Resting membrane potential , neuron

The M-channels (M for muscarine) are expressed in the peripheral sympathetic neurons and CNS. In the absence of acetylcholine, the M-channel opens at resting membrane potential and dampens neuronal responsiveness to synaptic inputs. Acetylcholine inhibits M-channel activity by activation of Ml receptor. 

Figure 11.5 Chloride distribution and the GABAa response. The change in membrane voltage (Fm) that results from an increase in chloride conductance following activation of GABAa receptors is determined by the resting membrane potential and the chloride equilibrium potential (Fci)- (a) Immature neurons accumulate CF via NKCC, while mature neurons possess a Cl -extruding transporter (KCC2). (b) In immature neurons GABAa receptor activation leads to CF exit and membrane depolarisation while in mature neurons the principal response is CF entry and h5q)erpolarisation. This is the classic inhibitory postsynaptic potential (IPSP)...

Figure 4.1 Types of changes in membrane potential. The resting membrane potential in a typical neuron is -70 mV. Movement of the membrane potential toward zero (less negative) is referred to as depolarization. The return of the membrane potential to its resting value is referred to as repolarization. Movement of the membrane potential further away from zero (more negative) is referred to as hyperpolarization.

The sinoatrial (SA) node is located in the wall of the right atrium near the entrance of the superior vena cava. The specialized cells of the SA node spontaneously depolarize to threshold and generate 70 to 75 heart beats/ min. The "resting" membrane potential, or pacemaker potential, is different from that of neurons, which were discussed in Chapter 3 (Membrane Potential). First of all, this potential is approximately -55 mV, which is less negative than that found in neurons (-70 mV see Figure 13.2, panel A). Second, pacemaker potential is unstable and slowly depolarizes toward threshold (phase 4). Two important ion currents contribute to this slow depolarization. These cells are inherently leaky to sodium. The resulting influx of Na+ ions occurs through channels that differ from the fast Na+ channels that cause rapid depolarization in other types of excitable cells. Toward the end of phase... 

However, in the SAnode, the action potential develops more slowly because the fast Na+ channels do not play a role. Whenever the membrane potential is less negative than -60 mV for more than a few milliseconds, these channels become inactivated. With a resting membrane potential of -55 mV, this is clearly the case in the SA node. Instead, when the membrane potential reaches threshold in this tissue, many slow Ca++ channels open, resulting in the depolarization phase of the action potential. The slope of this depolarization is less steep than that of neurons. 

The first systematic analysis of synaptic potentials in the CNS was in the early 1950s by Eccles and associates, who recorded intracellularly from spinal motor neurons. When a microelectrode enters a cell, there is a sudden change in the potential recorded by the electrode, which is typically about -70 mV (Figure 21-3). This is the resting membrane potential of the neuron. Two types of pathways—excitatory and inhibitory—impinge on the motor neuron. 

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... 

Shortly after the discovery of Ih in the heart, a very similar current was identified in the brain (29), and not long thereafter, two simultaneous works (30,31) reported that serotonin facilitated Ih in neurons of the thalamus and the nucleus prepositus hypoglossi. Like the effect of norepinephrine in the heart, this effect of serotonin was mediated via cAMP and involved a shift in the voltage dependence of 4 The net effect of this shift in voltage dependence is an increase in the net amount of inward current contributed by HCN channels at a given voltage and thus results in a slow depolarization of the resting membrane potential. 

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