Central monoamines and convulsive thresholds in mice and rats

Kilian, Marion; Frey, H.‐H.

doi:10.1016/0028-3908(73)90121-4

Cited by 254 publications

(58 citation statements)

References 21 publications

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“…5-HTP has beneficial effects in certain neurologic and psychiatric disorders [27,28], Although Chadwick et al [29] showed suppressive effects o f a monoamine oxidase inhibitor plus /,-trypto phan in epileptic patients, clinical efficacy o f serotonergic agents remains unclear. Our data are in agreement with those obtained in other epilepsy models [3][4][5][6], and justify the further investigation of serotonergic compounds in the treatment of human epilepsy. Drugs which act selec tively on the specific receptor subtype should be used to further clarify the role o f serotonin in epilepsy.…”

Section: Discussionsupporting

confidence: 82%

“…K in dling provides a viable model o f secondarily generalized seizures, and many experiments have been done to deter mine the neurophysiological and neurochemical bases of epilepsy [2], A number o f studies have provided evidence that brain serotonin plays an inhibitory role in a variety o f epilepsy models, such as electroconvulsive [3][4][5] and pen tylenetetrazol-induced seizures [4][5][6]. Serotonin has also been considered to possess an inhibitory action against the kindling development [7][8][9][10][11], but there are contradic tory results on the role o f this neurotransmitter in kindled seizures [8.…”

Section: Introductionmentioning

confidence: 99%

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Serotonergic Inhibition of Limbic and Thalamic Seizures in Cats

Wada¹,

Hasegawa²,

Nakamura³

et al. 1992

Neuropsychobiology

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To clarify the role of the serotonergic system in limbic and thalamic epileptic activity, we examined the effects of 5-hydroxytryρtophan (5-HTP, 20 and 40 mg/kg) on fully kindled seizures from the hippocampus and lateral geniculate nucleus. The intraperitoneal administration of 20 mg/kg 5-HTP exerted no anticonvulsant effect on hippocampal kindled seizures, and a higher dose (40 mg/kg) produced a signiñcant reduction in the behavioral seizure stage. 5-HTP at 20 mg/kg displayed no suppressive effect on lateral geniculate seizures, and 5-HTP at 40 mg/kg significantly reduced both the seizure stage and afterdischarge duration. Our data suggest that serotonergic mechanisms play an inhibitory role in seizures kindled from these brain regions.

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Section: Discussionsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 99%

Serotonergic Inhibition of Limbic and Thalamic Seizures in Cats

Wada¹,

Hasegawa²,

Nakamura³

et al. 1992

Neuropsychobiology

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“…Phentolamine given intracerebroventricularly induced spontaneous limb myoclonus in mice (Horton 1980). Moreover, the systemic administration of phentolamine increases suscetibility to electroshock-induced seizures in mice (Killian & Frey 1973). It should be noted that under our experimental conditions, the dose of phentolamine necessary to counteract the protective effect of tizanidine was rather high.…”

Section: Discussionmentioning

confidence: 95%

Tizanidine Protects Mice against Convulsions Induced by Lidocaine: Involvement of α₂‐Adrenoceptors

Altenburg

Farah²

1999

Pharmacology & Toxicology

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The effects of u-adrenoceptors agents on seizures induced by intraperitoneal administration of lidocaine (75 mg/kg) were studied in mice. Pretreatment with the selective a2-adrenoceptor agonist, tizanidine, decreased the incidence of seizures induced by lidocaine. Tizanidine increased the latency to the first seizure in those animals which progressed to seizures. The blockade of a2-adrenoceptors with yohimbine or phentolamine counteracted the protection induced by tizanidine. The seletive aradrenoceptor antagonist, prazosin, did not modify the protection induced by tizanidine. The aradrenoceptor agonist clonidine also increased the latency to the first seizure induced by lidocaine. The protective effect of clonidine was also reversed by pretreatment with the selective a2-adrenoceptor antagonist yohimbine. Taken together, these results suggest that a2-adrenoceptors are involved in seizures induced by lidocaine.

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“…Lowering of central monoamine levels by reserpine or a-methyl-ptyrosine lowers the convulsive threshold (Chen, Ensor & Bohner, 1954;Yeoh & Wolf, 1968;Kilian & Frey, 1973;Jobe, Stull & Geiger, 1974). Central noradrenaline appears to be important since selective lesions of the dorsal forebrain bundle by 6-hydroxydopamine injection enhances pentylenetetrazol (PTZ)-induced convulsions in rats (Mason & Corcoran, 1979).…”

Section: Introductionmentioning

confidence: 99%

Role of Central Β‐adrenoceptors in the Control of Pentylenetetrazol‐induced Convulsions in Rats

Louis

Papanicolaou

Summers

et al. 1982

British J Pharmacology

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1 The role of central P-adrenoceptors in the anticonvulsant effect of 0-adrenoceptor antagonists has been examined.2 Oral administration of (-)-and (+)-propranolol (0.05-1 mg/kg) and (±)-pindolol (0.025 -0.5 mg/kg) produced a dose-dependent decrease in duration of convulsions produced by pentylenetetrazol (PTZ 50 mg/kg, i.p.) in rats. 3 At the EC50 level, (-)-propranolol is seven times more effective than the (+)-isomer. 4 Oral administration of (-(1-10 mg/kg), two P-adrenoceptor antagonists that do not penetrate the blood brain barrier, had no significant effect on the duration of PTZ-induced convulsions.5 Intracerebroventricular administration of (-)-propranolol (0.5 pg/kg) or (-)-timolol (0.25 pg/kg) produced highly significant anticonvulsant effects whereas the (+ )-isomers at the same dose level were ineffective. (±)-Pindolol (0.25 pg/kg) was also much more effective given by this route than when given orally. The (+)-and (-)-isomers of the Pf-adrenoceptor selective antagonist practolol (10 pg/kg) exerted only weak anticonvulsant effects.6 This study provides evidence that P-adrenoceptor antagonists exert an anticonvulsant effect through central 32-adrenoceptors. At high dose levels, additional anticonvulsant activity is associated with membrane stabilization in those antagonists which possess this property.

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Central monoamines and convulsive thresholds in mice and rats

Cited by 254 publications

References 21 publications

Serotonergic Inhibition of Limbic and Thalamic Seizures in Cats

Serotonergic Inhibition of Limbic and Thalamic Seizures in Cats

Tizanidine Protects Mice against Convulsions Induced by Lidocaine: Involvement of α₂‐Adrenoceptors

Role of Central Β‐adrenoceptors in the Control of Pentylenetetrazol‐induced Convulsions in Rats

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Central monoamines and convulsive thresholds in mice and rats

Cited by 254 publications

References 21 publications

Serotonergic Inhibition of Limbic and Thalamic Seizures in Cats

Serotonergic Inhibition of Limbic and Thalamic Seizures in Cats

Tizanidine Protects Mice against Convulsions Induced by Lidocaine: Involvement of α2‐Adrenoceptors

Role of Central Β‐adrenoceptors in the Control of Pentylenetetrazol‐induced Convulsions in Rats

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Tizanidine Protects Mice against Convulsions Induced by Lidocaine: Involvement of α₂‐Adrenoceptors