Eloy G. Moreno‐Galindo

ORCID: 0000-0001-7448-1239
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About
Contact & Profiles
Research Areas
  • Ion channel regulation and function
  • Cardiac electrophysiology and arrhythmias
  • Receptor Mechanisms and Signaling
  • Neuroscience and Neuropharmacology Research
  • Circadian rhythm and melatonin
  • Sleep and Wakefulness Research
  • Photoreceptor and optogenetics research
  • Birth, Development, and Health
  • Ion Channels and Receptors
  • Cardiac Ischemia and Reperfusion
  • Neuroscience of respiration and sleep
  • Neuroendocrine regulation and behavior
  • Neurotransmitter Receptor Influence on Behavior
  • Electrostatic Discharge in Electronics
  • Nicotinic Acetylcholine Receptors Study
  • Biochemical Analysis and Sensing Techniques
  • Legionella and Acanthamoeba research
  • Neuroscience and Neural Engineering
  • Cannabis and Cannabinoid Research
  • Genetics and Neurodevelopmental Disorders
  • Cholinesterase and Neurodegenerative Diseases
  • Cardiac Arrhythmias and Treatments
  • Biochemical effects in animals
  • Stress Responses and Cortisol
  • Parasitic Infections and Diagnostics

Universidad de Colima
2015-2025

University of Utah
2016

Non‐technical summary Normal heart rate variability is critically dependent upon the G‐protein‐coupled, acetylcholine (ACh)‐activated inward rectifier K + current, I KACh . A unique feature of so‐called ‘relaxation’ gating property that contributes to increased current at hyperpolarized membrane potentials. Here, we consider a novel explanation for relaxation based recent finding G‐protein‐coupled receptors are intrinsically voltage sensitive and muscarinic agonists pilocarpine manifest...

10.1113/jphysiol.2010.204115 article EN The Journal of Physiology 2011-02-01

The cardiac muscarinic receptor (M2R) regulates heart rate, in part, by modulating the acetylcholine (ACh) activated K+ current IK,ACh through dissociation of G-proteins, that turn activate KACh channels. Recently, M2Rs were noted to exhibit intrinsic voltage sensitivity, i.e. their affinity for ligands varies a dependent manner. sensitivity M2R implies ACh (and thus effect) throughout time course electrical cycle. aim this study was investigate contribution rate and shape human sinus node...

10.1371/journal.pcbi.1006438 article EN cc-by PLoS Computational Biology 2018-10-10

The antimalarial drug mefloquine was found to inhibit the KATP channel by an unknown mechanism. Because is a Cationic amphiphilic and known insert into lipid bilayers, we postulate that interferes with interaction between PIP2 Kir channels resulting in inhibition. We studied inhibitory effects of on Kir2.1, Kir2.3, Kir2.3(I213L), Kir6.2/SUR2A expressed HEK-293 cells, IK1 IKATP from feline cardiac myocytes. order inhibition ≈ Kir2.3 (IC50 2 μM) > Kir2.1 30 μM). Similar results were obtained...

10.1097/fjc.0b013e31820b7c03 article EN Journal of Cardiovascular Pharmacology 2011-01-06

Choline (Ch) is a precursor and metabolite of the neurotransmitter acetylcholine (ACh). In canine guinea pig atrial myocytes, Ch was shown to activate an outward K(+) current in delayed rectifier fashion. This has been suggested modulate cardiac electrical activity play role fibrillation pathophysiology. However, exact nature identity this not convincingly established. We recently described unique ligand- voltage-dependent properties muscarinic activation ACh-activated (IKACh) showed that,...

10.1113/jphysiol.2013.255166 article EN The Journal of Physiology 2013-05-08

The endocannabinoid, <i>N</i>-arachidonoylethanolamine (anandamide; AEA) is known to interact with voltage-gated K<sup>+</sup> (Kv) channels in a cannabinoid receptor-independent manner. AEA modulates the functional properties of Kv channels, converting slowly inactivating current into apparent fast inactivation. In this study, we characterize mechanism action and binding site for on Kv1.5 expressed HEK-293 cells using patch-clamp techniques. exhibited high-potency block (IC<sub>50</sub> ≈...

10.1124/mol.109.063008 article EN Molecular Pharmacology 2010-02-04

Abstract Circadian rhythms synchronize to light through the retinohypothalamic tract (RHT), which is a bundle of axons coming from melanopsin retinal ganglion cells, whose synaptic terminals release glutamate ventral suprachiasmatic nucleus (SCN). Activation AMPA–kainate and NMDA postsynaptic receptors elicits increase in intracellular calcium required for triggering signaling cascade that ends phase shifts. During aging, there decline synchronization circadian light. With...

10.1002/jnr.25331 article EN Journal of Neuroscience Research 2024-04-01

Inwardly rectifying potassium (Kir) channels are broadly expressed in both excitable and nonexcitable tissues, where they contribute to a wide variety of cellular functions. Numerous studies have established that rectification Kir is not an inherent property the channel protein itself, but rather reflects strong voltage dependence block by intracellular cations, such as polyamines Mg2+. Here, we identify previously unknown mechanism inward Kir4.1/Kir5.1 absence these endogenous blockers....

10.1085/jgp.201912540 article EN cc-by-nc-sa The Journal of General Physiology 2021-04-05

The suprachiasmatic nucleus (SCN) is the main brain clock that regulates circadian rhythms in mammals. SCN synchronizes to LD cycle through retinohypothalamic tract (RHT), which projects ventral neurons via glutamatergic synapses. Released glutamate activates N-methyl-D-aspartate (NMDA) receptors, play a critical role activation of signaling cascades enable phase shifts. Previous evidence indicates presynaptic changes during postnatal development consist an increase RHT fibers impinging on...

10.1177/0748730418824198 article EN Journal of Biological Rhythms 2019-01-17
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