to opiates. It may be inferred that some property of opiates, possibly related to seizures, normally inhibits at least certain classes of behavior and this additionally supported electroencephalographically (e.g.…”

mentioning

confidence: 99%

Behavioral interactions between opiate and antiepileptic drugs in the mouse

Katz

Schmaltz

1981

Neuropharmacology

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Summary-Morphine and related opioid compounds are known to possess proconvulsant activity based upon both electroencephalographic and behavioral criteria. The present authors previously suggested that opiate-related seizures were behaviorally inhibitory, and this was further investigated in the present study. The effects of pretreatment with three pharmacologically distinct compounds (sodium valproic acid, trimethadione, taurine) upon normal behavioral activation to systemic morphine were examined in the mouse. Morphine consistently increased activity levels in comparison with vehicle. Each of the three experimental compounds itself was behaviorally inhibitory; nonetheless both sodium valproate and trimethadione facilitated behavioral responses to morphine. The effects of the same drugs upon activation produced by central administration of a long-lasting enkephalin analog (o-ala'-leu-enkephalinamide) were investigated, with similar results. These findings confirm a behavioral interaction between opiate and anticonvulsant drugs, although it may be selective for certain classes of anticonvulsant compounds.Previous studies (Cookson and Mann, 1978; Katz and Schmaltz, 1979) have proposed the existence of behavioral interactions between endogenous and exogenous opiates and anticonvulsant drugs, with anticonvulsants facilitating behavioral activation to opiates. It may be inferred that some property of opiates, possibly related to seizures, normally inhibits at least certain classes of behavior and this additionally supported electroencephalographically (e.g. Urea, Frenk, Liebeskind and Taylor, 1977;Tortella, Moreton and Khazan, 1978). To date, only a limited number of ~ticonvulsants have been evafuated for their effects upon opiates, either behaviorally or electroencephalographicaiiy. Given the range of anticonv&ant drugs with both related and distinctive modes of action, the generality of effects across drug categories might merit additional examination and comment.To investigate the presence and generality of previously reported behavioral interadtions, opiate and opioid running after pretreatment with a variety of anticonvulsant drugs was examined. In particular, the pharmacolo~cally distinct ~ticonvuisants, sodium valproate, trimethadione and taurine were examined for their effects upon behavioral activation induced either by systemic morphine or by central injection of a long-lasting enkephalin analog (D-ala'-leu-enkephalinamide).Examination of enkephalin analogs may shed further tight upon the reported behavioral effects. The

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Phenytoin reversal and prevention of morphine-induced catalepsy in the rat

Cited by 3 publications

References 18 publications

Cocaine‐ and morphine‐induced synaptic plasticity in the nucleus accumbens

Cocaine‐ and morphine‐induced synaptic plasticity in the nucleus accumbens

Facilitation of opiate-and enkephalin-induced motor activity in the mouse by phenytoin sodium and carbamazepine

Behavioral interactions between opiate and antiepileptic drugs in the mouse

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