After-hyperpolarization

SK channels are not activated by Ca2+ release through RyRs (Herrera et al 2001, this study), however SK channels are activated by InsP3R-mediated Ca2+ release in gastrointestinal smooth muscle (Bayguinov et al 2000). In UBSM, SK channels are activated by Ca2+ entry through VDCCs, and this likely contributes to the action potential after-hyperpolarization (Fig. IE). 

Nelson That s a good question. We hope that there would be a delay, or we wouldn t have an action potential. I guess the delay is about 30 ms, which is when we start seeing the prominent after-hyperpolarization. 

Both oci and (3 adrenoceptors are postsynaptic excitatory heteroreceptors. Their action is mediated via the activation of Ca2+ current. However, different mechanisms are involved Gq-mediated phospholipase C (PLC) activation and Gs-mediated AC stimulation, respectively (Kandel et al., 2000). When they present on glutamate pyramidal neurons, (3-adrenoceptors receptors decrease the Ca2+-activated after-hyperpolarization K+ influx, making the neurons more responsive for excitatory inputs. The a] adrenoceptors, however, increase membrane conductance and make the pyramidal cells less excitable (Devilbiss and Waterhouse 2000). 

Bayliss DA, Umemiya M, Berger AJ. Inhibition of N- and P-type calcium currents and the after-hyperpolarization in rat motoneurones by serotonin. J Physiol 1995 485(Pt 3) 635-647. 

Torres GE, Arfken CL, Andrade R. 5-Hydroxytryptamine4 receptors reduce after-hyperpolarization in hippocampus by inhibiting calcium-induced calcium release. Mol Pharmacol 1996 50 1316-1322. 

Mahyar et al. (2006) report the effect of the fruit essential oil of cumin on the epileptiform activity induced by pentylenetetrazol (PTZ), using the intracellular technique. The results demonstrate that extracellular application of the essential oil of cumin (1 and 3%) dramatically decreases the frequency of spontaneous activity induced by PTZ in a time- and concentration-dependent manner. In addition, it showed protection against PTZ-induced epileptic activity by increasing the duration and decreasing the amplitude of after-hyperpolarization potential (AHP) following the action potential, the peak of action potential and inhibition of the firing rate. 

Spruston The current clamp recordings from the SNS / mice imply that SNS contributes a dramatic amount of current during the rising phase of the action potential, because the amplitude is reduced dramatically. Is that a consistent observation Also, the after-hyperpolarization is much more negative in the SNS mice, implying that there is an actual contribution by SNS during the repolarizing phase of the action potential. 

Gold There were just two voltage traces illustrated and they were from different resting membrane potentials. These cells have a number of K currents that are subject to steady-state inactivation where the steep part of the inactivation curve coincides with resting membrane potential. The result is that differences in available current may explain the apparent differences in after-hyperpolarization. 

Single neurons are a convenient material for detailed analysis of drug-rceeptor interaclioas. Sympathetic ganglion neurons of bullfrogs were used for the study of action of VX (Heppner and Pickers, 1992). The amplitude of excitatory postsynaptic potentials (EPSPs) was increa.sed, the membrane was depolarized, the input resistance was reduced, and the duration of the spike after hyperpolarizatioti was shortened. The observed increase in neuronai excitability may be due to the decrease in after-hyperpolarization. The effects of... 

Doemer JF, Gissehnann G, Halt H, Wetzel CH (2007) Transient receptor potential channel A1 is directly gated by calcium ions. JBiolChem 282(18) 13180-9 Fischer A, Forssmann WG, Undem BJ (1998) Nociceptin-induced inhibition of tachykinergic neurotransmission in guinea pig bronchus. J Pharmacol Exp Ther 285(2) 902-7 Fowler JC, WonderUn WF, Weinreich D (1985) Prostaglandins block a Ca2 -dependent slow spike after hyperpolarization independent of effects on Ca2+ influx in visceral afferent neurons. Brain Res 345(2) 345-9... 

Alger, B. E., and Nicoll, R. A., 1980ft, Epileptiform burst after hyperpolarization calcium-dependent potassium potential in hippocampal CA1 pyramidal cells. Science 210 1122-1124. 

Schwartzkroin, P. A., and Stafstrom, C. E., 1980, Effects of EGTA on the calcium-activated after-hyperpolarization in hippocampal CA3 pyramidal cells. Science 210 1125-1126. 

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