The aim of this study was to evaluate the participation of ventromedial hypothalamic nucleus (VMH) muscarinic cholinoceptors in heat balance and central fatigue during treadmill exercise (24 m min(-1), 5% inclination). The animals were anesthetized with pentobarbital sodium (50 mg/kg body weight i.p.) and fitted with bilateral cannulae into the VMH 1 week prior to the experiments. Tail skin (T(tail)) and core body temperatures (T(b)) were measured after the injection of 0.2 microL of 5 x 10(-9) mol methylatropine (Matr) or 0.15 M NaCl solution (Sal) into the hypothalamus. Methylatropine injection into the VMH greatly increased heat storage rate (HSR) measured until fatigue (19.7+/-4.6 cal min(-1) Matr versus 9.7+/-3.3 cal min(-1) Sal; P<0.05) and attenuated the exercise-induced tail vasodilation as seen by T(tail) (23.98+/-0.43 degrees C Matr versus 25.52+/-0.85 degrees C Sal; at 6.5 min; P<0.05), indicating inhibition of the heat loss process. The 2 min delay and the increased DeltaT(b), which triggered the heat loss mechanisms observed in Matr-treated rats, are associated with increased HSR and may be responsible for the decreased running performance of these animals (21.0+/-2.9 min Matr versus 33.5+/-3.4 min Sal; P<0.001). In fact, a close negative correlation was observed between HSR and time to fatigue (r=-0.61; P<0.01). In conclusion, VMH muscarinic cholinoceptors facilitate tail heat loss mechanisms, and a delay in this adjustment would lead to a decrease in physical exercise performance due to excess heat storage.
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http://dx.doi.org/10.1016/j.brainresbull.2007.03.004 | DOI Listing |
Acetylcholine modulates the network physiology of the hippocampus, a crucial brain structure that supports cognition and memory formation in mammals . In this and adjacent regions, synchronized neuronal activity within theta-band oscillations (4-10Hz) is correlated with attentive processing that leads to successful memory encoding . Acetylcholine facilitates the hippocampus entering a theta oscillatory regime and modulates the temporal organization of activity within theta oscillations .
View Article and Find Full Text PDFTransl Psychiatry
January 2025
Research Center Juelich, Institute of Neuroscience and Medicine 10, Research Center Juelich, Juelich, Germany.
Genetic variation in the α5 nicotinic acetylcholine receptor (nAChR) subunit of mice results in behavioral deficits linked to the prefrontal cortex (PFC). rs16969968 is the primary Single Nucleotide Polymorphism (SNP) in CHRNA5 strongly associated with nicotine dependence and schizophrenia in humans. We performed single cell-electrophysiology combined with morphological reconstructions on layer 6 (L6) excitatory neurons in the medial PFC (mPFC) of wild type (WT) rats, rats carrying the human coding polymorphism rs16969968 in Chrna5 and α5 knockout (KO) rats.
View Article and Find Full Text PDFJ Comput Chem
January 2025
Departamento de Fisicoquímica, Facultad de Química, Universidad Nacional Autónoma de México, Coyoacán, CDMX, Mexico.
The G protein-coupled receptor (GPCR) pharmacology accounts for a significant field in research, clinical studies, and therapeutics. Computer-aided drug discovery is an evolving suite of techniques and methodologies that facilitate accelerated progress in drug discovery and repositioning. However, the structure-activity relationships of molecules targeting GPCRs are highly challenging in many cases since slight structural modifications can lead to drastic changes in biological functionality.
View Article and Find Full Text PDFCells
December 2024
Institute of Physiology, Department of Neurophysiology, University of Würzburg, Röntgenring 9, 97070 Würzburg, Germany.
We recorded transmembrane currents through single nicotinic acetylcholine receptors (nAChRs) in cell-attached patches at high temporal resolutions from cultured and transiently transfected HEK 293 cells. Receptor activation was elicited by acetylcholine (ACh) or epibatidine (Ebd) at concentrations ranging from 0.01 to 100 µM, binding to one (R or R) or both extracellular ligand binding sites (R).
View Article and Find Full Text PDFMicroPubl Biol
December 2024
Laboratory of Physiology, Department of Medicine, University of Patras, Pátrai, West Greece, Greece.
Cholinergic transmission fundamentally modulates information processing in the brain via muscarinic receptors. Using electrophysiological recordings of population spikes from the CA1 region, we found that the muscarinic receptor agonist carbachol (CCh, 1 μM) enhances the basal excitation level in the dorsal but not ventral hippocampus. Using a frequency stimulation protocol, we found that CCh transforms depression of neuronal output into facilitation (at 3-30 Hz) in the ventral hippocampus while only lessening depression in the dorsal hippocampus, suggesting that muscarinic transmission boosts basal neuronal activation in the dorsal hippocampus and strongly facilitates the output of the ventral hippocampus in a frequency-dependent manner.
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