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Evaluation of rewarding effects of nitazene analogs: results from conditioned place preference tests and in vivo microdialysis experiments in mice.
J Toxicol Sci
January 2025
Department of Pharmaceutical and Environmental Sciences, Tokyo Metropolitan Institute of Public Health.
In illicit drug markets, the most recently expanding new synthetic opioid subclass is benzimidazoles, also known as nitazenes, which were originally developed as analgesics in the 1950s. The emergence of this classical, potent drug family has attracted extensive research interest in the field of forensic toxicology; however, information on their psychological and physical dependence is very limited. Herein, we evaluated the rewarding effects of four nitazene analogs using a battery of in vivo experiments, with a positive control drug (isotonitazene).
View Article and Find Full Text PDFRegulation of Glutamate Transporter Type 1 by TSA and the Antiepileptic Mechanism of TSA.
Neurochem Res
January 2025
Huazhong University of Science and Technology, Tongji Medical College, Wuhan, Hubei, 430000, China.
Epilepsy (EP) is a neurological disorder characterized by abnormal, sudden neuronal discharges. Seizures increase extracellular glutamate levels, causing excitotoxic damage. Glutamate transporter type 1 (GLT-1) and its human homologue excitatory amino acid transporter-2 (EAAT2) clear 95% of extracellular glutamate.
View Article and Find Full Text PDFAgonists of the opioid δ-receptor improve irritable bowel syndrome-like symptoms via the central nervous system.
Br J Pharmacol
December 2024
Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Chiba, Japan.
Background And Purpose: Irritable bowel syndrome (IBS) is a common condition that is challenging to treat, and novel drugs are needed for this condition. Previously, a chronic vicarious social defeat stress (cVSDS) mouse model exhibits IBS-like symptoms. Also agonists of the opioid δ-receptor exert anti-stress effects in rodents with minimal adverse effects.
View Article and Find Full Text PDFDysbindin-1 Mutation Alters Prefrontal Cortex Extracellular Glutamate and Dopamine In Vivo.
Int J Mol Sci
November 2024
Department of Psychology, Binghampton University-State University of New York, Binghampton, NY 13902, USA.
Elevated risk for schizophrenia is associated with a variation in the gene encoding dysbindin-1, which may underpin cognitive impairments in this prevalent neuropsychiatric disorder. The cognitive symptoms of schizophrenia involve anomalies in glutamate and dopamine signaling, particularly within the prefrontal cortex (PFC). Indeed, mice with mutations exhibit spatial and working memory deficits that are associated with deficits in glutamate release and NMDA receptor function as determined by slice electrophysiology.
View Article and Find Full Text PDFSleep deprivation leads to non-adaptive alterations in sleep microarchitecture and amyloid-β accumulation in a murine Alzheimer model.
Cell Rep
November 2024
Center for Translational Neuromedicine, Faculty of Medical and Health Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, Denmark; Center for Translational Neuromedicine, University of Rochester Medical School, Elmwood Avenue 601, Rochester, NY 14642, USA. Electronic address:
Article Synopsis
- Impaired sleep is common with aging and is linked to the onset of Alzheimer's disease; researchers studied the effects of sleep deprivation on both healthy mice and a mouse model of Alzheimer's.
- After sleep deprivation, both groups showed increased EEG slow-wave activity, but only healthy mice exhibited enhanced norepinephrine oscillations typical of good sleep.
- The Alzheimer’s model mice didn't show this enhancement 24 hours post-deprivation, along with a buildup of amyloid-β protein, suggesting that their disrupted sleep patterns may increase the risk of developing Alzheimer's.
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