Hyperpolarizing after-potentials

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.

Fig. 6.24 A hypothetic scheme of the time behaviour of the spike linked to the opening and closing of sodium and potassium channels. After longer time intervals a temporary hyperpolarization of the membrane is induced by reversed transport of potassium ions inside the nerve cell. Nernst potentials for Na+ and K+ are also indicated in the figure. 

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. 

The two processes briefly lead to the charge even falling below the resting potential (hyperpolarization). The channels also close after a few milliseconds. The nerve cell is then ready for re-stimulation. 

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. 

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. 

The immediate short-term effects of dopamine are mediated by voltage and receptor-operated channels. The effects depend on the membrane potential of the postsynaptic cell, and its recent history, because these variables determine the state of the channels modulated by dopamine. At hyperpolarized potentials, rapidly inactivating channels are available, and modulating them can have effects on the transition from hyperpolarized Down states to depolarized Up states. After prolonged periods in the depolarized states, these channels are inactivated. If a dopamine pulse occurs at this time the effects on noninactivating channels will predominate. 

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