Adenosinergic mechanisms in anticonvulsant action of diazepam and sodium valproate

Malhotra, J; Seth, S D; Gupta, Suresh; Gupta, Yogendra Kumar

doi:10.1016/1382-6689(96)00020-8

Cited by 6 publications

(4 citation statements)

References 41 publications

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“…However, data indicating an alternative mechanism, i.e. other than adenosine receptor antagonism, have recently been found (Hornfeldt & Larson, 1994; Malhotra et al , 1996).…”

Section: Discussionmentioning

confidence: 99%

Effect of adenosine receptor modulation on pentylenetetrazole‐induced seizures in rats

Malhotra

Gupta

1997

British J Pharmacology

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1 The e ects of adenosine, the adenosine analogue, 2-chloroadenosine (2-CADO), the speci®c adenosine A 1 receptor agonist, N 6 -cyclopentyladenosine (CPA) and A 2 receptor agonist 5'-(Ncyclopropyl) carboxamidoadenosine (CPCA), were examined against seizures induced by acute administration of pentylenetetrazole (PTZ), 60 mg kg 71 , and PTZ kindled seizures, in rats. 2 Adenosine 1000 mg kg 71 , i.p., 5 min pretreatment and CPA 10 mg kg 71 i.p., 60 min pretreatment, showed signi®cant protection against acute PTZ-induced seizures while, CPCA up to 10 mg kg 71 was ine ective. The adenosine analogue 2-CADO in a dose of 5 mg kg 71 was only partially protective and on increasing the dose to 10 mg kg 71 , this protection was lost. 3 Theophylline, a non speci®c adenosine receptor antagonist at 50 mg kg 71 and the speci®c adenosine A 1 receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), at 1 mg kg 71 , if administered before the maximally protective doses of adenosine and CPA, completely reversed the protection a orded by them against PTZ seizures. While, pretreatment with the adenosine A 2 receptor antagonist, 3,7-dimethyl-1-propargylxanthine (DMPX), failed to reverse the protection. 4 Adenosine and the adenosine A 1 receptor agonist in doses that protected against seizures after acute PTZ administration, o ered only incomplete protection when tested against PTZ kindled seizures.5 The e ects of adenosine and adenosine receptor agonists on mean arterial pressure, heart rate and rectal temperature were studied, to rule out the possibility of their systemic e ects mediating the protection of PTZ seizures. All these agents produced a fall in mean arterial pressure, heart rate and hypothermia in the doses exhibiting an anticonvulsant response. While the e ect on blood pressure and heart rate was immediate i.e. seen within 5 min and, maintained throughout the observation period, the development of hypothermia lagged behind the onset of hypotension and bradycardia. However, there was no correlation between haemodynamic and hypothermic response and the anticonvulsant e ect. 6 The results indicate that the adenosine mediated anticonvulsant e ect is via stimulation of A 1 receptors. Hypotension and hypothermia do not appear to contribute to the protection observed with adenosine and the adenosine A 1 receptor agonists.

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“…However, data indicating an alternative mechanism, i.e. other than adenosine receptor antagonism, have recently been found (Hornfeldt & Larson, 1994; Malhotra et al , 1996).…”

Section: Discussionmentioning

confidence: 99%

Effect of adenosine receptor modulation on pentylenetetrazole‐induced seizures in rats

Malhotra

Gupta

1997

British J Pharmacology

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“…The animals were housed in a temperature-controlled room (20 ± 2°C) in groups of 3 per cage and had free access to chow and water. The rats were divided into 8 groups (12 in each) and received drugs as follows: (1) PTZ (control group) 2 mg/ml intravenous infusion; (2) DMSO (the WKE vehicle, 0.1 ml i.p., 30 min before PTZ infusion) + saline (0.1 ml i.p., 10 min before DMSO administration) + PTZ; (3) WKE (100 mg/kg i.p., 30 min before PTZ infusion) + saline + PTZ; (4) WKE + FMZ (5 mg/kg i.p., 10 min before WKE administration) + PTZ [ 8 ]; (5) WKE + ESM (150 mg/kg i.p., 10 min before WKE administration) + PTZ [ 8 ]; (6) WKE + DPZ (0.5 mg/kg i.p., 10 min before WKE administration) + PTZ [ 9 ]; (7) ESM + PTZ, and (8) DPZ + PTZ.…”

Section: Methodsmentioning

confidence: 99%

“…The amount of convulsant agent required for induction of the threshold or clonic convulsions was calculated by the following parameters: concentration of the convulsant in the injected liquid, infusion duration, infusion rate, and animal weight [ 10 ]. If animals did not show a seizure and/or clonic convulsion after receiving the 80 mg/kg of PTZ [ 9 ], the PTZ injection was stopped and the threshold and/or clonic dose of PTZ was considered as 100 mg/kg. In addition, animals were excluded from the study if the tail vein angiocath insertion was not successful for intravenous infusion of PTZ, or if leakage of injected fluid occurred under the skin of the animal.…”

Section: Methodsmentioning

confidence: 99%

Potential Mechanisms Involved in the Anticonvulsant Effect of Walnut Extract on Pentylenetetrazole-Induced Seizure

Asadi-Shekaari¹,

Eslami

Kalantaripour

et al. 2014

Med Princ Pract

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Objective: It was the aim of this study to determine the potential effect of walnut kernel extract (WKE) on experimentally induced seizures in rats and to evaluate the role of benzodiazepines and ethosuximide (ESM) within these pathways. Materials and Methods: Male Wistar rats were selected and divided into eight groups. Seizures were evoked by intravenous infusion of pentylenetetrazole (PTZ; 2 mg/ml/min). In combination with PTZ, animals were treated with vehicle or WKE (100 mg/kg i.p.), with or without cotreatment with either flumazenil (FMZ; 5 mg/kg i.p.), ESM (150 mg/kg i.p.) or diazepam (DPZ; 0.5 mg/kg i.p.). Results: WKE administration significantly increased the PTZ dose needed to induce the first myoclonic jerk (13.09 ± 1.29 vs. 49.71 ± 12.03 mg/kg; p < 0.001), decreased the severity of seizure grades and reduced the mortality rate to 0%. FMZ did not significantly reduce the anticonvulsant effect of WKE. The combination of DPZ and WKE showed a synergic anticonvulsant effect, whereas ESM had no significant influence (p > 0.05) on the WKE effects. Conclusion: These findings indicated that WKE was effective at reducing seizure severity, at increasing the dose to the first myoclonic jerk and highly efficacious at preventing mortality, because 100% of animals were protected. It seems that this positive effect could apply through signaling pathways other than benzodiazepine-mediated γ-aminobutyric acid receptors and may at least in part be similar to ESM.

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“…Dose used was 300 mg/kg and was given intraperitoneally. 13 Vehicle used was 5% gum acacia.  Pentylenetetrazole was obtained from Sigma Aldrich.…”

Section: Chemicalsmentioning

confidence: 99%

Evaluation of anticonvulsant activity of volatile oil extract of Nigella sativa seeds by chemically induced seizure model in albino rats

Bepari

Parashivamurthy

Niazi

2016

Int J Basic Clin Pharmacol

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Adenosinergic mechanisms in anticonvulsant action of diazepam and sodium valproate

Cited by 6 publications

References 41 publications

Effect of adenosine receptor modulation on pentylenetetrazole‐induced seizures in rats

Effect of adenosine receptor modulation on pentylenetetrazole‐induced seizures in rats

Potential Mechanisms Involved in the Anticonvulsant Effect of Walnut Extract on Pentylenetetrazole-Induced Seizure

Evaluation of anticonvulsant activity of volatile oil extract of Nigella sativa seeds by chemically induced seizure model in albino rats

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