The effect of sertraline and 8-OH-DPAT on the PTZ_induced seizure threshold: Role of the nitrergic system

Heydari, Azhdar; Davoudi, Shima

doi:10.1016/j.seizure.2016.12.005

Cited by 14 publications

(5 citation statements)

References 53 publications

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“…In line with previous reports, the current study identified marked decreases in the levels of 5-HT and its metabolite (5-HIAA), DA, and NE and reduced AChE activity in PTZ-injected rats, which was accompanied by apparent increases in the DOPAC and HVA levels. Deficiencies in the levels of biogenic amines have been demonstrated to trigger seizure susceptibility and the development of behavioral deficits and neuropathological deficits in clinical and experimental studies [44][45][46]. Earlier reports showed a disturbance in the synthesis, release, and reuptake of monoamines following the initiation of epileptic seizures [47].…”

Section: Discussionmentioning

confidence: 99%

Selenium Nanoparticles with Prodigiosin Rescue Hippocampal Damage Associated with Epileptic Seizures Induced by Pentylenetetrazole in Rats

omairi

Albrakati

Alsharif

et al. 2022

Biology

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Background: Prodigiosin (PDG) is a red pigment synthesized by bacterial species with important pharmaceutical and biological activities. Here, we investigated the neuroprotective and anticonvulsant activities of green biosynthesized selenium formulations with PDG (SeNPs-PDG) versus pentylenetetrazole (PTZ)-induced epileptic seizures. Methods: Rats were assigned into six experimental groups: control; PTZ (60 mg/kg, epileptic model); sodium valproate (200 mg/kg) + PTZ; PDG (300 mg/kg) + PTZ; sodium selenite (0.5 mg/kg) + PTZ; and SeNPs-PDG (0.5 mg/kg) + PTZ. The treatment duration is extended to 28 days. Results: SeNPs-PDG pre-treatment delayed seizures onset and reduced duration upon PTZ injection. Additionally, SeNPs-PDG enhanced the antioxidant capacity of hippocampal tissue by activating the expression of nuclear factor erythroid 2–related factor 2 and innate antioxidants (glutathione and glutathione derivatives, in addition to superoxide dismutase and catalase) and decreasing the levels of pro-oxidants (lipoperoxidation products and nitric oxide). SeNPs-PDG administration inhibited inflammatory reactions associated with epileptic seizure development by suppressing the production and activity of glial fibrillary acidic protein and pro-inflammatory mediators, including interleukin-1 beta, tumor necrosis factor-alpha, cyclooxygenase-2, inducible nitric oxide synthase, and nuclear factor kappa B. Moreover, SeNPs-PDG protected against hippocampal cell loss following PTZ injection by decreasing the levels of cytosolic cytochrome c, Bax, and caspase-3 and enhancing the expression of anti-apoptotic Bcl-2. Interestingly, SeNPs-PDG restored the PTZ-induced imbalance between excitatory and inhibitory amino acids and improved monoaminergic and cholinergic transmission. Conclusions: These promising antioxidative, anti-inflammatory, anti-apoptotic, and neuromodulatory activities indicate that SeNPs-PDG might serve as a naturally derived anticonvulsant agent.

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Section: Discussionmentioning

confidence: 99%

Selenium Nanoparticles with Prodigiosin Rescue Hippocampal Damage Associated with Epileptic Seizures Induced by Pentylenetetrazole in Rats

omairi

Albrakati

Alsharif

et al. 2022

Biology

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“…In rat studies, sertraline provided reductions in the severity of generalized tonic-clonic seizures as well as secondarily generalized seizures [ 261 ]. Sertraline prevented tonic-clonic seizures and the epileptiform EEG activity induced by pro-convulsive (4-AP and PTZ) agents [ 262 , 263 ]; an effect comparable to the clinically established ASM carbamazepine [ 264 , 265 ]. Vortioxetine, a new AD approved for the treatment of the major depressive disorder (MDD), is a multimodal and selective serotonin reuptake inhibitor (SSRI) antidepressant that combines 5-HT 1A receptor agonism with serotonin transporter (SERT) inhibition [ 266 ].…”

Section: Current Treatment Of Depression In Epilepsymentioning

confidence: 99%

Antidepressant Drugs for Seizures and Epilepsy: Where do we Stand?

Tallarico

Pisano

Leo

et al. 2023

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People with epilepsy (PWE) are more likely to develop depression and both these complex chronic diseases highly affect health-related quality of life (QOL). This comorbidity contributes to the deterioration of the QOL further than increasing the severity of epilepsy worsening prognosis. Strong scientific evidence suggests the presence of shared pathogenic mechanisms. The correct identification and management of these factors is crucial in order toto improve patients’ QOL. This review article discusses recent original research of the most common pathogenic mechanisms of depression in PWE, highlights the effects of antidepressant drugs (ADs) against seizures in PWE and in animal models of seizures and epilepsy. Newer ADs, such as selective serotonin reuptake inhibitors (SRRI) or serotonin-noradrenaline reuptake inhibitors (SNRI), particularly sertraline, citalopram, mirtazapine, reboxetine, paroxetine, fluoxetine, escitalopram, fluvoxamine, venlafaxine, duloxetine may lead to improvements in epilepsy severity instead the use of older tricyclic antidepressant (TCAs) can increase the occurrence of seizures. Most of data demonstrates the acute effects of ADs in animal models of epilepsy while there is a limited number of studies about the chronic antidepressant effects in epilepsy and epileptogenesis or on clinical efficacy. Much longer treatments are needed in order toto validate the effectiveness of these new alternatives in the treatment and the development of epilepsy while further clinical studies with appropriate protocols are warranted in order to understand the real potential contribution of these drugs in the management of PWE (besides their effects on mood).

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“…Depleting 5-HT increases seizure severity, and sertraline or optogenetic stimulation of raphe nuclei dose-dependently prevents respiratory arrest induced by audiogenic seizures or proconvulsants, respectively, in seizure-prone mice. , SSRIs, however, indiscriminately and indirectly activate all 5-HT receptors (5-HTRs); targeting individual 5-HTRs is a more precise strategy for effecting therapeutic outcomes. With few exceptions, many studies show that activating 5-HT 1A Rs, either systemically or via direct injections into the hippocampus, attenuates seizures induced by both GABA antagonists and glutamate agonists in wild-type animals. − Also, 5-HT 7 R antagonism appears to prevent audiogenic seizures in mouse models . Two recent, though small, clinical trials reported that the selective 5-HT 2C R agonist lorcaserin (Belviq) effectively treats seizures in childhood-onset epilepsies. , These data provide compelling evidence that distinct 5-HTRs can modulate critical inhibitory and excitatory neural circuitry that translates behaviorally.…”

Section: Introductionmentioning

confidence: 99%

(S)-5-(2′-Fluorophenyl)-N,N-dimethyl-1,2,3,4-tetrahydronaphthalen-2-amine, a Serotonin Receptor Modulator, Possesses Anticonvulsant, Prosocial, and Anxiolytic-like Properties in an Fmr1 Knockout Mouse Model of Fragile X Syndrome and Autism Spectrum Disorder

Armstrong

Casey

Saraf

et al. 2020

ACS Pharmacol. Transl. Sci.

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Fragile X syndrome (FXS) is a neurodevelopmental disorder characterized by intellectual disabilities and a plethora of neuropsychiatric symptoms. FXS is the leading monogenic cause of autism spectrum disorder (ASD), which is defined clinically by repetitive and/or restrictive patterns of behavior and social communication deficits. Epilepsy and anxiety are also common in FXS and ASD. Serotonergic neurons directly innervate and modulate the activity of neurobiological circuits altered in both disorders, providing a rationale for investigating serotonin receptors (5-HTRs) as targets for FXS and ASD drug discovery. Previously we unveiled an orally active aminotetralin, (S)-5-(2'-fluorophenyl)-N,N-dimethyl-1,2,3,4-tetrahydronaphthalen-2-amine (FPT), that exhibits partial agonist activity at 5-HT1ARs, 5-HT2CRs, and 5-HT7Rs and that reduces repetitive behaviors and increases social approach behavior in wild-type mice. Here we report that in an Fmr1 knockout mouse model of FXS and ASD, FPT is prophylactic for audiogenic seizures. No FPT-treated mice displayed audiogenic seizures, compared to 73% of vehicle-treated mice. FPT also exhibits anxiolytic-like effects in several assays and increases social interactions in both Fmr1 knockout and wild-type mice. Furthermore, FPT increases c-Fos expression in the basolateral amygdala, which is a preclinical effect produced by anxiolytic medications. Receptor pharmacology assays show that FPT binds competitively and possesses rapid association and dissociation kinetics at 5-HT1ARs and 5-HT7Rs, yet has slow association and rapid dissociation kinetics at 5-HT2CRs. Finally, we reassessed and report FPT’s affinity and function at 5-HT1ARs, 5-HT2CRs, and 5-HT7Rs. Collectively, these observations provide mounting support for further development of FPT as a pharmacotherapy for common neuropsychiatric symptoms in FXS and ASD.

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The effect of sertraline and 8-OH-DPAT on the PTZ_induced seizure threshold: Role of the nitrergic system

Cited by 14 publications

References 53 publications

Selenium Nanoparticles with Prodigiosin Rescue Hippocampal Damage Associated with Epileptic Seizures Induced by Pentylenetetrazole in Rats

Selenium Nanoparticles with Prodigiosin Rescue Hippocampal Damage Associated with Epileptic Seizures Induced by Pentylenetetrazole in Rats

Antidepressant Drugs for Seizures and Epilepsy: Where do we Stand?

(S)-5-(2′-Fluorophenyl)-N,N-dimethyl-1,2,3,4-tetrahydronaphthalen-2-amine, a Serotonin Receptor Modulator, Possesses Anticonvulsant, Prosocial, and Anxiolytic-like Properties in an Fmr1 Knockout Mouse Model of Fragile X Syndrome and Autism Spectrum Disorder

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