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Electrophysiological Studies of 5-Hydroxytryptamine Receptors on Enteric Neurons
Published in T.S. Gaginella, J.J. Galligan, SEROTONIN and GASTROINTESTINAL FUNCTION, 2020
Single electrical stimuli do not elicit synaptic potentials, but multiple stimuli elicit a sEPSP in most AH neurons.8,10,11,15 The mediators of sEPSPs in AH neurons are ACh acting at muscarinic receptors,15,16 several neuropeptides,17 and 5-HT (see below). The sEPSP in myenteric AH neurons results from transmitter-induced inhibition of background GK, resting GK,Ca18,23 and the simultaneous activation of a chloride conductance (GC1).25 In addition, the spike afterhyperpolarization is inhibited during the sEPSP. The depolarization and inhibition of the spike afterhyperpolarization result in an increase in the excitability and firing rate of AH neurons.5 Combined electrophysiological, morphological, and immunohistochemical studies indicate that some AH neurons may be sensory neurons.17
Baroreceptor and Chemoreceptor Afferent Processing in the Solitary Tract Nucleus
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
Robert B. Felder, Steven W. Mifflin
Several variations on the classical concepts of summation have recently been described, and may influence the responsiveness of NTS neurons to synaptic input. An early observation from extracellular recordings was that activation of NTS neurons by electrical stimulation of peripheral afferent nerves was followed by a prolonged refractory period,21,36 during which the ongoing spontaneous activity of the neuron was inhibited. A likely explanation for this period of reduced excitability might be a prolonged action potential afterhyperpolarization. A seemingly related observation was that paired stimulation of the same or different visceral afferent nerves converging on the same NTS neuron resulted in an inhibition of unit responses to the second stimulus over an interval of 30 to 400 ms.
Antiepileptic Action of Hydantoins
Published in Carl L. Faingold, Gerhard H. Fromm, Drugs for Control of Epilepsy:, 2019
Ronald A. Browning, Carl L. Faingold
It has been suggested by Yaari et al.25 that phenytoin actually works better when the extracellular potassium concentration is above normal as it is expected to be in the epileptic focus, thus providing another way in which phenytoin could exert selective effects against seizures. In most neurons the action potential is followed by an afterhyperpolarization mediated by a transient efflux of potassium which is important in reducing the number of inactivated sodium channels after each action potential. During high frequency discharge of neurons, as would occur in a seizure, the number of inactivated sodium channels would increase because of the increase in extracellular potassium, which would in turn decrease the potassium efflux and cause a reduction in afterhyperpolarization. Since phenytoin binds better to inactivated sodium channels, its action would be enhanced primarily as a result of a decrease in afterhyperpolarization which occurred because of the increased extracellular potassium.
BK channel openers NS1619 and NS11021 reverse hydrogen peroxide-induced membrane potential changes in skeletal muscle
Published in Journal of Receptors and Signal Transduction, 2020
Cagil Coskun, Hacer Sinem Buyuknacar, Figen Cicek, Ismail Gunay
Large conductance potassium (BK), which is also known by the abbreviations MaxiK, BigK and Slo1, channels are members of the Ca2+-activated potassium channel family that is activated by intracellular calcium, membrane potential, or both simultaneously. The channels have a vital role in cell membrane repolarization and after-hyperpolarization because of their unique large K+ conductance around 100–300 pS [1,2]. Channel opening causes fast repolarization and allows BK channels to regulate intracellular signals by modulating Ca2+ homeostasis and membrane potential [3]. In this way, the channels play an active role in many physiological processes, such as neurotransmitter release, hormone secretion, vascular tone regulation and muscle contraction [1]. Previous studies show the relationship between dysregulation of BK channels and diseases such as Alzheimer’s disease [4], neuromuscular diseases [5], hypertension [6] and periodic paralysis [7–9]. Therefore, dysregulation of BK channels may negatively affect cellular signal transduction and metabolic pathways with pathogenic results.
Approaches for the discovery of drugs that target K Na 1.1 channels in KCNT1-associated epilepsy
Published in Expert Opinion on Drug Discovery, 2022
Barbara Miziak, Stanisław J Czuczwar
The neuronal Na+ -activated potassium channel Slack (aka Slo2.2, KNa 1.1, or Kcnt1) participates in establishing and maintaining resting membrane potential and determining excitability and firing patterns, as well as generating slow afterhyperpolarization [43]. Afterhyperpolarization occurs after single action potentials [44,45] or bursts of action potential firing [46]. The KNa1.1 channel is mainly expressed in neuronal brain tissue [47,48], spinal cord [49], and peripheral sensory neurons including dorsal root ganglion neurons [49–51] and spiral ganglion neurons of the inner ear [52].
Potassium channels as prominent targets and tools for the treatment of epilepsy
Published in Expert Opinion on Therapeutic Targets, 2021
Intracellular space is enriched with K+ ions, so the reversal potential of K+ (EK) is quite negative (Figure 2a). The EK of the neurons is assumed to be ~ −100 mV [24], which is normally below the resting potentials of neurons. Thus, the opening of K+ channels is thought to shift the membrane potential toward a more hyperpolarized state and thus to tune down the firing frequency. In general, the classic Hodgkin–Huxley model [25] describes the transmembrane ionic currents underlying action potentials, which applies to mammalian central neurons as well [26]. In the silent state, the membrane potential of a neuron is resting at a negative value, typically ranging within −40 to −80 mV (negative charge inside the cell). During the rising phase of the action potential, voltage-dependent Na+ currents pass through Na+-selective channels and evoke further membrane depolarization. This results in the activation of voltage-dependent K+ currents, which shifting the membrane potential down to EK (i.e. back to a polarized state), and in inactivation and closure of Na+ channels (Figure 1b). Thus, the membrane potential actively declines to reach a deeper hyperpolarized state, displaying the afterhyperpolarization temporarily. In real neurons, there are several families of K+ and Na+ channels expressed by the same cell. Some types of Na+ channels inactivate incompletely, which results in the afterdepolarization [27], a second peak of depolarization, which follows the action potential (Figure 2c). The afterdepolarization is known to underlie bursting behavior in neurons [28] and causes a series of action potentials to occur at very high frequencies (up to 300 Hz in pyramidal cells). Neuronal ability to burst is of great importance as the oscillations of neuronal networks are strongly influenced by the intrinsic firing properties of individual neurons. A significant number of pyramidal neurons in primate neocortex [29] and hippocampus [30] typically display various kinds of bursting behavior.