Possible involvement of nitrergic and opioidergic systems in the modulatory effect of acute chloroquine treatment on pentylenetetrazol induced convulsions in mice

Hassanipour, Mahsa; Shirzadian, Armin; Boojar, Mahdi Mashhadi-Akbar; Abkhoo, Aminreza; Abkhoo, Alireza; Delazar, Sina; Amiri, Shayan; Rahimi, Nastaran; Ostadhadi, Sattar; Dehpour, Ahmad Reza

doi:10.1016/j.brainresbull.2015.11.020

Cited by 24 publications

(14 citation statements)

References 56 publications

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“…7, simultaneous administration of L-arginine 60 mg/kg and subeffective dose of atorvastatin (10 mg/kg) led to significant (F(2, 10)= 17.36, P<0.001) potentiation of the analgesic threshold (P<0.01). Larginine 60 mg/kg is considered as the subeffective dose based on our previous studies (Hassanipour et al, 2016).…”

Section: Co-administration Of Acute L-arginine and Atorvastatin 10 Mgmentioning

confidence: 99%

“…Moreover; to determine the role of NO in the expression phase of tolerance L-NAME (5 mg/kg), aminoguanidine (100 mg/kg), 7-NI (40 mg/kg) and ODQ (20 mg/kg) and Larginine 60 mg/kg (NO precursor) were administered only on 5 th day 30 min after morphine injection (75 min after atorvastatin). Sub-effective doses of NOS inhibitors, ODQ and L-arginine were selected based on our previous studies (Hassanipour et al, 2016;Javadi et al, 2013).…”

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confidence: 99%

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Atorvastatin attenuates the antinociceptive tolerance of morphine via nitric oxide dependent pathway in male mice

Hassanipour

Amini-Khoei

Shafaroodi

et al. 2016

Brain Research Bulletin

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Section: Co-administration Of Acute L-arginine and Atorvastatin 10 Mgmentioning

confidence: 99%

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confidence: 99%

Atorvastatin attenuates the antinociceptive tolerance of morphine via nitric oxide dependent pathway in male mice

Hassanipour

Amini-Khoei

Shafaroodi

et al. 2016

Brain Research Bulletin

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“…The induction of seizure by MES represents an experimental model of tonic–clonic seizures with similarities to human seizures ( 55 , 56 ). The model has also shown high sensitivity to compounds affecting opioidergic mechanisms ( 57 ).…”

Section: Discussionmentioning

confidence: 99%

Influence of methadone on the anticonvulsant efficacy of valproate sodium gabapentin against maximal electroshock seizure in mice by regulation of brain MDA TNF-α

Jafari

Hassanpour-Ezatti

2022

Front. Neurol.

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Methadone is the most frequently used opioid therapy worldwide, with controversial effects on oxidative stress homeostasis. This study investigated the effects of intraperitoneal (i.p.) co-administration of methadone (0.1, 0.3, 1, and 3 mg/kg) and valproate sodium (300 mg/kg) or gabapentin (50 mg/kg) in the mice maximal electroshock (MES)-induced seizure model. The adverse effect of drugs was assessed using the chimney test. The levels of tumor necrosis factor-alpha (TNF-α) and malondialdehyde (MDA) contents were measured in mice brains after a single seizure. Administration of methadone alone resulted in a significant reduction in the duration of hind limb extension (HLE) than that in the control group. Methadone pretreatment at doses of 0.1 and 0.3 mg/kg i.p. decreased, and at doses of 1 and 3 mg/kg i.p. had an increasing effect on anticonvulsant efficacy of gabapentin. Pretreatment with all doses of methadone significantly decreased the valproate anticonvulsive efficacy. At doses of 1 and 3 mg/kg i.p. methadone per se increased brain MDA levels after MES-induced seizure. Administration of methadone (0.3 mg/kg i.p.) enhanced and at 3 mg/kg decreased gabapentin effect on brain MDA level, but their co-treatment did not lead to further increase in MDA. Methadone at 0.3–3 mg/kg enhanced the effect of sodium valproate on MDA levels in the brain, but at all doses significantly potentiated its effect on brain TNF-α levels. The drugs did not produce any side effects on motor coordination in experimental animals. In conclusion, methadone showed different effects on anticonvulsant actions of gabapentin and valproate through regulation of brain levels of MDA and TNF-α.

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“…12,13 The role of NO in the CNS function, especially in modulating seizure threshold, has been well documented in the literature. [14][15][16][17] N-methyl D-aspartic acid (NMDA) receptors (NMDARs) are identified as excitatory synaptic transmission and play pivotal roles in the seizure pathogenesis, hypoxic brain damage, and other CNS diseases. 18 Additionally, the NMDAR-mediated NO signaling contributes to pathogenesis of seizures and other cortical brain dysfunctions.…”

Section: Introductionmentioning

confidence: 99%

Effect of Lenalidomide on Pentylenetetrazole-Induced Clonic Seizure Threshold in Mice: A Role for N-Methyl-D-Aspartic Acid Receptor/Nitric Oxide Pathway

Dafe¹,

Rahimi²,

Javadian³

et al. 2021

J Epilepsy Res

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Background and Purpose: Accumulating evidence suggest that lenalidomide, a structural analog of thalidomide, has neuro-modulatory and neuroprotective properties. In the present study, we investigated effects of acute administration of lenalidomide on clonic seizure threshold in mice induced by pentylenetetrazole (PTZ) and possible role of N-methyl-D-aspartic acid receptor (NMDAR) and nitric oxide (NO) pathway.Methods: We have utilized a clonic model of seizure in NMRI mice induced by PTZ to evaluate the potential effect of lenalidomide on seizure threshold. Different doses of lenalidomide (5, 10, 20, and 50 mg/kg, intraperitoneal [i.p.]) were administered 1 hour before PTZ. To evaluate probable role of NMDAR/NO signaling, the non-selective NO synthase inhibitor L-NG-nitroarginine methyl ester (L-NAME; 10 mg/kg, i.p.), neuronal NOS (nNOS) inhibitor 7-nitroindazole (7-NI; 30 mg/kg, i.p.), selective inducible NOS inhibitor aminoguanidine (AG; 100 mg/kg, i.p.), selective NMDAR antagonist MK-801 (0.01 mg/kg, i.p.), and selective NMDAR agonist D-serine (30 mg/kg, i.p.) were injected 15 minutes before lenalidomide.Results: Lenalidomide at 10 and 20 mg/kg significantly elevated the PTZ-induced seizure thresholds. Interestingly, L-NAME (10 mg/kg, i.p), 7-NI (30 mg/kg, i.p), and AG (100 mg/kg, i.p) reversed the anticonvulsive effect of lenalidomide (10 mg/kg). Moreover, treatment with the NMDAR agonist D-serine (30 mg/kg, i.p.) did not alter the anticonvulsive properties of lenalidomide (10 mg/kg, i.p). However, the NMDAR antagonist MK-801 (0.01 mg/kg, i.p) significantly reversed the anticonvulsive effects of lenalidomide (10 mg/kg).Conclusions: Our study demonstrated a role for the NMDAR/NO pathway in the anticonvulsive effects of lenalidomide on the PTZ-induced clonic seizures in mice.

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Possible involvement of nitrergic and opioidergic systems in the modulatory effect of acute chloroquine treatment on pentylenetetrazol induced convulsions in mice

Cited by 24 publications

References 56 publications

Atorvastatin attenuates the antinociceptive tolerance of morphine via nitric oxide dependent pathway in male mice

Atorvastatin attenuates the antinociceptive tolerance of morphine via nitric oxide dependent pathway in male mice

Influence of methadone on the anticonvulsant efficacy of valproate sodium gabapentin against maximal electroshock seizure in mice by regulation of brain MDA TNF-α

Effect of Lenalidomide on Pentylenetetrazole-Induced Clonic Seizure Threshold in Mice: A Role for N-Methyl-D-Aspartic Acid Receptor/Nitric Oxide Pathway

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