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Nigral dopamine neurons are transiently activated by high frequency glutamatergic inputs relaying reward-predicting sensory information. The tonic firing pattern of dopamine cells responds to these inputs with a transient burst of spikes that requires NMDA receptors. Here, we show that NMDA receptor activation further excites the cell by recruiting a calcium-activated non-selective cation current (ICAN) capable of generating a plateau potential. Burst firing in vitro is eliminated after blockade of ICAN with flufenamic acid, 9-phenanthrol, or intracellular BAPTA. ICAN is likely to be mediated by a transient receptor potential (TRP) channel, and RT-PCR was used to confirm expression of TRPM2 and TRPM4mRNA in substantia nigra pars compacta.We propose that ICAN is selectively activated during burst firing to boost NMDA currents and allow plateau potentials. This boost mechanism may render DA cells vulnerable to excitotoxicity.
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http://dx.doi.org/10.1113/jphysiol.2011.206631 | DOI Listing |
Front Cell Neurosci
July 2025
Department of Cellular and Systems Pharmacology, College of Pharmacy, University of Florida, Gainesville, FL, United States.
The basolateral amygdala (BLA) plays a crucial role in context-specific learning and memory by integrating valence-specific stimuli with internal physiological states. Cholinergic signaling systems modulate neural excitability to influence information processing in the BLA. Muscarinic acetylcholine receptors (mAChRs) are of particular interest because aberrant mAChR signaling in BLA circuits is associated with neuropsychiatric disorders, cognitive impairment, substance use, and age-related cognitive decline.
View Article and Find Full Text PDFMolecules
July 2025
Laboratory of Cardiovascular Pharmacology (LaFaC), Faculty of Health Sciences, Federal University of Grande Dourados (UFGD), Dourados 79.804-070, MS, Brazil.
We used molecular docking as a computational tool to predict the binding affinities and interactions of quercetin 3-O-malonylglucoside (Q3MG) with vascular target proteins. First, the proteins 1M9M (human endothelial nitric oxide synthase; eNOS) and 6ND0 (human large-conductance voltage- and calcium-activated K channels; BK) were downloaded from the Protein Data Bank and submitted to molecular docking studies, revealing Q3MG binding affinities for both proteins. The vascular effect of Q3MG was investigated in the perfused mesenteric vascular beds (MVBs) of spontaneously hypertensive rats.
View Article and Find Full Text PDFbioRxiv
May 2025
Department of Pharmacodynamics, College of Pharmacy, University of Florida, Gainesville, FL, United States.
The basolateral amygdala (BLA) plays a crucial role in context-specific learning and memory by integrating valence-specific stimuli with internal physiological states. Cholinergic signaling systems modulate neural excitability to influence information processing in the BLA. Muscarinic acetylcholine receptors (mAChRs) are of particular interest because aberrant mAChR signaling in BLA circuits is associated with neuropsychiatric disorders, cognitive impairment, substance use, and age-related cognitive decline.
View Article and Find Full Text PDFCytotechnology
April 2025
Department of Biology, College of Science, Salahaddin University-Erbil, Erbil, Kurdistan Region Iraq.
In a circadian cycle, the pineal gland produces and releases melatonin (MEL) into the bloodstream. By activating distinct melatonin receptors, MEL has been shown to variably change vascular endothelial dysfunction (VED) to various vascular beds. This study investigates the interaction of melatonin (MEL) and potassium ion (K) on angiotensin 1-7 (Ang 1-7) vasorelaxant in streptozotocin (STZ)-induced diabetes mellitus (DM) and non-diabetes mellitus (non-DM) male albino rat aortic rings.
View Article and Find Full Text PDFiScience
December 2024
Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
Neurodegeneration in central nervous system disorders is linked to dysregulated neuronal calcium. Direct inhibition of glutamate-induced neuronal calcium influx, particularly via N-methyl-D-aspartate receptors (NMDAR), has led to adverse effects and clinical trial failures. A more feasible approach is to modulate NMDAR activity or calcium signaling indirectly.
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