DSP-4 induced depletion of brain noradrenaline and increased 6-hertz psychomotor seizure susceptibility in mice is prevented by sodium valproate

Jahan, Kausar; Pillai, K. K.; Vohora, Divya

doi:10.1016/j.brainresbull.2018.08.002

Cited by 6 publications

(4 citation statements)

References 34 publications

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“…These observations were consistent with the increased risk of seizures in cyproheptadine-treated rats, which exhibited decreased brain norepinephrine content. Multiple experimental data in the literature support the regulatory and protective role of norepinephrine against seizures, with enhanced neuronal damage following focal status epilepticus if norepinephrine content is reduced in the brain [ 37 , 38 , 39 ]. Norepinephrine exerts its anticonvulsant effects through β2-adrenergic receptors by stimulating the autophagy pathway.…”

Section: Discussionmentioning

confidence: 99%

Investigation of the Mechanisms of Tramadol-Induced Seizures in Overdose in the Rat

et al. 2022

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Tramadol overdose is frequently associated with the onset of seizures, usually considered as serotonin syndrome manifestations. Recently, the serotoninergic mechanism of tramadol-attributed seizures has been questioned. This study’s aim was to identify the mechanisms involved in tramadol-induced seizures in overdose in rats. The investigations included (1) the effects of specific pretreatments on tramadol-induced seizure onset and brain monoamine concentrations, (2) the interaction between tramadol and γ-aminobutyric acid (GABA)A receptors in vivo in the brain using positron emission tomography (PET) imaging and 11C-flumazenil. Diazepam abolished tramadol-induced seizures, in contrast to naloxone, cyproheptadine and fexofenadine pretreatments. Despite seizure abolishment, diazepam significantly enhanced tramadol-induced increase in the brain serotonin (p < 0.01), histamine (p < 0.01), dopamine (p < 0.05) and norepinephrine (p < 0.05). No displacement of 11C-flumazenil brain kinetics was observed following tramadol administration in contrast to diazepam, suggesting that the observed interaction was not related to a competitive mechanism between tramadol and flumazenil at the benzodiazepine-binding site. Our findings do not support the involvement of serotoninergic, histaminergic, dopaminergic, norepinephrine or opioidergic pathways in tramadol-induced seizures in overdose, but they strongly suggest a tramadol-induced allosteric change of the benzodiazepine-binding site of GABAA receptors. Management of tramadol-poisoned patients should take into account that tramadol-induced seizures are mainly related to a GABAergic pathway.

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Section: Discussionmentioning

confidence: 99%

Investigation of the Mechanisms of Tramadol-Induced Seizures in Overdose in the Rat

et al. 2022

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“…Fluoxetine (5 mg/kg, i.p., kind gift from IPCA laboratories, India) was administered 30 min prior to DSP-4 or vehicle administration to protect serotonergic neurons. The choice of DSP-4 as a noradrenergic neurotoxin and the treatment regimen were based on prior studies from us and others confirming a robust depletion of NE levels in the hippocampus ( Yu et al, 1994 , Scullion et al, 2009 , Chalermpalanupap et al, 2018 , Jahan et al, 2018 , O’Neill et al, 2021 , Bromek et al, 2022 ). Mice received an injection of BrdU (100 mg/kg, i.p.)…”

Section: Methodsmentioning

confidence: 99%

Genetic loss of norepinephrine does not alter adult hippocampal neurogenesis in dopamine beta-hydroxylase deficient mice

Kapri

Vadodaria

Rommelfanger

et al. 2022

IBRO Neuroscience Reports

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“…However, the mechanisms behind the triggers currently remain unclear. Experiments on N-2-Chloroethyl-N-ethyl-2-bromobenzylamine hydrochloride deprived mice, a feature widely accepted to deplete noradrenaline [31], has demonstrated a five-fold increase in Aβ deposition with an increased size of senile plaques [32]. Surprisingly, other experiments conducted on mice with impaired ability to produce noradrenaline have failed to show increased senile plaque deposition.…”

Section: Introductionmentioning

confidence: 99%

Locus Coeruleus Dysfunction and Trigeminal Mesencephalic Nucleus Degeneration: A Cue for Periodontal Infection Mediated Damage in Alzheimer’s Disease?

Pisani

Arcangeli

et al. 2023

IJERPH

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Alzheimer’s disease (AD) is a leading neurodegenerative disease with deteriorating cognition as its main clinical sign. In addition to the clinical history, it is characterized by the presence of two neuropathological hallmark lesions; amyloid-beta (Aβ) and neurofibrillary tangles (NFTs), identified in the brain at post-mortem in specific anatomical areas. Recently, it was discovered that NFTs occur initially in the subcortical nuclei, such as the locus coeruleus in the pons, and are said to spread from there to the cerebral cortices and the hippocampus. This contrasts with the prior acceptance of their neuropathology in the enthorinal cortex and the hippocampus. The Braak staging system places the accumulation of phosphorylated tau (p-tau) binding to NFTs in the locus coeruleus and other subcortical nuclei to precede stages I-IV. The locus coeruleus plays diverse psychological and physiological roles within the human body including rapid eye movement sleep disorder, schizophrenia, anxiety, and depression, regulation of sleep-wake cycles, attention, memory, mood, and behavior, which correlates with AD clinical behavior. In addition, the locus coeruleus regulates cardiovascular, respiratory, and gastrointestinal activities, which have only recently been associated with AD by modern day research enabling the wider understanding of AD development via comorbidities and microbial dysbiosis. The focus of this narrative review is to explore the modes of neurodegeneration taking place in the locus coeruleus during the natural aging process of the trigeminal nerve connections from the teeth and microbial dysbiosis, and to postulate a pathogenetic mechanism due to periodontal damage and/or infection focused on Treponema denticola.

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DSP-4 induced depletion of brain noradrenaline and increased 6-hertz psychomotor seizure susceptibility in mice is prevented by sodium valproate

Cited by 6 publications

References 34 publications

Investigation of the Mechanisms of Tramadol-Induced Seizures in Overdose in the Rat

Investigation of the Mechanisms of Tramadol-Induced Seizures in Overdose in the Rat

Genetic loss of norepinephrine does not alter adult hippocampal neurogenesis in dopamine beta-hydroxylase deficient mice

Locus Coeruleus Dysfunction and Trigeminal Mesencephalic Nucleus Degeneration: A Cue for Periodontal Infection Mediated Damage in Alzheimer’s Disease?

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