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Ahmad Reza Dehpour - One of the best experts on this subject based on the ideXlab platform.
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Effects of Modafinil on Clonic Seizure Threshold Induced by Pentylenetetrazole in Mice: Involvement of Glutamate, Nitric oxide, GABA, and Serotonin Pathways
Neurochemical Research, 2018Co-Authors: Erfan Bahramnjead, Soheil Kazemi Roodsari, Payam Etemadi, Iraj Aghaei, Nastaran Rahimi, Ahmad Reza DehpourAbstract:Epilepsy is the third most common chronic brain disorder. Modafinil is an awakening agent approved for narcolepsy. In addition to its clinical uses some reports revealed that modafinil was associated with some alterations in Seizure Threshold. The purpose of this study was to clarify the effect of acute administration of modafinil in clonic Seizure Threshold (CST) induced by pentylenetetrazole in mice and the involvement of glutamate, nitric oxide, gamma amino butyric acid (GABA), and serotonin systems in this feature. Modafinil at 80 and 150 mg/kg showed anti- and pro-convulsant effects respectively and expressed maximum anti- and pro-convulsant activities at 30 min after injection. Both modulatory effects were blunted by pretreatment of l -NAME [nonspecific nitric oxide synthase (NOS) inhibitor; 10 mg/kg, i.p.], 7-nitroindazole (a neuronal NOS inhibitor; 40 mg/kg, i.p.), and aminoguanidine (an inducible NOS inhibitor; 50 mg/kg, i.p.). Injection of the NOS precursor l -arginine (60 mg/kg, i.p.) before modafinil did not change the anti-convulsant effect, while thoroughly reversed the pro-convulsant one. Our experiments displayed that administration of diazepam (a GABA_A receptor agonist; 0.02 mg/kg, i.p.) and MK-801 (a NMDA receptor antagonist; 0.05 mg/kg, i.p.) before different doses of modafinil significantly increased CST. Finally, pretreatment of citalopram (a selective serotonin reuptake inhibitor; 0.1 mg/kg, i.p.) did not modify the convulsant activities of modafinil. Therefore, nitric oxide system may mediate anti-convulsant activity, while glutamate, nitric oxide, and GABA pathways may involve in pro-convulsant property. Serotonin receptors have no role on convulsant effects of modafinil.
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the role of α2 adrenoceptors in the anti convulsant effects of cannabinoids on pentylenetetrazole induced Seizure Threshold in mice
European Journal of Pharmacology, 2013Co-Authors: Hamed Shafaroodi, Leila Moezi, Arsh Bahremand, Ahmad Reza DehpourAbstract:Abstract Cannabinoid system plays a pivotal role in the Seizure Threshold modulation which is mainly mediated through activation of the cannabinoid CB 1 receptor. There is also several evidence of interaction between cannabinoid system and α 2 -adrenoceptors in different paradigms. Using model of clonic Seizure induced by intravenous pentylenetetrazole (PTZ) in male mice, we investigated whether α 2 -adrenoceptors is involved in the effects of cannabinoids on the Seizure Threshold. Injection of the selective cannabinoid CB 1 agonist ACEA (2 mg/kg) significantly ( P 1 antagonist AM251 (1 mg/kg, i.p.). The highest doses of clonidine, a α 2 receptor agonist, (1 and 5 mg/kg) showed anticonvulsant effects while yohimbine, a α 2 receptor antagonist, (0.01, 0.1, 1, and 10 mg/kg) did not induce any significant effect on PTZ Seizure Threshold. Pretreatment with clonidine (0.1 and 0.5 mg/kg) significantly reversed the anticonvulsant effect of ACEA (2 mg/kg). Yohimbine (0.1, 1, and 10 mg/kg) pretreatment of mice enhanced the clonic Seizure Threshold of ACEA (1 mg/kg), significantly. Combination of non-effective doses of AM251 (0.1 mg/kg) and clonidine (0.01 mg/kg) showed additive effect in blocking the anticonvulsant effect of ACEA (2 mg/kg). In conclusion, our findings demonstrated that α 2 -adrenoceptors could be involved in the anticonvulsant properties of the specific cannabinoid CB 1 agonist ACEA, suggesting that CB 1 cannabinoid and α 2 receptors have functional interactions in modulation of clonic Seizure Threshold.
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The interaction of melatonin and agmatine on pentylenetetrazole-induced Seizure Threshold in mice.
Epilepsy & Behavior, 2011Co-Authors: Leila Moezi, Abolfazl Hojati, Hamed Shafaroodi, Ahmad Reza DehpourAbstract:article i nfo Melatonin, the major hormone produced by the pineal gland, has a number of functions in mammals, for example, its function as an anticonvulsant. Agmatine, a biogenic amine formed by decarboxylation of L- arginine by arginine decarboxylase, also has anticonvulsant effects. This study investigated the effect of the interaction of melatonin and agmatine on Seizure susceptibility in the mouse model of pentylenetetrazole (PTZ)-induced clonic Seizures. Further, the researchers investigated the involvement of melatonin receptors in this interaction using luzindole, a ML1/2 receptor antagonist and prazosin, a ML3 receptor antagonist. Melatonin, at 40 and 80 mg/kg, and agmatine, at 10 and 20 mg/kg, exerted anticonvulsant effects. Luzindole, at 1.25 and 2.5 mg/kg, or prazosin, at 0.5 mg/kg, did not change the Seizure Threshold as compared with that of vehicle-treated mice. The anticonvulsant effect of melatonin (40 and 80 mg/kg) was prevented by luzindole (2.5 mg/kg) (Pb0.001) but not prazosin (0.5 mg/kg), indicating the possible involvement of ML1/2 receptors in the anticonvulsant effect of melatonin. Agmatine (5 mg/kg) significantly increased the anticonvulsant effect of both the noneffective dose (20 mg/kg) (Pb0.05) and the effective dose (80 mg/kg) (Pb0.001) of melatonin. Luzindole (2.5 mg/kg), but not prazosin (0.5 mg/kg), decreased the anticonvulsant effect of agmatine (20 mg/kg) (Pb0.05). Luzindole (2.5 mg/kg), but not prazosin (0.5 mg/kg), also decreased the Seizure Threshold when agmatine (5 mg/kg) was administered before melatonin (20 mg/kg); the decrease was significant compared with that of the group that received only agmatine and melatonin (Pb0.001). In conclusion, melatonin and agmatine exhibit an additive effect in decreasing pentylenetetrazole-induced Seizure Threshold in mice, probably through ML1/2 receptors.
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morphine sensitization in the pentylenetetrazole induced clonic Seizure Threshold in mice role of nitric oxide and μ receptors
Epilepsy & Behavior, 2011Co-Authors: Hamed Shafaroodi, Leila Moezi, Nazanin Baradaran, Siavash Dehpour, Tina Kabiri, Ahmad Reza DehpourAbstract:Behavioral sensitization occurs after repeated administration of μ-opioid receptor agonists following a drug-free period. It seems that the changes in dopaminergic systems induced by μ-opioid receptor agonists play a crucial role in behavioral sensitization to opioids. Nitric oxide also plays a role in some behavioral effects of morphine, including sensitization to the locomotor-stimulating effect. This study investigated whether morphine sensitization appears in Seizure Threshold and the possible role of μ-opioid receptor and nitric oxide in this sensitization. Sensitization was produced by daily injections of morphine (0.1, 0.5, 1, 5, 15, or 30 mg/kg), followed by a 10-day washout period. Then the challenge test was performed using morphine (0.1, 0.5, 1, 5, 15, or 30 mg/kg) in different groups. To assess clonic Seizure Threshold, pentylenetetrazole (PTZ) was administered intravenously. Subcutaneous administration of morphine (0.1 and 0.5 mg/kg) induced sensitization in PTZ-induced clonic Seizures in mice. Intraperitoneal administration of L-NAME (20 mg/kg), a nonselective inhibitor of nitric oxide synthase, or naltrexone (10 mg/kg), an opioid receptor antagonist, along with morphine inhibited morphine-induced sensitization in PTZ-induced Seizure Threshold. In conclusion, at low doses, morphine induces sensitization in PTZ-induced clonic Seizures in mice probably as a result of the interaction with μ-receptors and nitric oxide.
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effect of acute and chronic photoperiod modulation on pentylenetetrazole induced clonic Seizure Threshold in mice
Epilepsy Research, 2008Co-Authors: Pouya Tahsilifahadan, Noushin Yahyavifirouzabadi, Kiarash Riazi, Mohammad Hossein Ghahremani, Ahmad Reza DehpourAbstract:Summary Changes in circadian rhythms have been shown to alter Seizure susceptibility and anticonvulsant properties of drugs. The present study attempts to elucidate the effect of acute and chronic light/dark (LD) cycle alterations on pentylenetetrazol-induced clonic Seizure Threshold (CST) in male NMRI mice. The acute effect was tested by comparing the effects of abrupt 6-h phase shifts that resulted in 6-h and 18-h photoperiods, during the 24-h period before CST determination, with the controls that were maintained on 12 h/12 h LD cycle. In order to test the effect of chronic LD cycle alteration on CST, three groups of mice were maintained on 12 h/12 h, 6 h/18 h and 18 h/6 h LD cycles for 2 weeks prior to CST testing. The effect of administration of exogenous melatonin (5, 10 and 20 mg/kg, i.p.) was also assessed on LD cycle related changes of CST. The results indicate that acute photoperiod change from 12 h/12 h to 18 h/6 h LD cycle lowers CST, while keeping animals under shorter photoperiod does not produce a significant effect. The pro-convulsant effect of acute increase in light period is reversed by a single injection of melatonin (10 and 20 mg/kg). Animals chronically maintained on both shorter and longer photoperiods show a significant decrease in CST compared to animals under 12 h/12 h LD cycle. However, in both groups chronic administration of melatonin (20 mg/kg) reversed the effect of LD cycle alteration on CST. In conclusion, our data demonstrate that acute increase and chronic modulation of the photoperiod increase Seizure susceptibility in mice. Moreover, the pro-convulsant effect of LD cycle alteration could be reversed by exogenous melatonin administration.
Thomas N. Ferraro - One of the best experts on this subject based on the ideXlab platform.
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bmal1 controls the diurnal rhythm and set point for electrical Seizure Threshold in mice
Frontiers in Systems Neuroscience, 2014Co-Authors: Jason R Gerstner, George G. Smith, Russell J. Buono, Thomas N. Ferraro, Olivia Lenz, Isaac J PerronAbstract:The epilepsies are a heterogeneous group of neurological diseases defined by the occurrence of unprovoked Seizures which, in many cases, are correlated with diurnal rhythms. In order to gain insight into the biological mechanisms controlling this phenomenon, we characterized time-of-day effects on electrical Seizure Threshold in mice. Male C57BL/6J wild-type mice were maintained on a 14h/10h light/dark cycle, from birth until 6 weeks of age for Seizure testing. Seizure Thresholds were measured using a step-wise paradigm involving a single daily electrical stimulus. Results showed that the current required to elicit both generalized and maximal Seizures was significantly higher in mice tested during the dark phase of the diurnal cycle compared to mice tested during the light phase. This rhythm was absent in BMAL1 knockout (KO) mice. BMAL1 KO also exhibited significantly reduced Seizure Thresholds at all times tested, compared to C57BL/6J mice. Results document a significant influence of time-of-day on electrical Seizure Threshold in mice and suggest that this effect is under the control of genes that are known to regulate circadian behaviors. Furthermore, low Seizure Thresholds in BMAL1 KO mice suggest that BMAL1 itself is directly involved in controlling neuronal excitability.
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Mouse strain variation in maximal electroshock Seizure Threshold.
Brain Research, 2002Co-Authors: Thomas N. Ferraro, Gregory T. Golden, George G. Smith, Denis Demuth, Russell J. Buono, Wade H. BerrettiniAbstract:Abstract Maximal electroshock Seizure Threshold (MEST) is a classical measure of Seizure sensitivity with a wide range of experimental applications. We determined MEST in nine inbred mouse strains and one congenic strain using a procedure in which mice are given one shock per day with an incremental (1 mA) current increase in each successive trial until a maximal Seizure (tonic hindlimb extension) is elicited. C57BL/6J and DBA/2J mice exhibited the highest and lowest MEST, respectively, with the values of other strains falling between these two extremes. The relative rank order of MEST values by inbred strain (highest to lowest) is as follows: C57BL/6J>CBA/J=C3H/HeJ>A/J>Balb/cJ=129/SvIMJ=129/SvJ>AKR/J>DBA/2J. Results of experiments involving a single electroconvulsive shock given to separate groups of mice at different current intensities suggest that determination of MEST by the method used is not affected by repeated sub-maximal Seizures. Overall, results document a distinctive mouse strain distribution pattern for MEST. Additionally, low within strain variability suggests that environmental factors which affect quantification of MEST are readily controlled under the conditions of this study. We conclude that MEST represents a useful tool for dissecting the multifactorial nature of Seizure sensitivity in mice.
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Quantitative genetic study of maximal electroshock Seizure Threshold in mice: evidence for a major Seizure susceptibility locus on distal chromosome 1.
Genomics, 2001Co-Authors: Thomas N. Ferraro, Gregory T. Golden, Denis Demuth, G G Smith, R L Longman, R L Snyder, I Szpilzak, N Mulholland, E Eng, Falk W. LohoffAbstract:We conducted a quantitative trait locus (QTL) mapping study to dissect the multifactorial nature of maximal electroshock Seizure Threshold (MEST) in C57BL/6 (B6) and DBA/2 (D2) mice. MEST determination involved a standard paradigm in which 8- to 12-week-old mice received one shock per day with a daily incremental increase in electrical current until a maximal Seizure (tonic hindlimb extension) was induced. Mean MEST values in parental strains were separated by over five standard deviation units, with D2 mice showing lower values than B6 mice. The distribution of MEST values in B6xD2 F2 intercrossed mice spanned the entire phenotypic range defined by parental strains. Statistical mapping yielded significant evidence for QTLs on chromosomes 1, 2, 5, and 15, which together explained over 60% of the phenotypic variance in the model. The chromosome 1 QTL represents a locus of major effect, accounting for about one-third of the genetic variance. Experiments involving a congenic strain (B6.D2-Mtv7(a)/Ty) enabled more precise mapping of the chromosome 1 QTL and indicate that it lies in the genetic interval between markers D1Mit145 and D1Mit17. These results support the hypothesis that the distal portion of chromosome 1 harbors a gene(s) that has a fundamental role in regulating Seizure susceptibility.
Hamed Shafaroodi - One of the best experts on this subject based on the ideXlab platform.
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the role of α2 adrenoceptors in the anti convulsant effects of cannabinoids on pentylenetetrazole induced Seizure Threshold in mice
European Journal of Pharmacology, 2013Co-Authors: Hamed Shafaroodi, Leila Moezi, Arsh Bahremand, Ahmad Reza DehpourAbstract:Abstract Cannabinoid system plays a pivotal role in the Seizure Threshold modulation which is mainly mediated through activation of the cannabinoid CB 1 receptor. There is also several evidence of interaction between cannabinoid system and α 2 -adrenoceptors in different paradigms. Using model of clonic Seizure induced by intravenous pentylenetetrazole (PTZ) in male mice, we investigated whether α 2 -adrenoceptors is involved in the effects of cannabinoids on the Seizure Threshold. Injection of the selective cannabinoid CB 1 agonist ACEA (2 mg/kg) significantly ( P 1 antagonist AM251 (1 mg/kg, i.p.). The highest doses of clonidine, a α 2 receptor agonist, (1 and 5 mg/kg) showed anticonvulsant effects while yohimbine, a α 2 receptor antagonist, (0.01, 0.1, 1, and 10 mg/kg) did not induce any significant effect on PTZ Seizure Threshold. Pretreatment with clonidine (0.1 and 0.5 mg/kg) significantly reversed the anticonvulsant effect of ACEA (2 mg/kg). Yohimbine (0.1, 1, and 10 mg/kg) pretreatment of mice enhanced the clonic Seizure Threshold of ACEA (1 mg/kg), significantly. Combination of non-effective doses of AM251 (0.1 mg/kg) and clonidine (0.01 mg/kg) showed additive effect in blocking the anticonvulsant effect of ACEA (2 mg/kg). In conclusion, our findings demonstrated that α 2 -adrenoceptors could be involved in the anticonvulsant properties of the specific cannabinoid CB 1 agonist ACEA, suggesting that CB 1 cannabinoid and α 2 receptors have functional interactions in modulation of clonic Seizure Threshold.
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The interaction of melatonin and agmatine on pentylenetetrazole-induced Seizure Threshold in mice.
Epilepsy & Behavior, 2011Co-Authors: Leila Moezi, Abolfazl Hojati, Hamed Shafaroodi, Ahmad Reza DehpourAbstract:article i nfo Melatonin, the major hormone produced by the pineal gland, has a number of functions in mammals, for example, its function as an anticonvulsant. Agmatine, a biogenic amine formed by decarboxylation of L- arginine by arginine decarboxylase, also has anticonvulsant effects. This study investigated the effect of the interaction of melatonin and agmatine on Seizure susceptibility in the mouse model of pentylenetetrazole (PTZ)-induced clonic Seizures. Further, the researchers investigated the involvement of melatonin receptors in this interaction using luzindole, a ML1/2 receptor antagonist and prazosin, a ML3 receptor antagonist. Melatonin, at 40 and 80 mg/kg, and agmatine, at 10 and 20 mg/kg, exerted anticonvulsant effects. Luzindole, at 1.25 and 2.5 mg/kg, or prazosin, at 0.5 mg/kg, did not change the Seizure Threshold as compared with that of vehicle-treated mice. The anticonvulsant effect of melatonin (40 and 80 mg/kg) was prevented by luzindole (2.5 mg/kg) (Pb0.001) but not prazosin (0.5 mg/kg), indicating the possible involvement of ML1/2 receptors in the anticonvulsant effect of melatonin. Agmatine (5 mg/kg) significantly increased the anticonvulsant effect of both the noneffective dose (20 mg/kg) (Pb0.05) and the effective dose (80 mg/kg) (Pb0.001) of melatonin. Luzindole (2.5 mg/kg), but not prazosin (0.5 mg/kg), decreased the anticonvulsant effect of agmatine (20 mg/kg) (Pb0.05). Luzindole (2.5 mg/kg), but not prazosin (0.5 mg/kg), also decreased the Seizure Threshold when agmatine (5 mg/kg) was administered before melatonin (20 mg/kg); the decrease was significant compared with that of the group that received only agmatine and melatonin (Pb0.001). In conclusion, melatonin and agmatine exhibit an additive effect in decreasing pentylenetetrazole-induced Seizure Threshold in mice, probably through ML1/2 receptors.
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morphine sensitization in the pentylenetetrazole induced clonic Seizure Threshold in mice role of nitric oxide and μ receptors
Epilepsy & Behavior, 2011Co-Authors: Hamed Shafaroodi, Leila Moezi, Nazanin Baradaran, Siavash Dehpour, Tina Kabiri, Ahmad Reza DehpourAbstract:Behavioral sensitization occurs after repeated administration of μ-opioid receptor agonists following a drug-free period. It seems that the changes in dopaminergic systems induced by μ-opioid receptor agonists play a crucial role in behavioral sensitization to opioids. Nitric oxide also plays a role in some behavioral effects of morphine, including sensitization to the locomotor-stimulating effect. This study investigated whether morphine sensitization appears in Seizure Threshold and the possible role of μ-opioid receptor and nitric oxide in this sensitization. Sensitization was produced by daily injections of morphine (0.1, 0.5, 1, 5, 15, or 30 mg/kg), followed by a 10-day washout period. Then the challenge test was performed using morphine (0.1, 0.5, 1, 5, 15, or 30 mg/kg) in different groups. To assess clonic Seizure Threshold, pentylenetetrazole (PTZ) was administered intravenously. Subcutaneous administration of morphine (0.1 and 0.5 mg/kg) induced sensitization in PTZ-induced clonic Seizures in mice. Intraperitoneal administration of L-NAME (20 mg/kg), a nonselective inhibitor of nitric oxide synthase, or naltrexone (10 mg/kg), an opioid receptor antagonist, along with morphine inhibited morphine-induced sensitization in PTZ-induced Seizure Threshold. In conclusion, at low doses, morphine induces sensitization in PTZ-induced clonic Seizures in mice probably as a result of the interaction with μ-receptors and nitric oxide.
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mouth breathing increases the pentylenetetrazole induced Seizure Threshold in mice a role for atp sensitive potassium channels
Epilepsy & Behavior, 2008Co-Authors: Seyed Esfandiar Akhavan Niaki, Hamed Shafaroodi, Mehdi Ghasemi, Bijan Shakiba, Ali Fakhimi, Ahmad Reza DehpourAbstract:Nasal obstruction and consequent mouth breathing have been shown to change the acid-base balance, producing respiratory acidosis. Additionally, there exists a large body of evidence maintaining that acidosis affects the activity of ATP-sensitive potassium (K(ATP)) channels, which play a crucial role in the function of the central nervous system (CNS), for example, in modulating Seizure Threshold. Thus, in the study described here, we examined whether mouth breathing, induced by surgical ligation of nostrils, could affect the Seizure Threshold induced by pentylenetetrazole in male NMRI mice. Using the selective K(ATP) channel opener (diazoxide) and blocker (glibenclamide), we also evaluated the possible role of K(ATP) channels in this process. Our data revealed that Seizure Threshold was increased 6 to 72 hours after nasal obstruction, reaching a peak 48 hours afterward, compared with either control or sham-operated mice (P<0.01). There was a significant decrease in pH of arterial blood samples and increase in CO(2) partial pressure (PCO(2)) during this time. Systemic injection of glibenclamide (1 and 2mg/kg, ip, daily) significantly prevented the increase in Seizure Threshold in 48-hour bilaterally nasally obstructed mice, whereas it had no effect on Seizure Threshold in sham-operated mice. Systemic injection of diazoxide (25mg/kg, ip, daily) had no effect on Seizure Threshold in all groups, whereas higher doses (50 and 100mg/kg, ip, daily) significantly increased Seizure Threshold in both 48-hour-obstructed and sham-operated mice. The decrease in Seizure Threshold induced by glibenclamide (2mg/kg, ip, daily) was prevented by diazoxide (25mg/kg, ip, daily). These results demonstrate for the first time that mouth breathing, which could result in respiratory acidosis, increases Seizure Threshold in mice and K(ATP) channels may play a role in this effect.
Jarogniew J Luszczki - One of the best experts on this subject based on the ideXlab platform.
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Influence of aminophylline on the anticonvulsive action of gabapentin in the mouse maximal electroshock Seizure Threshold model
Journal of Neural Transmission, 2007Co-Authors: Jarogniew J Luszczki, K. Jankiewicz, M. JankiewiczAbstract:Accumulating evidence indicates that aminophylline [theophylline_2 · ethylenediamine] markedly attenuates the anticonvulsant action of conventional antiepileptic drugs in experimental animal models of epilepsy and evokes severe Seizure activity in patients treated with this methylxanthine. The objective of this study was to determine the influence of acute (single) and chronic (twice daily for 14 consecutive days) treatments with aminophylline on the anticonvulsant potential of gabapentin (a second-generation antiepileptic drug) in the mouse maximal electroshock Seizure Threshold model. Additionally, the effects of acute and chronic administration of aminophylline on the adverse effect potential of gabapentin in terms of motor coordination impairment were assessed in the chimney test. To evaluate pharmacokinetic characteristics of interaction between drugs, total brain concentrations of gabapentin and theophylline were estimated with high-pressure liquid chromatography and fluorescence polarization immunoassay, respectively. Results indicated that gabapentin (at doses of 75 and 100 mg/kg, i.p.) increased the Threshold for electroconvulsions in mice. Aminophylline in non-convulsive doses of 50 and 100 mg/kg (i.p.), both in acute and chronic experiments, did not attenuate the anticonvulsant potential of gabapentin in the maximal electroshock Seizure Threshold test in mice. Similarly, aminophylline at a dose of 100 mg/kg had no impact on the adverse effect potential of gabapentin in the chimney test. Pharmacokinetic evaluation of total brain concentrations of gabapentin and theophylline revealed no significant changes in total brain concentrations of the drugs after both, acute and chronic applications of aminophylline in combination with gabapentin. The data show that aminophylline did not alter the ability of gabapentin to protect mice against Seizures induced by electroconvulsive shock. The observed interaction between gabapentin and aminophylline in both acute and chronic experiments was pharmacodynamic in nature.
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Time-course and dose-response relationships of imperatorin in the mouse maximal electroshock Seizure Threshold model.
Neuroscience Research, 2007Co-Authors: Jarogniew J Luszczki, Kazimierz GłowniakAbstract:Abstract This study was designed to evaluate the anticonvulsant effects of imperatorin (a furanocoumarin isolated from fruits of Angelica archangelica ) in the mouse maximal electroshock Seizure Threshold model. The Threshold for electroconvulsions in mice was determined at several times: 15, 30, 60 and 120 min after i.p. administration of imperatorin at increasing doses of 10, 20, 30, 40, 50 and 100 mg/kg. The evaluation of time–course relationship for imperatorin in the maximal electroshock Seizure Threshold test revealed that the agent produced its maximum antielectroshock action at 30 min after its i.p. administration. In this case, imperatorin at doses of 50 and 100 mg/kg significantly raised the Threshold for electroconvulsions in mice by 38 and 68% ( P P
Leila Moezi - One of the best experts on this subject based on the ideXlab platform.
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the role of α2 adrenoceptors in the anti convulsant effects of cannabinoids on pentylenetetrazole induced Seizure Threshold in mice
European Journal of Pharmacology, 2013Co-Authors: Hamed Shafaroodi, Leila Moezi, Arsh Bahremand, Ahmad Reza DehpourAbstract:Abstract Cannabinoid system plays a pivotal role in the Seizure Threshold modulation which is mainly mediated through activation of the cannabinoid CB 1 receptor. There is also several evidence of interaction between cannabinoid system and α 2 -adrenoceptors in different paradigms. Using model of clonic Seizure induced by intravenous pentylenetetrazole (PTZ) in male mice, we investigated whether α 2 -adrenoceptors is involved in the effects of cannabinoids on the Seizure Threshold. Injection of the selective cannabinoid CB 1 agonist ACEA (2 mg/kg) significantly ( P 1 antagonist AM251 (1 mg/kg, i.p.). The highest doses of clonidine, a α 2 receptor agonist, (1 and 5 mg/kg) showed anticonvulsant effects while yohimbine, a α 2 receptor antagonist, (0.01, 0.1, 1, and 10 mg/kg) did not induce any significant effect on PTZ Seizure Threshold. Pretreatment with clonidine (0.1 and 0.5 mg/kg) significantly reversed the anticonvulsant effect of ACEA (2 mg/kg). Yohimbine (0.1, 1, and 10 mg/kg) pretreatment of mice enhanced the clonic Seizure Threshold of ACEA (1 mg/kg), significantly. Combination of non-effective doses of AM251 (0.1 mg/kg) and clonidine (0.01 mg/kg) showed additive effect in blocking the anticonvulsant effect of ACEA (2 mg/kg). In conclusion, our findings demonstrated that α 2 -adrenoceptors could be involved in the anticonvulsant properties of the specific cannabinoid CB 1 agonist ACEA, suggesting that CB 1 cannabinoid and α 2 receptors have functional interactions in modulation of clonic Seizure Threshold.
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The interaction of melatonin and agmatine on pentylenetetrazole-induced Seizure Threshold in mice.
Epilepsy & Behavior, 2011Co-Authors: Leila Moezi, Abolfazl Hojati, Hamed Shafaroodi, Ahmad Reza DehpourAbstract:article i nfo Melatonin, the major hormone produced by the pineal gland, has a number of functions in mammals, for example, its function as an anticonvulsant. Agmatine, a biogenic amine formed by decarboxylation of L- arginine by arginine decarboxylase, also has anticonvulsant effects. This study investigated the effect of the interaction of melatonin and agmatine on Seizure susceptibility in the mouse model of pentylenetetrazole (PTZ)-induced clonic Seizures. Further, the researchers investigated the involvement of melatonin receptors in this interaction using luzindole, a ML1/2 receptor antagonist and prazosin, a ML3 receptor antagonist. Melatonin, at 40 and 80 mg/kg, and agmatine, at 10 and 20 mg/kg, exerted anticonvulsant effects. Luzindole, at 1.25 and 2.5 mg/kg, or prazosin, at 0.5 mg/kg, did not change the Seizure Threshold as compared with that of vehicle-treated mice. The anticonvulsant effect of melatonin (40 and 80 mg/kg) was prevented by luzindole (2.5 mg/kg) (Pb0.001) but not prazosin (0.5 mg/kg), indicating the possible involvement of ML1/2 receptors in the anticonvulsant effect of melatonin. Agmatine (5 mg/kg) significantly increased the anticonvulsant effect of both the noneffective dose (20 mg/kg) (Pb0.05) and the effective dose (80 mg/kg) (Pb0.001) of melatonin. Luzindole (2.5 mg/kg), but not prazosin (0.5 mg/kg), decreased the anticonvulsant effect of agmatine (20 mg/kg) (Pb0.05). Luzindole (2.5 mg/kg), but not prazosin (0.5 mg/kg), also decreased the Seizure Threshold when agmatine (5 mg/kg) was administered before melatonin (20 mg/kg); the decrease was significant compared with that of the group that received only agmatine and melatonin (Pb0.001). In conclusion, melatonin and agmatine exhibit an additive effect in decreasing pentylenetetrazole-induced Seizure Threshold in mice, probably through ML1/2 receptors.
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morphine sensitization in the pentylenetetrazole induced clonic Seizure Threshold in mice role of nitric oxide and μ receptors
Epilepsy & Behavior, 2011Co-Authors: Hamed Shafaroodi, Leila Moezi, Nazanin Baradaran, Siavash Dehpour, Tina Kabiri, Ahmad Reza DehpourAbstract:Behavioral sensitization occurs after repeated administration of μ-opioid receptor agonists following a drug-free period. It seems that the changes in dopaminergic systems induced by μ-opioid receptor agonists play a crucial role in behavioral sensitization to opioids. Nitric oxide also plays a role in some behavioral effects of morphine, including sensitization to the locomotor-stimulating effect. This study investigated whether morphine sensitization appears in Seizure Threshold and the possible role of μ-opioid receptor and nitric oxide in this sensitization. Sensitization was produced by daily injections of morphine (0.1, 0.5, 1, 5, 15, or 30 mg/kg), followed by a 10-day washout period. Then the challenge test was performed using morphine (0.1, 0.5, 1, 5, 15, or 30 mg/kg) in different groups. To assess clonic Seizure Threshold, pentylenetetrazole (PTZ) was administered intravenously. Subcutaneous administration of morphine (0.1 and 0.5 mg/kg) induced sensitization in PTZ-induced clonic Seizures in mice. Intraperitoneal administration of L-NAME (20 mg/kg), a nonselective inhibitor of nitric oxide synthase, or naltrexone (10 mg/kg), an opioid receptor antagonist, along with morphine inhibited morphine-induced sensitization in PTZ-induced Seizure Threshold. In conclusion, at low doses, morphine induces sensitization in PTZ-induced clonic Seizures in mice probably as a result of the interaction with μ-receptors and nitric oxide.