Methylphenidate affects memory, brain-derived neurotrophic factor immunocontent and brain acetylcholinesterase activity in the rat

Scherer, Emilene B. S.; Cunha, Maira J. da; Matté, Cristiane; Schmitz, Felipe; Netto, Carlos Alexandre; Wyse, Ângela T. S.

doi:10.1016/j.nlm.2010.06.002

Cited by 70 publications

(42 citation statements)

References 63 publications

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“…McFadyen-Leussis et al [65] showed that prenatal exposure to MPH increased exploratory activity but also evoked anxiety-related behavior with no benefits on learning and memory tasks in mice. We have demonstrated previously that rats presented lower performance in the Water maze test after they had received MPH (2 mg/kg) from the 15th to the 45th day of age [66]. On the other hand, acute treatment in adult mice of 5 mg/kg of MPH improved, while the dose 50 mg/kg worsened object recognition memory and aversive memory [67].…”

Section: Discussionmentioning

confidence: 99%

Methylphenidate Causes Behavioral Impairments and Neuron and Astrocyte Loss in the Hippocampus of Juvenile Rats

et al. 2016

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Although the use, and misuse, of methylphenidate is increasing in childhood and adolescence, there is little information about the consequences of this psychostimulant chronic use on brain and behavior during development. The aim of the present study was to investigate hippocampus biochemical, histochemical, and behavioral effects of chronic methylphenidate treatment to juvenile rats. Wistar rats received intraperitoneal injections of methylphenidate (2.0 mg/kg) or an equivalent volume of 0.9 % saline solution (controls), once a day, from the 15th to the 45th day of age. Results showed that chronic methylphenidate administration caused loss of astrocytes and neurons in the hippocampus of juvenile rats. BDNF and pTrkB immunocontents and NGF levels were decreased, while TNF-α and IL-6 levels, Iba-1 and caspase 3 cleaved immunocontents (microglia marker and active apoptosis marker, respectively) were increased. ERK and PKCaMII signaling pathways, but not Akt and GSK-3β, were decreased. SNAP-25 was decreased after methylphenidate treatment, while GAP-43 and synaptophysin were not altered. Both exploratory activity and object recognition memory were impaired by methylphenidate. These findings provide additional evidence that early-life exposure to methylphenidate can have complex effects, as well as provide new basis for understanding of the biochemical and behavioral consequences associated with chronic use of methylphenidate during central nervous system development.

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Section: Discussionmentioning

confidence: 99%

Methylphenidate Causes Behavioral Impairments and Neuron and Astrocyte Loss in the Hippocampus of Juvenile Rats

et al. 2016

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“…The assay was performed according to the manufacturer's recommendations and how described by Scherer and colleagues [53].…”

Section: Brain-derived Neurotrophic Factor (Bdnf) Levelsmentioning

confidence: 99%

“…Supernatant from homogenized tissue was added to the reaction mixture and preincubated for 3 min. The hydrolysis was monitored by formation of the thiolate dianion of DTNB at 412 nm for 2-3 min (intervals of 30 s) [54], with modifications [53,55]. All samples were run in triplicate.…”

Section: Ache Activity Assaymentioning

confidence: 99%

D-Galactose Causes Motor Coordination Impairment, and Histological and Biochemical Changes in the Cerebellum of Rats

et al. 2016

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Classical galactosemia is an inborn error of carbohydrate metabolism in which patients accumulate high concentration of galactose in the brain. The most common treatment is a galactose-restricted diet. However, even treated patients develop several complications. One of the most common symptoms is motor coordination impairment, including affected gait, balance, and speech, as well as tremor and ataxia. In the present study, we investigated the effects of intracerebroventricular galactose administration on motor coordination, as well as on histological and biochemical parameters in cerebellum of adult rats. Wistar rats received 5 μL of galactose (4 mM) or saline by intracerebroventricular injection. The animals performed the beam walking test at 1 and 24 h after galactose administration. Histological and biochemical parameters were performed 24 h after the injections. The results showed motor coordination impairment at 24 h after galactose injection. Galactose also decreased the number of cells in the molecular and granular layers of the cerebellum. The immunohistochemistry results suggest that the cell types lost by galactose are neurons and astrocytes in the spinocerebellum and neurons in the cerebrocerebellum. Galactose increased active caspase-3 immunocontent and acetylcholinesterase activity, decreased acetylcholinesterase immunocontent, glutathione, and BDNF levels, as well as caused protein and DNA damage. Our results suggest that galactose induces histological and biochemical changes in cerebellum, which can be associated with motor coordination impairment.

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“…Mature BDNF protein was assessed using the E-Max ELISA kit (Promega) according to the manufacturer's recommendations and to Scherer and colleagues [40]. Briefly, cerebral cortex and hippocampus were individually homogenized in lysis buffer containing: 137 mM NaCl, 20 mM Tris-HCl (pH 8.0), Igepal (1%), glycerol (10%), 1 mM phenylmethanesulfonyl fluoride (PMSF), 0.5 mM sodium vanadate, 0.1 mM EDTA, and 0.1 mM EGTA, and centrifuged for 3 min at 14,000 rpm at 4°C.…”

Section: Analysis Of Bdnf Immunocontentmentioning

confidence: 99%

Physical Exercise Reverses Cognitive Impairment in Rats Subjected to Experimental Hyperprolinemia

et al. 2011

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This study investigated whether physical exercise would reverse proline-induced performance deficits in water maze tasks, as well as its effects on brain-derived neurotrophic factor (BDNF) immunocontent and brain acetylcholinesterase (AChE) activity in Wistar rats. Proline administration followed partial time (6th-29th day of life) or full time (6th-60th day of life) protocols. Treadmill exercise was performed from 30th to 60th day of life, when behavioral testing was started. After that, animals were sacrificed for BDNF and AChE determination. Results show that proline impairs cognitive performance, decreases BDNF in cerebral cortex and hippocampus and increases AChE activity in hippocampus. All reported effects were prevented by exercise. These results suggest that cognitive, spatial learning/memory, deficits caused by hyperprolinemia may be associated, at least in part, to the decrease in BDNF levels and to the increase in AChE activity, as well as support the role of physical exercise as a potential neuroprotective strategy.

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Methylphenidate affects memory, brain-derived neurotrophic factor immunocontent and brain acetylcholinesterase activity in the rat

Cited by 70 publications

References 63 publications

Methylphenidate Causes Behavioral Impairments and Neuron and Astrocyte Loss in the Hippocampus of Juvenile Rats

Methylphenidate Causes Behavioral Impairments and Neuron and Astrocyte Loss in the Hippocampus of Juvenile Rats

D-Galactose Causes Motor Coordination Impairment, and Histological and Biochemical Changes in the Cerebellum of Rats

Physical Exercise Reverses Cognitive Impairment in Rats Subjected to Experimental Hyperprolinemia

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