Action potentials resting membrane potential

A) On the initation of an action potential the membrane potential moves from the resting potential upward toward the Na equilibrium potential and then downward toward the equilibrium potential. 

Figure 1.4 Ionic basis for excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). Resting membrane potential ( — 70 mV) is maintained by Na+ influx and K+ efflux. Varying degrees of depolarisation, shown by different sized EPSPs (a and b), are caused by increasing influx of Na. When the membrane potential moves towards threshold potential (60-65 mV) an action potential is initiated (c). The IPSPs (a b ) are produced by an influx of Cl. Coincidence of an EPSP (b) and IPSP (a ) reduces the size of the EPSP (d)...

The initiation of an epileptic attack involves "pacemaker" cells these differ from other nerve cells in their unstable resting membrane potential, i.e a depolarizing membrane current persists after the action potential terminates. 

The neurotoxins isolated from Aph. flos-aquae were shown to have similar chemical and biological properties to paralytic shellfish poisons (PSP) (25,29,38) Sawyer et al. in 1968 (25) were the first to demonstrate that the crude preparation of aphantoxins behave like saxitoxin, the major paralytic shellfish poison. They showed that the toxins had no effect on the resting membrane potential of frog sartorius muscle blocked action potential on de-sheathed frog sciatic nerve and also abolished spontaneous contractions in frog heart. Sasner et al. (1981) (29) using the lab cultured strain reported similar results. 

In normal atrial and ventricular myocytes, phase 4 is electrically stable, with the resting membrane potential held at approximately -90 mV and maintained by the outward potassium leak current and ion exchangers previously described. It is during phase 4 that the Na+ channels necessary for atrial and ventricular myocyte depolarization recover completely from inactivation. In myocytes capable of automaticity, the membrane potential slowly depolarizes during this period to initiate an action potential (discussed later). 

Adenosine receptors are found on myocytes in the atria and sinoatrial and A-V nodes. Stimulation of these receptors acts via a G-protein signaling cascade to open an acetylcholine-sensitive outward potassium current. This leads to hyperpolarization of the resting membrane potential, a decrease in the slope of phase 4 spontaneous depolarization, and shortening of the action potential duration. 

K+ channels are responsible for setting the resting membrane potential and for the repolarizing phase of action potentials. In addition, K+ channels mediate afterhyperpolarizations to terminate periods of high neuronal activity and to modulate firing rates. When located in presynaptic nerve terminals, these actions of K+ channels will contribute to the regulation of transmitter release. In fact, most types of the huge superfamily of K+ channels, in particular delayed rectifier, fast transient, and Ca2+-sensitive K+ channels, have been found in a variety of nerve terminals and... 

---