Postirradiation Emesis
John Kucharczyk, David J. Stewart, Alan D. Miller in Nausea and Vomiting: Recent Research and Clinical Advances, 2017
Among the many classes of identified 5-HT receptors,151,196 only the 5-HT3 receptor appears to be linked to an ion channel. Thus, for several types of neurons studied,193,194,197–199 including the submucosal plexus,186200 agonist binding at the 5-HT3 receptor produces an electrophysiological response with the following characteristics: A rapid-onset depolarization of the membrane potential associated with an inward currentA reversal potential near zero millivolts, or slightly positive that is Altered by changes in extracellular concentrations of monovalent cationsReduced or abolished by 5-HT3 receptor antagonistsA rapid desensitizationIs impervious to manipulations of second messenger
Transmitter Regulation of Mesencephalic Dopamine Cells
Peter W. Kalivas, Charles D. Barnes in Limbic Motor Circuits and Neuropsychiatry, 2019
Both principal and secondary VTA cells also receive innervation at GABAA receptors7 (Figure 1). This can be isolated by blocking the excitatory synaptic inputs with CNQX and APV; it is reversibly blocked by bicuculline or Picrotoxin. The rise-time and duration of the GABA-mediated synaptic potential are somewhat larger than that of the non-NMDA glutamate component, as is usually observed in central neurons. This potential results from an increase in membrane chloride conductance; it reverses polarity at the chloride equilibrium potential. When intracellular recordings are made with electrodes that contain potassium acetate or potassium methylsulphate, the synaptic potential is hyperpolarizing at the resting potential, and this reversal potential is about -72 mV. Under these conditions the GABAA input is unequivocally inhibitory. When intracellular recordings are made with an electrode that contains potassium chloride, the chloride concentration inside the cell rises and the reversal potential becomes less negative. The synaptic potential mediated through GABAA receptors is now depolarizing and reverses close to -40 mV. Because this is less negative than the threshold for spike generation, GABA is an excitatory transmitter under these artificial circumstances.
Physiology
John D Firth, Professor Ian Gilmore in MRCP Part 1 Self-Assessment, 2017
At any given time in the cardiac cycle, the membrane potential is chiefly determined by the conductance of the membrane to a number of key ions. When the conductance to a particular ion increases, the membrane potential moves towards the ‘reversal potential’ of that ion, which is the potential at which the electromotive force to move that ion across the membrane exactly balances the concentration gradient. Because sodium and calcium concentrations are considerably higher outside the cell than inside, the reversal potentials for these ions are positive, i.e. these ions act as a depolarizing influence. The concentration gradient for potassium operates in the opposite way and this ion is a major repolarization force.
Loss of mGluR1-LTD following cocaine exposure accumulates Ca2+-permeable AMPA receptors and facilitates synaptic potentiation in the prefrontal cortex
Published in Journal of Neurogenetics, 2021
Hongyu Ruan, Wei-Dong Yao
In LTD experiments, stable EPSCs were first obtained for 10 min as the baseline, followed by 10 min application of mGluR drugs to the bath, and EPSCs were then recorded for another 60 min. LTD was measured as the percentage of the averaged EPSCs between 50 and 60 min post drug application to the baseline EPSC. For Naspm (1-naphthylacetyl spermine trihydrochloride) sensitivity measurement, stable EPSCs were recorded for 10 min as the baseline, followed by 10–15 min application of the drug delivered to the bath to measure the reduction of EPSC. For the rectification measurement, EPSCs were recorded at −60 mV and +60 mV, respectively. Rectification index was calculated as the EPSC amplitude at +60 mV divided by that at −60 mV. EPSC reversal potential was assumed to be ∼0 mV for mPFC L5 neurons in our preparation. Cells were otherwise held at −60 mV during voltage-clamp experiments.
Interaction of low frequency external electric fields and pancreatic β-cell: a mathematical modeling approach to identify the influence of excitation parameters
Published in International Journal of Radiation Biology, 2018
Sajjad Farashi, Pezhman Sasanpour, Hashem Rafii-Tabar
In Equations (3) and (4), VhXand VmXdenote the Nernst or reversal potential for inactivation and activation functions, respectively. The conductivity of the voltage-sensitive channel is determined by the product of activation and inactivation functions and based on the structure of the channel the product of terms will be expressed by different expressions.
Potassium channels as prominent targets and tools for the treatment of epilepsy
Published in Expert Opinion on Therapeutic Targets, 2021
ES Nikitin, LV Vinogradova
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.
Related Knowledge Centers
- Electrochemical Gradient
- Glutamate Receptor
- Membrane Potential
- Potassium
- Sodium
- Neurotransmitter
- Ion Channel
- Receptor
- Biological Membrane
- Ligand-Gated Ion Channel