Introduction: Psychostimulants such as amphetamine (AMPH) induce manic-like symptoms in humans and studies have suggested that bipolar disorder (BD) may be associated to dopamine dysfunction. Glial fibrillary acidic protein (GFAP) up-regulation is considered a marker of astrogliosis, and it has been associated to behavioral sensitization.
Purpose: We aimed to investigate the behavioral effects of acute and chronic AMPH on rat locomotion and assess GFAP levels in rat cortex and hippocampus.
Methods: Rats were administered either acute (single dose) or chronic (seven days) d-amphetamine IP injection. Locomotion was assessed with an open-field test and GFAP immunoquantity was measured using ELISA.
Results: Chronic, but not acute, administration of AMPH increased GFAP levels in rat hippocampus. No differences were observed in rat cortex.
Conclusions: Repeated exposure to AMPH leads to an astroglial response in the hippocampus of rats.
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http://dx.doi.org/10.1016/j.pnpbp.2006.03.016 | DOI Listing |
Int J Clin Exp Pathol
December 2024
Department of Neurology, Huanggang Central Hospital of Yangtze University Huanggang 438000, Hubei, China.
Objectives: Sulforaphane (SFN), an isothiocyanate in cruciferous plants, has been reported to be effective in treating central nervous system diseases. However, how SFN protects the central nervous system needs further study. The aim of this study was to investigate the neuroprotective effect of SFN and its possible mechanism of action.
View Article and Find Full Text PDFNeurobiol Stress
January 2025
Department of Translational Neuroscience, Wake Forest University, School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA.
With the recent rise in the rate of alcohol use disorder (AUD) in women, the historical gap between men and women living with this condition is narrowing. While there are many commonalities in how men and women are impacted by AUD, an accumulating body of evidence is revealing sex-dependent adaptations that may require distinct therapeutic approaches. Preclinical rodent studies are beginning to shed light on sex differences in the effects of chronic alcohol exposure on synaptic activity in a number of brain regions.
View Article and Find Full Text PDFJ Nutr
January 2025
USDA-ARS, Jean Mayer Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA. Electronic address:
Background: Acute neuroinflammatory and oxidative-stress (OS)-inducing stressors, such as high energy and charge (HZE) particle irradiation, produce accelerated aging in the brain. Anti-inflammatory and antioxidant foods, such as blueberries (BB), attenuate neuronal and cognitive deficits when administered to rodents before or both before and after HZE particle exposure. However, the effects of post-stressor treatments are unknown and may be important to repair initial damage and prevent progressive neurodegeneration.
View Article and Find Full Text PDFNeurosci Lett
January 2025
Neurophysiology Research Center, Cellular and Molecular Medicine Research Institute, Urmia University of Medical Sciences, Urmia, Iran. Electronic address:
Brain aging is the leading risk factor for most neurodegenerative diseases and has been linked with high rates of neuron loss. Thus, identifying molecular mechanisms underlying neuron loss and pharmacological modulation may be of great importance for slowing or preventing age-related diseases. Herein, we investigated the roles of miR-92a, Akt, mTOR, and NF-κB in age-associated apoptosis in the hippocampus (a critical structure involved in brain aging) of male rats alone and in combination with prazosin.
View Article and Find Full Text PDFToxicology
January 2025
School of Forensic Medicine, National Health Commission (NHC) Key Laboratory of Drug Addiction Medicine, Kunming Medical University, Kunming, Yunnan 650500, China. Electronic address:
Methamphetamine (METH), a synthetic stimulant, has seen an escalating abuse situation globally over the past decade. Although the molecular mechanism underlying METH-induced neurotoxicity has been explored, the dysfunction of brain-derived neurotrophic factor (BDNF) neuroprotection in the context of METH neurotoxicity remains insufficiently understood. Our previous studies have found that METH induced neurotoxicity and BDNF expression in rat primary neurons, necessitating further research into this paradox.
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