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

Prieto-Martín, Ana I.; Lloréns, Silvia; Pardal-Fernández, José Manuel; Muñoz, Luis J.; López, Dolores E.; Escribano, Julio; Nava, Eduardo; Cabo, Carlos de

doi:10.1016/j.lfs.2012.01.010

Cited by 15 publications

(12 citation statements)

References 55 publications

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“…Rundfeldt and his team [35] proposed that NO has dual roles either as a convulsant or an anticonvulsant in the same animal experiment depending on the dose applied. Analogous report was that NO increase may play different actions depending on whether this change occurs before or after the beginning of the seizure attack [36]. In this study, L-ARG (500 mg/kg, i.p.)…”

Section: Discussionmentioning

confidence: 58%

The involvement of neuronal nitric oxide synthase in antiepileptic action of alpha-asarone on pentylenetetrazol molding rats

Zhu

Liu

et al. 2014

Bio-Medical Materials and Engineering

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The aim of the present study was to research the role of nitric oxide (NO) as a mediator of alpha (Į)-asarone effect at the pentylenetetrazol (PTZ)-induced epileptiform discharge in rat. Į-Asarone that was injected intraperitoneally twenty minutes before PTZ injection suppressed the clonic discharge effectively and the significant actions lasted for 30 min with no change of clonic amplitude. Administration ofĮ-asarone did not influence interictal discharge. Four kinds of NO regulators were administered, including non-selective NG-nitro-L-arginine methyl ester (L-NAME), selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI), inducible nitric oxide synthase (iNOS) inhibitor, aminoguanidine (AG) and NO substrate, L-arginine (ARG) and their influence on the actions of Į-asarone were studied, and all of the regulators were administered fifteen minutes before Į-asarone injection. L-NAME and 7-NI reversed the anticlonic activity of Į-asarone, and a significant increase of clonic activity was induced by L-NAME later in L-NAME +.Į-asarone + PTZ group. There were no significant differences between AG + Į-asarone + PTZ and Į-asarone + PTZ group. L-ARG played a dual role in this study. It aggravated clonic discharge in the early stage but relieved interictal discharge in the late stage compared with PTZ group alone, and the beneficial effect ofĮ-asarone was also reversed. All the above results suggest that nNOS/NO pathway mediates the anticonvulsant effect ofĮ-asarone, and NO played a biphasic role in PTZ modeling process, while iNOS was unrelated to the inhibition effect of Į-asarone on PTZ induced epileptiform activity.

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Section: Discussionmentioning

confidence: 58%

The involvement of neuronal nitric oxide synthase in antiepileptic action of alpha-asarone on pentylenetetrazol molding rats

Zhu

Liu

et al. 2014

Bio-Medical Materials and Engineering

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“…12,34 Also, opposite responses of NOS to generalized seizures along the anterior-posterior axis of the brain have been recently proved. 35 Increase in iNOS expression has been found in brains of surgical patients with prolonged history of epilepsy, 16 as well as in some spontaneously epileptic animals. 17 Having in mind potential therapeutic applications, numerous attempts were also made to elucidate the effects of NOS inhibitors on the activity of different antiepileptic drugs.…”

Section: Discussionmentioning

confidence: 99%

Homocysteine thiolactone-induced seizures in adult rats are aggravated by inhibition of inducible nitric oxide synthase

et al. 2013

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Homocysteine and its metabolites (homocysteine thiolactone (HT)) induce seizures via different but still not well-known mechanisms. The role of nitric oxide (NO) in epileptogenesis is highly contradictory and depends on, among other factors, the source of NO production. The aim of the present study was to examine the effects of aminoguanidine, selective inhibitor of inducible NO synthase (iNOS), on HT-induced seizures. Aminoguanidine (50, 75, and 100 mg/kg, intraperitoneally (i.p.)) was injected to rats 30 min prior to inducing HT (5.5 mmol/kg, i.p.). Seizure behavior was assessed by seizure incidence, latency time to first seizure onset, number of seizure episodes, and their severity during observational period of 90 min. Number and duration of spike and wave discharges (SWDs) were determined in electroencephalogram (EEG). Seizure latency time was significantly shortened, while seizure incidence, number, and duration of HT-induced SWD in EEG significantly increased in rats receiving aminoguanidine 100 mg/kg before subconvulsive dose of HT. Aminoguanidine in a dose-dependent manner also significantly increased the number of seizure episodes induced by HT and their severity. It could be concluded that iNOS inhibitor (aminoguanidine) markedly aggravates behavioral and EEG manifestations of HT-induced seizures in rats, showing functional involvement of iNOS in homocysteine convulsive mechanisms.

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“…There are three types of NOS: neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS) [11]. Nitric oxide has been implicated in the pathophysiology of epilepsy, but available data are conflicting, and the actual role of NO in epilepsy still remains to be clarified [12]. Some researchers have demonstrated that NO may act as an endogenous anticonvulsant [13][14][15][16][17], while others suggest a proconvulsant role for NO [18,19].…”

Section: Introductionmentioning

confidence: 99%

The effect of acute aripiprazole treatment on chemically and electrically induced seizures in mice: The role of nitric oxide

Shafaroodi

Oveisi

Hosseini

et al. 2015

Epilepsy & Behavior

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

Cited by 15 publications

References 55 publications

The involvement of neuronal nitric oxide synthase in antiepileptic action of alpha-asarone on pentylenetetrazol molding rats

The involvement of neuronal nitric oxide synthase in antiepileptic action of alpha-asarone on pentylenetetrazol molding rats

Homocysteine thiolactone-induced seizures in adult rats are aggravated by inhibition of inducible nitric oxide synthase

The effect of acute aripiprazole treatment on chemically and electrically induced seizures in mice: The role of nitric oxide

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