Effects of chronic treatment with methylphenidate on oxidative stress and inflammation in hippocampus of adult rats

Motaghinejad, Majid; Motevalian, Manijeh; Shabab, Behnaz

doi:10.1016/j.neulet.2015.12.015

Cited by 58 publications

(38 citation statements)

References 34 publications

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“…While lithium in the mentioned doses can prevent the MPH-induced decline of antioxidant enzyme activity and increases GPx and SOD activity (Fig-8 & 9). Previous studies showed that MPH at highest therapeutic doses used can decrease SOD and GPx activities in rat hippocampus (Motaghinejad, Motevalian, 2015e). It has been proven that lithium is capable of modulating the oxidant-antioxidant activities and therefore showing the neuroprotective effects (Bhalla and Dhawan, 2009).…”

Section: Discussionmentioning

confidence: 98%

“…Our recent study showed the effect of various doses of MPH (2, 5, 10 and 20 mg/kg) on adult rat hippocampal cells (Motaghinejad, Motevalian, 2015e), and another study showed the effects of various doses of lithium in neuroprotection against some neurodegenerative disorders (Marmol, 2008). According to these findings, the harmful dose of MPH and protective doses of lithium were chosen to be studied together in order to confer the protective effects of lithium in this model.…”

Section: Discussionmentioning

confidence: 99%

“…MPH showed neurotoxic properties in some areas of the brain, such as the hippocampus (Fagundes et al, 2007). Methamphetamine-like agents may cause neurotoxicity in some areas of the brain (Motaghinejad et al, 2015e). Several studies have clearly shown that caspase protein family and DNA fragmentation are involved in methamphetamine-induced neurodegeneration (Andreazza, Frey, 2007.…”

Section: Introductionmentioning

confidence: 99%

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The neuroprotective effect of lithium against high dose methylphenidate: Possible role of BDNF

et al. 2016

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The neuroprotective effect of lithium against high dose methylphenidate: Possible role of BDNF

et al. 2016

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“…Studies have confirmed that MP reduces the expression of neurotrophins (Sadasivan et al 2012), and induces apoptosis, oxidative damage, and DNA fragmentation in brain cells (Banihabib et al 2014;Andreazza et al 2007;Motaghinejad et al 2016, 2017a, b; Gomes et al 2008). Acute and chronic MP also increases the expression of proinflammatory cytokines, while chronic MP increases microglial activation in several brain regions including the cortex, hippocampus, and basal ganglia (Sadasivan et al 2012;Motaghinejad et al 2016, 2017b).…”

Section: Introductionmentioning

confidence: 95%

Chronic oral methylphenidate treatment increases microglial activation in rats

et al. 2018

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Methylphenidate (MP) is a widely prescribed psychostimulant used to treat attention deficit hyperactivity disorder. Previously, we established a drinking paradigm to deliver MP to rats at doses that result in pharmacokinetic profiles similar to treated patients. In the present study, adolescent male rats were assigned to one of three groups: control (water), low-dose MP (LD; 4/10 mg/kg), and high dose MP (HD; 30/60 mg/kg). Following 3 months of treatment, half of the rats in each group were euthanized, and the remaining rats received only water throughout a 1-month-long abstinence phase. In vitro autoradiography using [H] PK 11195 was performed to measure microglial activation. HD MP rats showed increased [H] PK 11195 binding compared to control rats in several cerebral cortical areas: primary somatosensory cortex including jaw (68.6%), upper lip (80.1%), barrel field (88.9%), and trunk (78%) regions, forelimb sensorimotor area (87.3%), secondary somatosensory cortex (72.5%), motor cortices 1 (73.2%) and 2 (69.3%), insular cortex (59.9%); as well as subcortical regions including the thalamus (62.9%), globus pallidus (79.4%) and substantia nigra (22.7%). Additionally, HD MP rats showed greater binding compared to LD MP rats in the hippocampus (60.6%), thalamus (59.6%), substantia nigra (38.5%), and motor 2 cortex (55.3%). Following abstinence, HD MP rats showed no significant differences compared to water controls; however, LD MP rats showed increased binding in pre-limbic cortex (78.1%) and ventromedial caudate putamen (113.8%). These findings indicate that chronic MP results in widespread microglial activation immediately after treatment and following the cessation of treatment in some brain regions.

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“…(ii) Neurotoxicity-and/or neurodegeneration-based models, e.g. pesticide and perflouroalkyl substances (Lien et al, 2016;Mostafalou and Abdollahi, 2016) [62,63], that implicate both neurons and glial cells (Motaghinejad et al, 2016;Shah and Lahiri, 2016) [64,65]. (iii) N-methyl-D-aspartate (NMDA) neonatally-injected antagonist models in rodents, e.g.…”

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confidence: 99%

Regional Dysregulation and Aberrant Functional Connectivity in ADHD

Archer¹,

Abedini²

2017

Journal of Neuroscience and Neuropsychology

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The trajectory of neurodevelopmental adversity determining attention-deficit/hyperactivity disorder (ADHD) from childhood to adulthood which is recognized increasingly by the long-term impairment and the burgeoning persistence beyond childhood, through adolescence, to adulthood poses a prolonged history defined by a concatenation of symptom profiles and an underlying dysregulation accompanied by aberrant brain regional networks. Abnormalities within the "default mode network" and disharmonizing fluctuations afflicting brain regional connectivity, even inducing dysconnectivity, appear to be associated both with symptoms profiles and the relative efficacy of putative interventional outcomes. Co-morbidity in ADHD, a persistently debilitating and potentially regressive issue, is viewed from a perspective of eating disorders and substance use disorders although several other combinations proliferate. Among the factors contributing to dysregulation and aberrant connectivity in brain development are included genetic and epigenetic proclivities, neurotoxins and neurodegeneration, predisposing characteristics and environmental pressures. Finally, the likelihood of perinatal stress trauma and/or inflammation as contributory circumstances ought to be considered.

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Effects of chronic treatment with methylphenidate on oxidative stress and inflammation in hippocampus of adult rats

Cited by 58 publications

References 34 publications

The neuroprotective effect of lithium against high dose methylphenidate: Possible role of BDNF

The neuroprotective effect of lithium against high dose methylphenidate: Possible role of BDNF

Chronic oral methylphenidate treatment increases microglial activation in rats

Regional Dysregulation and Aberrant Functional Connectivity in ADHD

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