Opiate and non-opiate aspects of morphine induced seizures

Frenk, Hanan; Liban, Alexander; Balamuth, Ron; Urca, Gideon

doi:10.1016/0006-8993(82)90692-8

Cited by 29 publications

(6 citation statements)

References 17 publications

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“…Naltrexone was similarly unable to block the convulsions observed in naive animals produced by lethal doses of morphine. This is consistent with the findings of others who have been unable to block morphine's convulsive effects (7). These results may be explained by assuming that large doses of systemic morphine induce both opiate receptor-dependent and nonspecific effects.…”

Section: Discussionsupporting

confidence: 92%

Morphine responsiveness and seizure proneness

Mansour

Valenstein

1984

Experimental Neurology

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Previous research demonstrated that following amygdala kindling, animals showed a heightened sensitivity to morphine's convulsive effects and an exaggerated Straub tail response. These effects were evident to 3 months after their last convulsion and could be blocked by naloxone pretreatment. The present paper extends these findings by demonstrating that animals given metrazol or electroshock (ECS) convulsions also showed an enhanced morphine response that was blocked by naltrexone. Both metrazol- and ECS-treated animals convulsed in response to doses of morphine that produced little or no effect in control animals. In addition, it was shown that brain damage induced by electrode implantation or neocortex penetration by skull screws also increased an animal's sensitivity to morphine even in the absence of prior convulsions. This effect, however, could not be blocked by naltrexone. Finally, as opiate receptors vary with the diurnal rhythm, we determined that following amygdala kindling, animals are more sensitive to morphine's convulsive action during their dark phase when receptor number and sensitivity are highest. The results indicated that seizure proneness, whether induced by a history of prior convulsions or brain damage, increased sensitivity to morphine. This effect may be due to a change in opiate receptors only when prior convulsions have occurred.

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Section: Discussionsupporting

confidence: 92%

Morphine responsiveness and seizure proneness

Mansour

Valenstein

1984

Experimental Neurology

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“…It is not known, however, if there is enough metabolism of morphine in the spinal cord for this to be possible at doses used. These reactions have been experimentally reproduced in mice and rats with high doses of opioids given by different routes (Frenk et al. 1982; Werz & McDonald 1982, Shohami et al.…”

Section: Discussionmentioning

confidence: 99%

“…Studies on animals or spinal neuronal cultures have led to different theories explaining central hyperactivity. Morphine, like other alkaloid opioids, interacts with opioid and nonopioid receptors in the central nervous system (Frenk et al. 1982; Werz et al.…”

Section: Discussionmentioning

confidence: 99%

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Myoclonus and urinary retention following subarachnoid morphine injection in a dog

Kona‐Boun

Pîbarot

Quesnel

2003

Veterinary Anaesthesia and Analgesia

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“…Accordingly, some early studies showed that morphine suppresses audiogenic seizures and delays the onset of pentetrazole‐ and flurothyl‐induced convulsions (Frenk et al, 1979; Thompson et al, 2009). When doses which are much higher than those producing analgesia are used, morphine and related opiates may produce convulsions (Frenk, 1983; Frenk et al, 1982). Meanwhile, morphine‐pretreated animals show a faster acquisition of seizure activity (Hofmann et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

The effect of selective opioid receptor agonists and antagonists on epileptiform activity in morphine‐dependent infant mice hippocampal slices

Panahi

Saboory

Rabbani

et al. 2017

Intl J of Devlp Neuroscience

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Hippocampal slices of mouse brain were used to estimate how selective agonist and antagonist of opioid receptors alter Low-Mg artificial cerebrospinal fluid (LM-ACSF)-induced epileptiform activities in normal and morphine-dependent mice. Brain slices were obtained from control and morphine-dependent mice. The morphine-dependent group received morphine once a day for 5 consecutive days, and the control group received saline. All injections were administered subcutaneously (s.c) in a volume of 0.1mL on postnatal days 14-18. Brain slices were perfused with LM-ACSF along with selective agonist and antagonist of μ, κ and δ opioid receptors. Changes in spike count per unit of time were used as indices to quantify the effects of LM-ACSF exposure in the slices. In both groups, DAMGO (selective μ opioid receptor agonist) and DPDPE (selective δ opioid receptor agonist) suppressed while Dyn-A (selective κ opioid receptor agonist) potentiated the epileptiform activity. Meanwhile, BFN-A (selective μ opioid receptor antagonist) recovered epileptiform activity in normal brain slices but not in morphine-dependent ones. NTI (selective δ opioid receptor antagonist) and nor-BNI (selective κ opioid receptor antagonist) decreased epileptiform activity. It seems that the excitatory effect of morphine on epileptiform activity was mediated through kappa receptors and its inhibitory effect was mediated via the mu receptor and, to a lesser degree, through the delta receptor. The pattern of effect was similar in normal and morphine-dependent slices, but the intensity of the effect was significantly stronger in normal mice. Finding of this study might be considered for further research and attention in epilepsy treatment.

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Opiate and non-opiate aspects of morphine induced seizures

Cited by 29 publications

References 17 publications

Morphine responsiveness and seizure proneness

Morphine responsiveness and seizure proneness

Myoclonus and urinary retention following subarachnoid morphine injection in a dog

The effect of selective opioid receptor agonists and antagonists on epileptiform activity in morphine‐dependent infant mice hippocampal slices

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