Clonidine, but not ritanserin, suppresses kainic acid-induced automatisms in developing rats

Velı́šek, Libor; Bohačenková, L.; Čapková, Markéta; Mareš, Pavel

doi:10.1016/0031-9384(94)90074-4

Cited by 17 publications

(2 citation statements)

References 22 publications

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“…These outcomes suggest that systemic clonidine administration inhibits both the development and maintenance of icilin-evoked shaking. One clue to the mechanism by which clonidine inhibited icilin-evoked shaking in our experiments may reside in its wide-ranging efficacy against WDS induced by a panoply of pharmacological manipulations, including kainic acid, naloxone-precipitated morphine withdrawal, carbachol, benzylideneaminooxycarbonic acid derivatives, and thyrotropin (TRH)-releasing hormone analogues (Jahn and Mixich, 1976; Byrska et al, 1980; Turski et al, 1981; Wei, 1983; Ohno et al, 1987; Velísek et al, 1994). The fact that dissimilar pharmacological manipulations evoke a similar behavioral stimulant effect, WDS, suggests that a common downstream signaling pathway underlies the phenomenon and that alpha 2 -adrenoceptor activation by clonidine inhibits the normal activation or recruitment of the said pathway.…”

Section: Discussionmentioning

confidence: 81%

Icilin-evoked behavioral stimulation is attenuated by alpha2-adrenoceptor activation

et al. 2011

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Icilin is a transient receptor potential cation channel subfamily M (TRPM8) agonist that produces behavioral activation in rats and mice. Its hallmark overt pharmacological effect is wet-dog shakes (WDS) in rats. The vigorous shaking associated with icilin is dependent on NMDA receptor activation and nitric oxide production, but little else is known about the biological systems that modulate the behavioral phenomenon. The present study investigated the hypothesis that alpha2-adrenoceptor activation inhibits icilin-induced WDS. Rats injected with icilin (0.5, 1, 2.5, 5 mg/kg, i.p.) displayed dose-related WDS that were inhibited by pretreatment with a fixed dose of clonidine (0.15 mg/kg, s.c.). Shaking behavior caused by a fixed dose (2.5 mg/kg) of icilin was also inhibited in a dose-related manner by clonidine pretreatment (0.03–0.15 mg/kg, s.c.) and reduced by clonidine posttreatment (0.15 mg/kg, s.c.). Pretreatment with a peripherally restricted alpha2-adrenoceptor agonist, ST91 (0.075, 0.15 mg/kg), also decreased the incidence of shaking elicited by 2.5 mg/kg of icilin. Pretreatment with yohimbine (2 mg/kg, i.p.) enhanced the shaking induced by a low dose of icilin (0.5 mg/kg). The imidazoline site agonists, agmatine (150 mg/kg, i.p.) and 2-BFI (7 mg/kg, i.p.), did not affect icilin-evoked shaking. These results suggest that alpha2-adrenoceptor activation inhibits shaking induced by icilin and that increases in peripheral, as well as central, alpha2-adrenoceptor signaling oppose the behavioral stimulant effect of icilin.

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Section: Discussionmentioning

confidence: 81%

Icilin-evoked behavioral stimulation is attenuated by alpha2-adrenoceptor activation

et al. 2011

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“…In other experimental models, 5-HT 2A -R antagonists have failed to be effective in seizure control. Ritanserin was ineffective on kainic acid-induced seizures ( Velisek et al, 1994 ) and ketanserin did not affect the seizure threshold for picrotoxin in mice ( Pericic et al, 2005 ) or on ethanol withdrawal seizures ( Grant et al, 1994 ), but antagonized cocaine-induced convulsions in a dose-dependent manner ( Ritz and George, 1997 ). The 5-HT 2A/2C -R and calcium antagonist dotarizine inhibited electroconvulsive shock (ECS)-induced seizures but had no effect on pentylenetetrazole (PTZ)-induced convulsions in rats ( Lazarova et al, 1995 ) ( Table 1 ).…”

Section: The 5-ht 2a -Rs In the Regulation Of Epilmentioning

confidence: 99%

Central serotonin-2A (5-HT2A) receptor dysfunction in depression and epilepsy: the missing link?

2015

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5-Hydroxytryptamine 2A receptors (5-HT2A-Rs) are G-protein coupled receptors. In agreement with their location in the brain, they have been implicated not only in various central physiological functions including memory, sleep, nociception, eating and reward behaviors, but also in many neuropsychiatric disorders. Interestingly, a bidirectional link between depression and epilepsy is suspected since patients with depression and especially suicide attempters have an increased seizure risk, while a significant percentage of epileptic patients suffer from depression. Such epidemiological data led us to hypothesize that both pathologies may share common anatomical and neurobiological alteration of the 5-HT2A signaling. After a brief presentation of the pharmacological properties of the 5-HT2A-Rs, this review illustrates how these receptors may directly or indirectly control neuronal excitability in most networks involved in depression and epilepsy through interactions with the monoaminergic, GABAergic and glutamatergic neurotransmissions. It also synthetizes the preclinical and clinical evidence demonstrating the role of these receptors in antidepressant and antiepileptic responses.

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Role of Serotonin2A (5-HT2A) Receptors in Epilepsy

Crunelli

Venzi

Deurwaerdère

et al. 2018

5-Ht2a Receptors in the Central Nervous System

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Clonidine, but not ritanserin, suppresses kainic acid-induced automatisms in developing rats

Cited by 17 publications

References 22 publications

Icilin-evoked behavioral stimulation is attenuated by alpha2-adrenoceptor activation

Icilin-evoked behavioral stimulation is attenuated by alpha2-adrenoceptor activation

Central serotonin-2A (5-HT2A) receptor dysfunction in depression and epilepsy: the missing link?

Role of Serotonin2A (5-HT2A) Receptors in Epilepsy

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