Involvement of the nitric oxide pathway in the anticonvulsant effect of tramadol on pentylenetetrazole-induced seizures in mice

Lesani, Ali; Javadi‐Paydar, Mehrak; Khodadad, Tina Kabiri; Asghari-Roodsari, Alaleh; Shirkhodaei, Mahyar; Norouzi, Abbas; Dehpour, Ahmad Reza

doi:10.1016/j.yebeh.2010.08.006

Cited by 17 publications

(16 citation statements)

References 38 publications

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“…In some cases, NOS inhibitors have potentiated the antiepileptic effect of these drugs (Baran et al, 1997;Borowicz et al, 1997Borowicz et al, , 2000Łuszczki et al, 2006, 2011De Sarro et al, 2000;Bahremand et al, 2010), while at other times they showed counteractive actions (Baran et al, 1997;Borowicz et al1998;Czuczwar et al, 1999;Lesani et al, 2010;Yahyavi-Firouz-Abadi et al, 2006) or even lack of effect (Borowicz et al, 1997(Borowicz et al, , 1998(Borowicz et al, , 2000Baran et al, 1997;Czuczwar et al, 1999;Łuszczki et al, 2006, 2011.…”

Section: Discussionmentioning

confidence: 99%

“…However, although abundant experimental research has demonstrated a functional involvement of NO in the control of epileptic phenomena, the available data are conflicting and it cannot be concluded whether this atypical messenger acts as a pro-convulsant or an anticonvulsant agent (Barbiro-Michaely et al, 2011;Hrnčić et al, 2010Hrnčić et al, , 2011Przegaliñski et al, 1996;Tutka et al, 1997;Masukawa et al, 1998;Borowicz et al, 2000;Lesani et al, 2010;Łuszczki et al, 2006, 2011Sardo et al, 2008;Itoh and Watanabe, 2009;Nieoczym et al, 2010). Besides, there is still little information available describing changes in either NOS activity or expression after repeated epileptic seizures comparing different brain regions (e.g.…”

Section: Introductionmentioning

confidence: 99%

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Opposite caudal versus rostral brain nitric oxide synthase response to generalized seizures in a novel rodent model of reflex epilepsy

et al. 2012

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Opposite caudal versus rostral brain nitric oxide synthase response to generalized seizures in a novel rodent model of reflex epilepsy

et al. 2012

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“…However, the obtained results were inconsistent to some level. In particular, the results showed that NOS inhibitors could increase ( (82) or not affect antiepileptic efficacy (81). Recently, it has been shown that co-administration of an iNOS inhibitor significantly decreased the beneficial effects of pioglitazone on PTZ-induced seizures in mice (83).…”

Section: Anticonvulsive Eff Ects Of No In Homocysteine Thiolactone Sementioning

confidence: 96%

Modulation of Epileptic Activity in Rats: Focus on Sleep, Physical Exercise and Nitric Oxide–mediated Neurotransmission in a Model of Homocysteine Thiolactone–induced Seizures

Hrnčić

Rašić-Marković

Šušić

et al. 2014

Serbian Journal of Experimental and Clinical Research

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Epilepsy is a chronic neurological disorder characterised by recurrent epileptic seizures. Understanding the mechanisms by which it initiates and develops, as well as its modulating factors, are of great scientifi c interest. Experimental models of epilepsy are useful for understanding these mechanisms.Homocysteine, an amino acid endogenously generated in the body, together with its reactive metabolite, homocysteine thiolactone (HCT), is recognised as a risk factor for a variety of diseases. HCT-induced seizures are a model of generalised epilepsy in which the coexistence of two types of epileptic activity has been documented. Th e complex interplay between sleep and epilepsy is still only poorly understood. Additionally, the relationship between physical exercise and epilepsy is quite intriguing, especially the mechanism underlying this relationship. Th e role of nitric oxide (NO)-mediated neurotransmission in the development of epileptic activity is highly debated in the existing scientifi c literature .In this review article, we described the modulation of epileptic activity in rats and focused on sleep, physical activity and NO-mediated signalling. First, we explain the characteristics of the experimental models of epileptic activity and the unique features of HCT-induced seizures. Second, the modulating eff ects of sleep and regular physical exercise training on epileptic activity, along with works from the authors, are discussed. Finally, the anticonvulsive eff ects of NO that is produced via nNOS and iNOS in HCT-induced seizures are reviewed. SAŽETAKEpilepsija je hronično neurološko oboljenje koje karakteriše rekurentna pojava epileptičnih napada. Razumevanje menahizama nastanka i širenja epileptične aktivnosti, kao i foktora modulacije ovih procesa, od izuzetnog je naučno-stručnog značaja. Eksperimentalni modeli epilepsije su značajni za razumevanje upravo ovih mehanizama. Homocistein, aminokiselina koja se endogeno sintetiše u organizmu, zajedno sa svojim reaktivnim metabolitom homocistein tiolaktonom (HCT), je prepoznat kao faktor rizika za nastanak različitih bolesti. Epilepsije izazvane HCT-om predstavljaju model generalizovane epileptične aktivnosti u kome je pokazana koegzistencija dva tipa napada. Složeni uzajamni odnos između spavanja i epilepsije još uvek nije dovoljno razjašnjen. Takođe, međuodnos fi zičke aktivnosti i epilepsije je krajnje interesantan, naročito mehanizmi ovih odnosa. Uloga neurotransmisije posredovane azot monoksidom (NO) u nastanku epileptične aktivnosti je vrlo kontradiktorna u postojećoj literaturi. Predmet ovog rada bila je modulacija epileptične aktivnosti kod pacova sa posebnim osvrtom na spavanje, fi zičku aktivnost i neurotransmisiju posredovanu NO. Najpre su razmotreni koncepti eksperimentalnih modela epileptične aktivnosti sa osobenostima HCT epilepsija. Zatim su diskutovani modulatorni efekti spavanja i regularnog fi zičkog veržbanja na epileptičnu aktivnost zajedno sa rezultatima radova autora. Na posletku, dat je osvrt na antikonvulzivnu ulogu NO i doprinos nNOS i...

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“…7 Although TR, as opposed to typical opioids, does not have a remarkable opioid side effects (eg, respiratory depression, sedation, constipation), sometimes it has unfavorable side effects with respect to seizure potential. 8,9 At therapeutic doses, TR slightly suppresses the severity of seizure. However, at high doses, TR paradoxically induces seizure.…”

Section: Introductionmentioning

confidence: 99%

“…10 Other hypotheses about the seizure-inducing mechanism of TR are inhibition of the serotonin and nitric oxide (NO) pathways. 9,[16][17][18] Also, opioid receptors' agonist activity of TR has been confirmed to induce seizures due to GABA pathway inhibition. 19,20 Furthermore, seizures in patients receiving TR at recommended doses have been reported.…”

Section: Introductionmentioning

confidence: 99%

Evidence for the Involvement of the Dopaminergic System in Seizure and Oxidative Damage Induced by Tramadol

et al. 2018

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Tramadol (TR) is a synthetic analgesic drug with central function that can induce seizures even at therapeutic doses. The exact mechanism of TR effect on seizure generation is not clear, but inhibition of the serotonin and nitric oxide pathways and inhibitory effects on GABA receptors are the most common hypotheses about the seizure-inducing mechanism of the TR. This study aimed to evaluate the role of dopaminergic system on the seizure and oxidative damage induced by TR using agonist and antagonist drugs of this system in the Albino mice. Clonic seizure induced by TR was evaluated as seizure threshold. Haloperidol (0.2 mg/kg, IP), a predominantly D receptor antagonist, and cabergolin (0.5 mg/kg, IP), a dopamine agonist specific for the D receptors, were injected 60 minutes before the seizure induction. The seizure threshold was significantly increased by dopaminergic antagonist, but it was decreased significantly by pretreatment with the selective agonist. Oxidative stress biomarkers (reactive oxygen species, lipid peroxidation, and protein carbonyl content) significantly increased and glutathione content significantly decreased in brain mitochondria by TR compared with the control group, whereas oxidative markers were decreased significantly after pretreatment with haloperidol compared with the TR group. This study revealed that the dopaminergic system is involved in TR-induced seizure, and meanwhile, inhibition of dopamine D receptors can increase the TR threshold seizure and decrease the oxidative damage in the brain mitochondria. Conversely, stimulation of dopamine D receptors by cabergolin can decrease the TR threshold seizure and glutathione content in the brain mitochondria.

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Involvement of the nitric oxide pathway in the anticonvulsant effect of tramadol on pentylenetetrazole-induced seizures in mice

Cited by 17 publications

References 38 publications

Opposite caudal versus rostral brain nitric oxide synthase response to generalized seizures in a novel rodent model of reflex epilepsy

Opposite caudal versus rostral brain nitric oxide synthase response to generalized seizures in a novel rodent model of reflex epilepsy

Modulation of Epileptic Activity in Rats: Focus on Sleep, Physical Exercise and Nitric Oxide–mediated Neurotransmission in a Model of Homocysteine Thiolactone–induced Seizures

Evidence for the Involvement of the Dopaminergic System in Seizure and Oxidative Damage Induced by Tramadol

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