This experiment tested the effect of clozapine on the sympathetic and thermogenic effects induced by orexin A. The firing rates of the sympathetic nerves to interscapular brown adipose tissue (IBAT), along with IBAT and colonic temperatures were monitored in urethane-anesthetized male Sprague-Dawley rats before and for 5 h after an injection of orexin A (1.5 nmol) into the lateral cerebral ventricle. The same procedure was carried out in rats treated with orexin A plus an intraperitoneal administration of clozapine (8 mg/kg bw), an atypical antipsychotic that is largely used in the therapy of schizophrenia. The same variables were monitored in rats with clozapine alone. A group of rats with saline injection served as control. The results show that orexin A increases the sympathetic firing rate, IBAT and colonic temperatures. Clozapine blocks completely the reactions due to orexin A. These findings suggest that clozapine influences strongly the thermogenic role of orexin A. Furthermore, the remarkable hyperthermic role played by orexin A is confirmed.
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Stroke
January 2025
New Drug Screening Center, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China (H.S., H.W., C.W., G.L., M.H., H.Z., F.H., H.L.).
Background: Activating glutamatergic neurons in the ipsilesional motor cortex can promote functional recovery after stroke. However, the underlying molecular mechanisms remain unclear. Clarifying key molecular mechanisms involved in recovery could help understand the development of neuromodulation strategies after stroke.
View Article and Find Full Text PDFJ Neuroinflammation
December 2024
Department of Neurosurgery, Stanford University School of Medicine, 1050 Arastradero Road, Building A, Palo Alto, Stanford, CA, 94304, United States of America.
Norepinephrine (NE) modulates cognitive function, arousal, attention, and responses to novelty and stress, and it also regulates neuroinflammation. We previously demonstrated behavioral and immunomodulatory effects of beta-adrenergic pharmacology in mouse models of Alzheimer's disease (AD). The current studies were designed to block noradrenergic signaling in 5XFAD mice through (1) chemogenetic inhibition of the locus coeruleus (LC), (2) pharmacologic blocking of β-adrenergic receptors, and (3) conditional deletion of β1- or β2-adrenergic receptors (adrb1 or adrb2) in microglia.
View Article and Find Full Text PDFNorepinephrine (NE) modulates cognitive function, arousal, attention, and responses to novelty and stress, and also regulates neuroinflammation. We previously demonstrated behavioral and immunomodulatory effects of beta-adrenergic pharmacology in mouse models of Alzheimer's disease (AD). The current studies were designed to block noradrenergic signaling in 5XFAD mice through chemogenetic inhibition of the locus coeruleus (LC), pharmacologic blocking of β-adrenergic receptors, and conditional deletion of β1- or β2-adrenergic receptors (adrb1 or adrb2) in microglia.
View Article and Find Full Text PDFEur J Neurol
December 2024
Institute of Neurology, Catholic University of the Sacred Heart, Rome, Italy.
Expert Opin Drug Saf
December 2024
Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX, USA.
Introduction: Drug-induced parkinsonism (DIP) is one of the most common iatrogenic movement disorders. It is characterized by tremors, slowness of movement, and shuffling gait with postural instability, clinically indistinguishable from idiopathic Parkinson's disease. Prior exposure to antipsychotic medications or other dopamine receptor blocking agents (DRBAs) is required for the diagnosis.
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