Depressing functional serotonin or depleting serotonin levels in rat brains with either p-chlorophenylalanine, 5,6-dihydroxytryptamine or raphe lesions greatly enhanced hypothermia induced by chloropromazine (CPZ). Depressing the firing of raphe units or decreasing serotonin turnover in the brain with either a serotonin precursor (tryptophan) or the inhibitors of serotonin re-uptake (Lilly 1 10140 and chlorimipramine) also greatly enhanced the CPZ-induced hypothermia. The data indicate that serotonergic activity in the brain plays a role in the elaboration or modulation of CPZ hypothermia.
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http://dx.doi.org/10.1159/000137241 | DOI Listing |
Metab Brain Dis
January 2025
Department of Zoology, Faculty of Science, Alexandria University, Alexandria, 21515, Egypt.
Exaggerated neuronal excitation by glutamate is a well-known cause of excitotoxicity, a key factor in numerous neurodegenerative disorders. This study examined the neurotoxic effect of monosodium glutamate (MSG) in the brain cortex of rats and focused on assessing the potential neuroprotective effects of omega-3 polyunsaturated fatty acids (ω-3 PUFAs). Four groups of adult male rats (n = 10) were assigned as follows; normal control, ω-3 PUFAs (400 mg/kg) alone, MSG (4 mg/g) alone, and MSG plus ω-3 PUFAs (4 mg/g MSG plus 400 mg/kg ω-3 PUFAs).
View Article and Find Full Text PDFRSC Adv
January 2025
Department of Pharmaceutical Chemistry, Faculty of Pharmacy, King Abdulaziz University P.O. Box 80260 Jeddah 21589 Saudi Arabia +966 553399718.
A mutual prodrug of sertraline-methylpropyphenazone (SER-MP) was prepared and characterized using a spectral method. The yield of the prepared SER-MP was 90%, and its purity reached 98.8%.
View Article and Find Full Text PDFFront Psychiatry
January 2025
Xinjiang Clinical Medical Research Center of Mental Health, The Psychological Medicine Center, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.
Behavioral addictive disorders (BADs) have become a significant societal challenge over time. The central feature of BADs is the loss of control over engaging in and continuing behaviors, even when facing negative consequences. The neurobiological underpinnings of BADs primarily involve impairments in the reward circuitry, encompassing the ventral tegmental area, nucleus accumbens in the ventral striatum, and prefrontal cortex.
View Article and Find Full Text PDFAm J Psychiatry
January 2025
Nathan Kline Institute for Psychiatric Research, Orangeburg, NY (Stern, Collins, Bragdon, Eng, Recchia, Tobe, Iosifescu); Department of Psychiatry (Stern, Bragdon, Eng, Recchia, Iosifescu) and Neuroscience Institute (Stern, Iosifescu), New York University Langone Medical Center, New York; Department of Psychiatry, University of Miami Medical School, Miami (Coffey); Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York (Leibu, Murrough); Center for the Developing Brain, Child Mind Institute, New York (Tobe); Department of Psychiatry, Brigham and Women's Hospital, Boston (Burdick); Harvard Medical School, Boston (Burdick); Department of Psychiatry, Baylor College of Medicine, Houston (Goodman).
Objective: Sensory phenomena (SP) are aversive sensations driving repetitive behaviors in obsessive-compulsive disorder (OCD) and Tourette's disorder that are not well addressed by standard treatments. SP are related to the functioning of an interoceptive-sensorimotor circuit that may be modulated by the 5-HT receptor antagonist ondansetron. The present study employed an experimental medicine approach to test the effects of 4 weeks of high-dose ondansetron compared to placebo on SP severity and brain connectivity in a cohort of individuals with OCD and/or Tourette's disorder.
View Article and Find Full Text PDFMol Neurobiol
January 2025
Cellular and Molecular Neurobiology and Drug Targeting Laboratory, Department of Zoology, Indira Gandhi National Tribal University, Amarkantak-484 887, MP, India.
Depression is one of the most disabling mental disorders worldwide and characterized by symptoms including worthlessness, anhedonia, sleep, and appetite disturbances. Recently, studies have suggested that tryptophan (Trp) metabolism plays a key role in depressed mood through serotonin and kynurenine pathway involving enzyme tryptophan 5-monooxygenase (TPH) and indoleamine-2,3-dioxygenase (IDO) respectively. Moreover, during neuroinflammation, IDO is activated by proinflammatory cytokines and affects neurogenesis, cognition, disturbed hypothalamic-pituitary-adrenal (HPA) axis, and gut homeostasis by altering the gut bacteria and its metabolites like Trp derivatives.
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