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Chapter: Biochemical Pharmacology : The ionic basis of cell excitation

The origin of cell excitation

The first, very important means of action potential genera-tion consists in synaptic transmission.

The origin of cell excitation

The mechanisms we have discussed above account for the propagation and for the termination of the action potential. However, so far we have relied on external electrodes for its initiation. Under physiological conditions, action potentials can be evoked in various ways.

The first, very important means of action potential genera-tion consists in synaptic transmission. A synapse connects a presynaptic cell (always a neuron) to a postsynaptic cell (a neuron or muscle cell). In brief, a synapse works as fol-lows:


1.  Excitation of the presynaptic cell leads to the release of a neurotransmitter substance.


2.  The neurotransmitter binds to a receptor on the postsy-naptic cell, very commonly a ligand-gated channel.


3.  The receptor channel opens and locally depolarizes the membrane.


4.  The local depolarization is picked up by adjacent voltage-gated channels and propagated across the entire membrane of the postsynaptic cell.


A very widespread receptor channel is the nicotinic acetyl-choline receptor, which is found on all skeletal muscle cells. Upon binding of the transmitter (acetylcholine), this chan-nel opens up to both K+ and Na+. This would drag the mem-brane potential towards the mean value between the two ions' equilibrium potentials (Figure 4.10). In the process, however, the firing level of the postsynaptic membrane is reached (see Figure 4.6), the adjacent voltage-gated sodium channels open, and the action potential starts propagating along the postsynaptic membrane in the usual way. We will see more about synapses in a later chapter.

Another principal means of action potential generation con-sists in spontaneous, rhythmic membrane depolarization. This occurs in specialized pacemaker cells in heart and smooth muscle. Therefore, while these tissues are modulat-ed by neuronal and hormonal influences, they are capable of self-stimulation in the absence of any neuronal control.

Figure 4.10. Overview of nerve impulse transmission in chemi-cal synapses. The action potential in the presynaptic nerve cell in-duces release of the neurotransmitter (e.g., acetylcholine) into the synaptic cleft. The transmitter binds to its receptor, e.g. the nico-tinic acetylcholine receptor (NAR). The NAR is a ligand-gated channel; it will open and become permeable to both K+ and Na+. This will move the membrane potential toward the average of the two respective equilibrium potentials; however, in the process, the firing level of adjacent voltage-gated sodium channels will be ex-ceeded, and a full action potential will be triggered (inset).

There are two major differences between action potentials that occur in nerve cells or skeletal muscle cells on the one hand, and in heart muscle cells on the other:


1.  The duration of the action potential in the heart is much longer – several hundred milliseconds as opposed to sev-eral milliseconds in nerve and skeletal muscle. While each skeletal muscle contraction is triggered and sus-tained by a repetitive burst of many action potentials, in the heart there is only one action potential per heart beat.


2.  While sodium is the major ion species responsible for excitation in nerve cells and skeletal muscle, in the heart pacemaker cells this role is taken by calcium. Calcium also has a prominent role in the excitation of smooth muscle cells.


Two types of calcium channels control the spontaneous for-mation of an action potential. These channels differ in their respective response to the prevailing membrane potential. One of them (the CaT channel) opens slowly but steadily at low potentials, thereby ramping up the membrane potential to the firing level. At this point, the Ca L channel responds and induces rapid and complete membrane depolarization (Figure 4.11).

Figure 4.11. Generation of spontaneous action potentials in the cardiac conduction system. Depolarization starts as a slowly ascending prepotential that is due to the CaT channel. Once the corresponding threshold is reached, the CaL channel opens, and the action potential is triggered. It is terminated by inactivation of the Ca++ channels, and by the opening of KV channels (which have the same role here as in the skeletal muscle and nerves).

The heart also provides us with the `classical' example of the third major way to trigger an action potential, which is by electrical coupling to a neighbouring cell via gap junc-tions (Figure 4.12). The excitation that is spontaneously generated in the small number of specialized pacemaker cells in the conduction system5 spreads in this way across the entire heart and ensures coordinated action. The speed of conduction varies in different parts of the heart, and the atria are excited and will contract before the ventricles. Groups of smooth muscle cells in many organs are likewise connected to each other and thus behave as functional units in a similar way.


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