Pacemaker cells have high resting membrane potentials of -50 to -40 mV, whereas normal cells have their resting membrane potential around -70 mV. Which ions, and what kind of channels are responsible for the high resting potential of pacemaker cells?
$\begingroup$ According to my knowledge their is a slow influx of sodium ions which causes action potential and during depolarization their is influx of calcium ions and while repolarizing their is efflux of potassium ions. But I want to know specifically what is the reason behind slow influx of sodium at the start of action potential and if their are any other ions involved in this. $\endgroup$– 9HeadsApr 28, 2015 at 6:52
The pacemaker potential is interesting (to a biologist) as it involves your typical Na/K channels, Ca channel, as well as a funny current (If) or alternatively called hyperpolarization-activated current.
The funny current is a mixed sodium-potassium current that activates upon hyperpolarization at voltages in the diastolic range (normally from -60/-70 mV to -40 mV). When at the end of a SA potential the membrane repolarizes below the If threshold (about -40/-50 mV), the funny current is activated and supplies inward current, which is responsible for starting the diastolic depolarization phase (DD); by this mechanism, the funny current controls the rate of spontaneous activity of sinoatrial myocytes, hence the cardiac rate.
Pacemaker activity (or spontaneous electrical activity) of the sino-atrial node is based on the presence of a special phase called the diastolic depolarization during the action potential, in which cells depolarize spontaneously towards the AP threshold. Animal studies (mostly conducted on rabbit heart) have identified that this net inward current during the diastolic depolarization phase is the result of a complex interaction of multiple inwardly and outwardly directed ion currents....
Verkerk, Arie O., Antoni CG van Ginneken, and Ronald Wilders. "Pacemaker activity of the human sinoatrial node: role of the hyperpolarization-activated current, I f." International journal of cardiology 132.3 (2009): 318-336.
The SAN is a complex tissue with regional differences in morphological and electrical properties.Animal studies have revealed that pacemaking in SAN cells follows from diastolic depolarization driven by a net inward current, which results from an interaction of multiple ion currents. Inward currents are activated during diastole: hyperpolarization-activated pacemaker current (If), background Na+ current (Ib,Na), sustained inward current (Ist), T- and L-type Ca2+ currents (ICa,T and ICa,L, respectively), and Ca2+-release activated Na+–Ca2+ exchange current (INCX). Conversely, outward currents are deactivated: rapid delayed rectifier K+ current (IKr) and slow delayed rectifier K+ current (IKs). The relative contributions of these currents to diastolic depolarization are a matter of debate.
Verkerk, Arie O., et al. "Pacemaker current (If) in the human sinoatrial node." European heart journal 28.20 (2007): 2472-2478.
Might I suggest you read up on the papers mentioned above?
You might also be interested in this:
Noma, Akinori. "Ionic mechanisms of the cardiac pacemaker potential." Japanese heart journal 37.5 (1996): 673-682.
1$\begingroup$ The Last reference provided by you was very useful and it had answers to most of my doubts and questions. $\endgroup$– 9HeadsApr 28, 2015 at 8:49