L-Arginine potentiates excitatory amino acid-induced seizures elicited in the deep prepiriform cortex

Sarro, G. De; Paola, Eugenio Donato Di; Sarro, Angela De; Vidal, María

doi:10.1016/0014-2999(93)90797-l

Cited by 110 publications

(34 citation statements)

References 21 publications

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“…Intracerebrally applied NO synthase inhibitors displayed anticonvulsant activity upon seizures evoked by NMDA or kainate, injected into the deep prepiriform cortex (De Sarro et al, 1991). In the same paradigm, L-arginine, potent NO donor, enhanced NMDA and kainate-induced convulsions (De Sarro et al, 1993). Systemic NNA was demonstrated to impair the convulsive activity of intracerebroventricular glutamate in mice (Tutka et al, 1996).…”

Section: Discussionmentioning

confidence: 97%

NG-nitro-L-arginine, a nitric oxide synthase inhibitor, and seizure susceptibility in four seizure models in mice

Drelewska

et al. 1996

J. Neural Transmission

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Nitric oxide may be involved in seizure phenomena even though data often seem to be contradictory. This prompted us to study the influence of nitric oxide upon electrically and chemically induced seizures. The effects of nitric oxide synthase inhibitor, NG-nitro-L-arginine (NNA), on pentylenetetrazol-, aminooxyacetic acid-, aminophylline-induced seizures or electroconvulsive shock were evaluated. NNA was applied at 1, 10 and 40 mg/ kg 0.5 and 2.0 h before chemical seizures and at 1 and 40 mg/kg 0.5 and 2.0 h prior to electroconvulsions. The nitric oxide synthase inhibitor (up to 40 mg/ kg) did not affect the susceptibility of mice to pentylenetetrazol, amino-oxyacetic acid or electroconvulsions. However, NNA significantly enhanced the convulsive properties of aminophylline when applied at 40 mg/kg, 0.5 h before the test. The CD50 value for aminophylline-induced clonus and tonus/ mortality was decreased from 233 to 191 and from 242 to 212 mg/kg, respectively. However, this pretreatment also led to a significant increase in the plasma levels of theophylline. Our results suggest that differential effects of NNA on chemically-induced convulsions might in some cases be associated with a pharmacokinetic interaction.

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Section: Discussionmentioning

confidence: 97%

NG-nitro-L-arginine, a nitric oxide synthase inhibitor, and seizure susceptibility in four seizure models in mice

Drelewska

et al. 1996

J. Neural Transmission

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“…Furthermore, some reports have suggested that a NO donator, L-ARG, aggravates the severity of experimental epileptic attacks, and NO has been speculated to have a pro-convulsive effect [25]. However, some examples are in disagreement.…”

Section: Discussionmentioning

confidence: 99%

The involvement of neuronal nitric oxide synthase in the anti-epileptic action of curcumin on pentylenetetrazol-kindled rats

Zhu

Liu

et al. 2015

BME

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Abstract. In this study, it was investigated whether a NO signaling pathway is involved in the anti-epileptic effect of curcumin on pentylenetetrazol (PTZ)-kindled rats. PTZ-kindled rats received different doses of curcumin that were administered intraperitoneally for 24 days. Either a non-selective inhibitor of nitric oxide synthase (NOS) (N-nitro-L-arginine methyl ester (L-NAME)), a selective inhibitor of neuronal NOS (7-Nitroindazole (7-NI)), a selective inhibitor of inducible NOS (aminoguanidine (AG)), or a NO precursor (L-arginine (L-ARG)) was administered chronically to evaluate the role of NO in curcumin's anti-seizure effect. A chronic administration of curcumin (200 mg/kg) was most effective for decreasing the mean frequency of epileptiform discharge. Furthermore, a pretreatment with L-NAME or 7-NI augmented the anti-epileptic effect of curcumin. In contrast, AG failed to significantly alter the anti-epileptic effect of curcumin. A pretreatment with L-ARG temporally reversed the anti-epileptic effect of curcumin in the early stage, but in the late stage, it potentiated curcumin's anti-epileptic effect. These findings suggest that the L-arginine-nitric oxide pathway may be involved in the anti-epileptic properties of curcumin, and that the role of nNOS (and not iNOS) is prominent in this neuroprotective feature.

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“…NO may have biphasic influences (ie both excitatory and inhibitory) based on a complex interaction among glutamatergic, GABAergic, and other (eg opioid) neuronal systems, all of which are modulated by NO (Lovick and Key, 1996;Wang et al, 1997;Hall and Behbehani, 1998;Lin et al, 2000). This may account for the contradictory results that NO appears to both enhance and suppress not only anxiety but also other functions such as pain (Moore et al, 1993;McDonald et al, 1994), seizure activity (Buisson et al, 1993;De Sarro et al, 1993), and neurotoxicity (Contestabile et al, 2003). These findings are contributing to a more complete understanding of the role of NO in brain function, which would potentially have many ramifications for more effective treatment of not only anxiety but other brain dysfunctions as well.…”

Section: Discussionmentioning

confidence: 99%

Antagonism by NOS Inhibition of the Behavioral Effects of Benzodiazepine and GABAA Receptor Agonists in the Mouse Elevated Plus-Maze

Elfline

Branda

Babich

et al. 2004

Neuropsychopharmacol

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Earlier we implicated nitric oxide (NO) in mediation of the behavioral effects of benzodiazepines. Since benzodiazepines work through facilitation of GABAergic inhibitory neurotransmission, this study was designed to determine whether the direct-acting g-aminobutyric acid A (GABA A ) receptor agonist THIP (4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol) evokes behavioral effects similar to those of benzodiazepines and whether behavioral effects of THIP are also NO dependent. When challenged with either chlordiazepoxide or THIP in an elevated plus-maze paradigm, male NIH Swiss mice exhibited a dose-related increase in open-arm activity. The chlordiazepoxide-induced effects were sensitive to antagonism by a benzodiazepine antagonist, and the effects of THIP were blocked by a GABA A receptor antagonist. Pretreatment with the NO synthase (NOS) inhibitor L-N G -nitro arginine antagonized the effects of both chlordiazepoxide and THIP; similar pretreatment with the D-isomer, D-N G -nitro arginine, which is inactive as an NOS inhibitor, was without effect on chlordiazepoxide and THIP. These findings indicate that chlordiazepoxide and THIP evoke similar behavioral effects in mice in the elevated plus-maze through actions on different parts of the GABA A receptor, and that NO appears to play a key role in mediation of the behavioral effects of both chlordiazepoxide and THIP.

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L-Arginine potentiates excitatory amino acid-induced seizures elicited in the deep prepiriform cortex

Cited by 110 publications

References 21 publications

NG-nitro-L-arginine, a nitric oxide synthase inhibitor, and seizure susceptibility in four seizure models in mice

NG-nitro-L-arginine, a nitric oxide synthase inhibitor, and seizure susceptibility in four seizure models in mice

The involvement of neuronal nitric oxide synthase in the anti-epileptic action of curcumin on pentylenetetrazol-kindled rats

Antagonism by NOS Inhibition of the Behavioral Effects of Benzodiazepine and GABAA Receptor Agonists in the Mouse Elevated Plus-Maze

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