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Background: ADHD is the most common developmental disorder affecting approximately three to seven percent of school-aged children and 2.5 percent of adults worldwide. The drug of choice for the pharmacotherapy of ADHD is Methylphenidate (MPH). However, there is growing concerns about side effects resulting from its potential interference with brain anatomical and behavioral development.
Aim: This article focuses on the adverse effects of MPH on the rat's hippocampus.
Methods: The animals received an oral dose of 5 mg/kg MPH or normal saline, as the vehicle, on a daily basis for 30 days. Y-maze test, passive avoidance, Barnes maze and field potential recording were conducted. Western blot for detecting the neurotrophic factor of GDNF and immunohistochemistry of astrogliosis were performed.
Results: Our results revealed that MPH treatment suppressed the willingness of rats to explore new environments. Also, it had no effect on improving long-term potentiation, long-term memory and spatial memory in the MPH group as opposed to the control group. There was also a significant increase of astrogliosis in the treated rats' hippocampi. On the other hand, there was not a significant relationship between MPH administration and the decrement of the GDNF level.
Conclusion: We encourage the need to conduct more research on the adverse effects of MPH on the brain.
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http://dx.doi.org/10.1016/j.jchemneu.2020.101818 | DOI Listing |
Mol Psychiatry
September 2025
Institute of Neurology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Alzheimer's disease (AD), a leading cause of dementia, represents a critical unmet global medical need. While the precise mechanisms underlying AD pathogenesis remain elusive, increasing evidence underscores the pivotal role of neuroinflammation in driving cognitive impairment. N6-methyladenosine (m6A), an epigenetic modification regulating RNA metabolism, has been found to be dysregulated in AD.
View Article and Find Full Text PDFNat Commun
September 2025
Department of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Parkinson's disease (PD) is characterized by the selective degeneration of midbrain dopaminergic neurons and aggregation of α-synuclein. Emerging evidence implicates the gut microbiome in PD, with microbial metabolites proposed as potential pathological mediators. However, the specific microbes and metabolites involved, and whether gut-derived metabolites can reach the brain to directly induce neurodegeneration, remain unclear.
View Article and Find Full Text PDFeNeuro
September 2025
NMD Laboratory at the Department of Biomedical Engineering, Florida International University, Miami, FL, 33174, USA.
Understanding the roles of astrocytic calcium signaling in multiple brain regulatory mechanisms including metabolism, blood flow, neuromodulation and neuroinflammation has remained one of the enduring challenges in glial biology. To delineate astrocytic contribution from concurrent neuronal activity, it is vital to establish robust control and manipulate astrocytes using a technique like optogenetics due to its high cellular specificity and temporal resolution. The lack of an experimental paradigm to induce controlled calcium signaling in astrocytes has hindered progress in the field.
View Article and Find Full Text PDFiScience
September 2025
iBET, Instituto de Biologia Experimental e Biológica, Oeiras, Portugal.
Growing evidence suggests that reactive astrocytes can acquire different functional subtypes, playing critical roles in neurological disorders. Human induced pluripotent stem cell (hiPSC)-derived three-dimensional (3D) CNS models have been proposed to study reactive astrocytes. Still, lack of reproducibility and immature/activated astrocyte phenotypes typical of these models limit their utility to address neuroinflammation.
View Article and Find Full Text PDFInvest Ophthalmol Vis Sci
August 2025
Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri, United States.
Purpose: We tested whether Müller cells utilize autophagy to support immune privilege in the eye.
Methods: The essential autophagy gene Atg5 was deleted in retinal Müller cells. Inflammation was induced by intravitreal injection of lipopolysaccharide (LPS) that was monitored by hematoxylin and eosin (H&E) staining, immunofluorescent confocal microscopy, and flow cytometry.