Effect of adenosinergic modulation on the anticonvulsant effect of
phenobartinone and carbamazepine

Malhotra, J; Yk, Gupta

doi:10.1358/mf.1999.21.2.529233

Cited by 11 publications

(4 citation statements)

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“…Recently, it has also been reported that resveratrol stimulates the release of endogenous adenosine in humans [11]. Since adenosine is an inhibitory neurotransmitter and since several lines of evidence suggest a role of the adenosinergic system in seizure [8,9], the involvement of an adenosinergic mechanism in resveratrol-induced protection cannot be ruled out in our study. We carried out experiments involving the combination of subanticonvulsant doses of adenosine and resveratrol against PTZ-induced seizures.…”

Section: Discussionmentioning

confidence: 79%

“…DMPX at 1 mg/kg did not reverse the protection of resveratrol against PTZ-induced seizures, as none of the animals exhibited convulsions after pretreatment with DMPX in the resveratrol-treated group. The dose of DMPX was selected on the basis of our earlier studies [9].…”

Section: Effects Of Adenosine Receptor Antagonists On Resveratrol Promentioning

confidence: 99%

“…Therefore, the present study was carried out to investigate the effect of resveratrol against PTZ-induced seizures in rats. Adenosine, an endogenous inhibitory neuromodulator, has been shown to exert antiepileptic activity and has also been shown to modulate the antiepileptic activity of some antiepileptic drugs [9]. Therefore, it was considered worthwhile to study the effects of adenosine and adenosine receptor antagonists on the anticonvulsant effect of resveratrol.…”

Section: Introductionmentioning

confidence: 99%

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Protective Effect of Resveratrol against Pentylenetetrazole-Induced Seizures and Its Modulation by an Adenosinergic System

Gupta

Chaudhary

Srivastava³

2002

Pharmacology

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The effect of trans-resveratrol (resveratrol), a polyphenolic compound with potent antioxidant activity, was investigated against pentylenetetrazole (PTZ) induced seizures in rats. Resveratrol (20, 40, and 80 mg/kg i.p.) administered 20 min prior to convulsive challenge with PTZ (60 mg/kg i.p.) dose dependently reduced the percent incidence of generalized tonic-clonic convulsions. Resveratrol (40 mg/kg) also potentiated the effect of sodium valproate (150 mg/kg) and diazepam (2 mg/kg) against PTZ-induced seizures. Since adenosine, an endogenous anticonvulsant, has been demonstrated to modulate the action of various antiepileptics, experiments were also carried out to determine whether an adenosinergic mechanism is involved in the anticonvulsant action of resveratrol. When a subanticonvulsant dose of adenosine (500 mg/kg) was administered together with resveratrol, a significant reduction in the percent incidence of generalized tonic-clonic convulsions was observed. Moreover, the nonspecific adenosine receptor antagonist theophylline (50 mg/kg i.p.) significantly reversed the resveratrol-induced protection, whereas the specific adenosine A₂ receptor antagonist 3,7-dimethyl-1-propargylxanthine (1 mg/kg i.p.) could not reverse the resveratrol-induced protection. The findings of the present study suggest an antiepileptic potential of resveratrol and that an adenosinergic mechanism may play a role in its anticonvulsant activity.

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Section: Discussionmentioning

confidence: 79%

Section: Effects Of Adenosine Receptor Antagonists On Resveratrol Promentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Protective Effect of Resveratrol against Pentylenetetrazole-Induced Seizures and Its Modulation by an Adenosinergic System

Gupta

Chaudhary

Srivastava³

2002

Pharmacology

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“…These findings suggest that the effects of CBZ may also result from effects on both adenosine A 1 and A 2 receptors. However, binding studies and the observation that a specific adenosine A 1 receptor antagonist have no effect on the anticonvulsant action of CBZ suggest that the alteration of adenosine A 1 receptor activity is not an important mechanism for the anticonvulsant efficacy of CBZ (43,49,50).…”

Section: Mechanisms Of Action Of Carbamazepine and Derivatives 123mentioning

confidence: 99%

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Ambrósio

Soares-da-Silva

Carvalho

et al. 2002

Neurochemical Research

259

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Carbamazepine (CBZ) has been extensively used in the treatment of epilepsy, as well as in the treatment of neuropathic pain and affective disorders. However, the mechanisms of action of this drug are not completely elucidated and are still a matter of debate. Since CBZ is not very effective in some epileptic patients and may cause several adverse effects, several antiepileptic drugs have been developed by structural variation of CBZ, such as oxcarbazepine (OXC), which is used in the treatment of epilepsy since 1990. (S)-(-)-10-acetoxy-10,11-dihydro-5H-dibenz [b,f]azepine-5-carboxamide (BIA 2-093) and 10,11-dihydro-10-hydroxyimino-5H-dibenz[b,f] azepine-5-carboxamide (BIA 2-024), which were recently developed by BIAL, are new putative antiepileptic drugs, with some improved properties. In this review, we will focus on the mechanisms of action of CBZ and its derivatives, OXC, BIA 2-093 and BIA 2-024. The available data indicate that the anticonvulsant efficacy of these AEDs is mainly due to the inhibition of sodium channel activity.

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Caffeine Protects Against Anticonvulsant-Induced Neurotoxicity in the Developing Rat Brain

et al. 2017

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Phenobarbital is the most commonly used drug for the treatment of neonatal seizures but may induce neurodegeneration in the developing brain. Methylxanthine caffeine is used for the treatment of apnea in newborn infants and appears to be neuroprotective, as shown by antiapoptotic and anti-inflammatory effects in oxidative stress models in newborn rodents and reduced rates of cerebral palsy in human infants treated with caffeine. We hypothesized that caffeine may counteract the proapoptotic effects of phenobarbital in newborn rats. Postnatal day 4 (P4) rats received phenobarbital (50 mg/kg) +/- caffeine (10 mg/kg) for three consecutive days. Brains examined at 6, 12, and 24 h after last injection of phenobarbital showed a drastic increase of apoptotic cell death (TUNEL+), which was attenuated by co-treatment with caffeine at 6 and 24 h but not at 12 h. Phenobarbital also increased protein levels of apoptosis inducing factor (AIF) and cleaved caspase-3, which was reduced by caffeine co-administration at all time points investigated. RNA expression of the pro-inflammatory cytokines TNFα, IFNγ, and IL-1β, but not IL-18, was upregulated by phenobarbital. Co-treatment with caffeine significantly decreased these upregulations at all time points investigated, while caffeine without phenobarbital resulted in increased expression of TNFα, IL-1β, and IL-18, but not IFNγ at 6 h. Downregulation of the adenosine A1 and A2a receptors, both of which bind caffeine, by 24 h of phenobarbital exposure was partly antagonized by caffeine. These results raise the possibility that the phenobarbital-induced adverse effects could be reduced by a co-treatment with caffeine.

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Effect of adenosinergic modulation on the anticonvulsant effect of phenobartinone and carbamazepine

Cited by 11 publications

References 0 publications

Protective Effect of Resveratrol against Pentylenetetrazole-Induced Seizures and Its Modulation by an Adenosinergic System

Protective Effect of Resveratrol against Pentylenetetrazole-Induced Seizures and Its Modulation by an Adenosinergic System

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Caffeine Protects Against Anticonvulsant-Induced Neurotoxicity in the Developing Rat Brain

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