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ObjectivesTo evaluate oxidative damage through the thiobarbituric acid-reactive species (TBARS) and protein carbonyl groups; antioxidant enzymatic system – superoxide dismutase (SOD) and catalase (CAT); and energetic metabolism in the brain of spontaneously hypertensive adult rats (SHR) after both acute and chronic treatment with methylphenidate hydrochloride (MPH).MethodsAdult (60 days old) SHRs were treated during 28 days (chronic treatment), or 1 day (acute treatment). The rats received one i.p. injection per day of either saline or MPH (2 mg/kg). Two hours after the last injection, oxidative damage parameters and energetic metabolism in the cerebellum, prefrontal cortex, hippocampus, striatum and cortex were evaluated.ResultsWe observed that both acute and/or chronic treatment increased TBARS and carbonyl groups, and decreased SOD and CAT activities in many of the brain structures evaluated. Regarding the energetic metabolism evaluation, the acute and chronic treatment altered the energetic metabolism in many of the brain structures evaluated.ConclusionWe observed that both acute and chronic use of methylphenidate hydrochloride (MPH) in adult spontaneously hypertensive rats (SHRs) was associated with increased oxidative stress and energetic metabolism alterations. These data also reinforce the importance of the SHR animal model in further studies regarding MPH. [ABSTRACT FROM PUBLISHER]

Objective: Methylphenidate hydrochloride is the most widely used medication for treatment and management of attention-deficit hyperactivity disorder. However, the chronic effects of methylphenidate hydrochloride on anxiety- and depressive-like rat behaviors remain poorly investigated. In this context, the present study evaluated the effects of treatment with methylphenidate hydrochloride on anxiety-and depressive-like behaviors using young and adult rats during the light and the dark cycle. Method: Male Wistar rats (25 or 60 days old) received a once-daily (in either the light or dark cycle) methylphenidate hydrochloride (2mg/kg) or saline intraperitoneal injection for 28 days. We performed elevated plus maze and forced swimming test two hours after the last injection. Results: The light/dark cycle was a significant factor in the anxiety-like behaviors; however, no significant interaction between all three factors (cycle, age and methylphenidate hydrochloride) was found. Nevertheless, we observed a nominally significant interaction between the light/dark cycle and age in the forced swimming test. Conclusion: Our results have shown that age and the light/dark cycle are more significant modulators of anxiety- and depressive-like behaviors than methylphenidate hydrochloride treatment. [ABSTRACT FROM AUTHOR]

Methylphenidate is a central nervous system stimulant used for the treatment of attention-deficit hyperactivity disorder. Na+, K+-ATPase is a membrane-bound enzyme necessary to maintain neuronal excitability. Considering that methylphenidate effects on central nervous system metabolism are poorly known and that Na+, K+-ATPase is essential to normal brain function, the purpose of this study was to evaluate the effect of this drug on Na+, K+-ATPase activity in the cerebrum of young and adult rats. For acute administration, a single injection of methylphenidate (1.0, 2.0, or 10.0 mg/Kg) or saline was given to rats on postnatal day 25 or postnatal day 60, in the young and adult groups, respectively. For chronic administration, methylphenidate (1.0, 2.0, or 10.0 mg/Kg) or saline injections were given to young rats starting at postnatal day 25 once daily for 28 days. In adult rats, the same regimen was performed starting at postnatal day 60. Our results showed that acute methylphenidate administration increased Na+, K+-ATPase activity in hippocampus, prefrontal cortex, and striatum of young and adult rats. In young rats, chronic administration of methylphenidate also enhanced Na+, K+-ATPase activity in hippocampus and prefrontal cortex, but not in striatum. When tested in adult rats, Na+, K+-ATPase activity was increased in all cerebral structures studied. The present findings suggest that increased Na+, K+-ATPase activity may be associated with neuronal excitability caused by methylphenidate. [ABSTRACT FROM AUTHOR]

Abstract: Dopamine may alter the phosphorylation state of DARPP-32 that plays a central role in the dopaminergic neurons biology. Studies have shown that DARPP-32/protein phosphatase 1 cascade is a major target for psychostimulants drugs. Methylphenidate is a psychostimulant that acts blocking the dopamine transporter has been used as an effective treatment for Attention Deficit Hyperactivity Disorder. We investigated if methylphenidate could alter DARPP-32 expression in five brain regions (striatum, hippocampus, prefrontal cortex, cortex and cerebellum) in young and adult rats. Our results showed that methylphenidate treatment is able to alter DARPP-32 expression in rat brain. Acute methylphenidate treatment has reduced hippocampal DARPP-32 protein levels in old rats, while chronic methylphenidate treatment has decreased them in old rat hippocampus and young rat cerebellum. It was found an increased cortical expression after chronic methylphenidate administration in old rats. Our results provide the first experimental demonstration that methylphenidate induces changes in total DARPP-32 expression that are posology- and age-related in some rat brain areas, although further studies are needed to shed more light on the mechanisms behind these findings. [Copyright &y& Elsevier]

Malathion [S-(1,2-dicarbethoxy) ethyl-0,0-dimethyl-phosphorodithioate] is an organophosphorus compound that is widely used as pesticide especially in developing countries. This pesticide affects the central nervous system by inhibiting acetylcholinesterase, leading to an increase of acetylcholine in the synaptic cleft, and subsequent activation of cholinergic muscarinic and nicotinic receptors. In humans, intoxication with organophosphates causes a wide range of neurological symptoms, including memory deficits. The present study was aimed to investigate the effects of the acute (1 h prior the test) and subacute (once a day for 28 days) exposure to malathion at doses of 25, 50, 100 and 150 mg/kg in rats tested in the step-down inhibitory avoidance task, open-field habituation and elevated plus-maze tests. Interestingly, the acute and subacute treatment with malathion impaired aversive-memory in the step-down inhibitory avoidance task, but did not alter the animal performance in the elevated plus-maze and in the habituation to the open-field tests, and neither modified spontaneous locomotion. The activity of acetylcholinesterase enzyme was significantly reduced after subacute, but not acute, treatment with malathion (25, 100 and 150 mg/kg). Our results suggest that malathion impairs aversive-memory retention but not non-associative memory, without affecting anxiety-related behaviors. These findings support the view that the inhibition of acetylcholinesterase enzyme is not correlated with cognitive deficits observed in acute and subacute malathion-treated rats. [ABSTRACT FROM AUTHOR]

Objective: Methylphenidate hydrochloride is the most widely used medication for treatment and management of attention-deficit hyperactivity disorder. However, the chronic effects of methylphenidate hydrochloride on anxiety- and depressive-like rat behaviors remain poorly investigated. In this context, the present study evaluated the effects of treatment with methylphenidate hydrochloride on anxiety- and depressive-like behaviors using young and adult rats during the light and the dark cycle., Method: Male Wistar rats (25 or 60 days old) received a once-daily (in either the light or dark cycle) methylphenidate hydrochloride (2mg/kg) or saline intraperitoneal injection for 28 days. We performed elevated plus maze and forced swimming test two hours after the last injection., Results: The light/dark cycle was a significant factor in the anxiety-like behaviors; however, no significant interaction between all three factors (cycle, age and methylphenidate hydrochloride) was found. Nevertheless, we observed a nominally significant interaction between the light/ dark cycle and age in the forced swimming test., Conclusion: Our results have shown that age and the light/dark cycle are more significant modulators of anxiety- and depressive-like behaviors than methylphenidate hydrochloride treatment.