Action potentials 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. 

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. 

K channels are associated with the recovery or repolarization of excitable cells after depolarization. In general, they function to inhibit excitatory processes. As mentioned before, ASM exhibits only a low level of electrical excitability without the development of action potentials. Instead, ASM displays slow wave activity thought to represent action potentials which are suppressed by the opening of K channels, with the efflux of from the cell rectifying any tendency to depolarization (Small atU., 1993). Thus, ASM is strongly rectified (i.e. more resistant to depolarization than to hyperpolarization). 

Arrhythmias occur within a few seconds after reperfusion, following ischemic periods of 10-30 min long. They start by a spontaneous stimulus in the reperfused zone and change afterward in a re-entry multiple wavelet type of ventricular tachycardia (VT) or ventricular fibrillation (VF). Extremely short action potential, short refractory period and slow conduction are the main contributing factors. Increased hyperpolarization and elevated intracellular calcium that act negatively on gap conductance impair conduction. Unidirectional conduction is favored by the marked heterogeneity in extracellular potassium, action potential and refractory period. The extra stimulus is initiated in the reperfused zone, probably by early (EAD) and late (DAD) afterdepolirizations. 

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. 

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... 

Fig. 20. SA spikes depolarizing after-potentials. Hyperpolarizing current injected through the recording electrode enhances the amplitude of the depolarizing after-potential until all-or-none SA spikes evoked by the after-potential initiate full-blown action potentials.

The membrane potential when gates finally close is lower than the resting potential, and the membrane is hyperpolarized because the neuron has shghtly more on the outside than it has Na" on the inside. After the impulse has passed through the neuron, the action potential is over, and the cell membrane returns to the resting potential. 

Ionotropic receptors are ligand-gated ion channels (left half of the table). The receptors for stimulatory transmitters (indicated in the table by a ) mediate the inflow of cations (mainly Na""). When these open after binding of the transmitter, local depolarization of the postsynaptic membrane occurs. By contrast, inhibitory neurotransmitters (GABA and glycine) allow cr to flow in. This increases the membrane s negative resting potential and hinders the action of stimulatory transmitters hyperpolarization, 0). 

If seizures do occur, it is important to prevent hypoxemia and acidosis. Although administration of oxygen does not prevent seizure activity, hyperoxemia may be beneficial after onset of seizures. Hypercapnia and acidosis may lower the seizure threshold, and so hyperventilation is recommended during treatment of seizures. In addition, hyperventilation increases blood pH, which in turn lowers extracellular potassium. This action hyperpolarizes the transmembrane potential of axons, which favors the resting (or low-affinity) state of the sodium channels, resulting in decreased local anesthetic toxicity. 

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