5 Important Functions of Nerve Cells (With Diagram)

Some of the most important functions of nerve cells are as follows:

1. Conduction of Nerve Impulses 2. Ion Gradients across the Membrane 3. Initiation of the Action Potential 4. Conduction of the Action Potential 5. Synaptic Transmission.

The tissues of the nervous system contain a variety of cells, but one of the most highly differentiated and specialized is the neuron or nerve fiber itself. The pri­mary and specialized functions of these cells are the conduction and transmission of impulses from one part of an organism to another. In some instances, the impulse may travel several feet, and a single neuron may bridge the entire distance.

In certain respects, neurons are similar to most other cells (Fig. 24-21) and the cell body contains the typical spectrum of organelles. It is the processes or extensions that make neurons easily distinguishable from other cells. Processes that receive transmitted impulses and conduct them toward the cell body are called dendrites and processes that conduct impulses away from the cell body are called axons.

The axons terminate in a special structure called the end-plate, which is responsible for initiating the transmission of the impulse to the next cell. The junctions between successive nerve cells or between a nerve cell and an effector cell (such as a gland or muscle cell) are called synapses. At each synapse, the two cells are sepa­rated by a narrow gap called a synaptic cleft. A nerve is formed by a bundle of many neurons.

Neurons develop from the neural tube of the early embryo and in many animals continue development until sometime after birth. The development of motor neurons that have elongated axons is best understood. These cells are derived from tissue on the ventral side of the neural tube. In an action reminiscent of amoe­boid movement, the cytoplasm of these cells flows out­ward in a strand like manner with progressive and con­tinuous amoeboid like activity at the end of the strand.

The long, thin strand becomes the axon of the neuron and may give rise to several smaller branches. By the time growth is complete the axon may contain thou­sands of times as much cytoplasmic material as the cell body and may extend for thousands of cell body diameters. Growth of an axon is maintained by the continuous flow of cytoplasm from the nerve cell body. Even after growth ceases, axoplasmic flow continues and serves to carry substances produced in the cell body toward the axonal endings.

Mature nerve cells also exhibit a second form of intracellular transport called axonal transport. Axonal transport is more rapid than axo­plasmic flow and conveys materials in both directions along the nerve cell process. Indeed, it is the retro­grade movement by which herpes and rabies viruses make their way to the cell bodies of nerve cells.

Axo­nal transport carries membranous elements and small vesicles filled with neurotransmitters or their precur­sors toward the nerve endings. Much of the membranous material is incorporated into the plasma membrane or axolemma along the way, but the re­mainder reaches the nerve ending. The axoplasm of nerve cells contains large numbers of actin and myso- sin filaments as well as microtubules (Fig. 24-21). These are believed to play a role in both axoplasmic flow and axonal transport.

1. Conduction of Nerve Impulses:

Neurons conduct signals or impulses from one part of the body to another. Under normal circumstances each impulse begins at the dendrites (occasionally at the cell body) and spreads across the cell to the axonal endings. Experimentally, an impulse can be initiated anywhere on the cell surface and can be elicited by ap­plying a variety of stimuli including electrical shock, pressure (pinching), heat, cold, and pH changes.

The impulse results from transitory physicochemical changes occurring in the cell’s plasma membrane, and once initiated it is propagated along the membrane without dependence on a continuing stimulus. The ve­locity with which the impulse travels along the fiber is not dependent on the strength of the stimulus, that is, it does not travel faster if initiated by a stronger stim­ulus.

The rate of movement of an impulse varies ac­cording to neuron type but is in the range of 2-100 ml sec, a speed far too slow to compare the impulse to the movement of an electron through a wire during elec­trical flow. As the impulse passes along the plasma membrane, two major changes occur. One is a change in electrical potential across the membrane and the second is a change in membrane permeability.

Resting Potentials and Action Potentials:

The cyto­plasm or axoplasm within the axon and the extracel­lular fluid contain a number of ions and are good elec­trical conductors. On the other hand’, the axolemma acts as an insulator, albeit a weak one. When one member of a pair of microelectrodes connected to a voltmeter is inserted into the axoplasm and the other electrode is placed in the extracellular fluid, an elec­trical potential across the membrane is measured (Fig. 24-22).

When the cell is not conducting an im­pulse, the potential is called the resting potential and maintains a constant value. For most nerve cells, the resting potential is 50-90 mV, with the inner (axoplas­mic) surface of the membrane negative relative to the outside. When a neuron is stimulated and the impulse passes the region of the electrodes, a brief change in potential is recorded; this transitory change in poten­tial is called an action potential. By placing elec­trodes at several points along the axon, it is possible to follow the action potential as it travels along the pro­cess.

As the action potential passes each recording electrode (Fig. 24-23), the internal voltage rapidly changes from – 90 mV through 0 mV to + 20 or + 30 mV. Within 0.5 to 1.0 msec, the membrane recovers, and the – 90 mV resting potential is restored. The im­pulse sweeping along the axon represents a net transi­tory change in potential of 110-120 mV.

2. Ion Gradients across the Membrane:

The resting potential of the nerve cell membrane stems from an unequal distribution of ions between the axoplasm and the extracellular fluid. The fluid bathing the membrane’s surface contains Na⁺, Cl^–, and HCO₃^– in higher concentrations than the axo­plasm, whereas the axoplasm contains higher concentrations of K⁺ and organic anions than the extracellu­lar fluid. In addition to concentration differences across the membrane for individual ionic species, there is also a relatively higher concentration of nega­tive ions inside the cell than outside. As a result, the outside surface of the axolemma is positive rela­tive to the inside surface.

The nerve cell membrane is permeable to sodium and potassium ions and these ions are continuously diffusing from the side of the membrane where they are at higher concentration to the side where they are at lower concentration. To maintain the concentration differences of these two cations, metabolic energy is used to pump inwardly diffusing Na⁺ out of the cell and outwardly diffusing K⁺ into the cell.

The mecha­nism proposed to account for such a sodium/potassium pump is depicted in Figure 15-40 and involves cyclic changes in the tertiary structure of an enzyme carrier located in the axolemma. Sodium ions together with ATP are bound to an enzyme site exposed at the inside membrane surface and K ⁺ is bound to the outer sur­face. The binding causes a conformational change in the carrier that moves the ions through the mem­brane. The ATP is hydrolyzed and the ions are re­leased.

3. Initiation of the Action Potential:

Much of what we know today about the molecular ba­sis of impulse conduction by nerve cells is based on the pioneering studies of A. Hodgkin, A. Huxley, and J. Eccles, who received the Nobel Prize in 1963 for their work. According to the presently accepted model, ap­plication of a stimulus to the neuron is followed by the rapid diffusion of Na⁺ across the axolemma from the exterior into the axoplasm. The unusually rapid in­ward diffusion of Na ⁺ is apparently due to a transient increase in the size of the pores or “gates” in the plasma membrane permeable to Na⁺. The inward rush of Na⁺ reverses the electrical potential across the membrane.

This is followed almost immediately by an opening of the membrane’s potassium gates and a rapid efflux of K⁺; the latter flow of ions restores the former potential. Only a small percentage of the Na⁺ and K⁺ initially present outside and inside the cell need traverse the membrane to cause the reverse po­larization followed by the repolarization.

Indeed, the nerve fiber can conduct an impulse many times in suc­cession without appreciably diminishing the concen­tration gradients across the membrane. Between suc­cessive conductions the Na⁺ /K⁺ gates close and the Na ⁺ /K⁺ pump restores the original ion concentra­tions. It is estimated that the normal distribution of Na ⁺ and K ⁺ across the membrane can be restored in less than 5 x 10^-3 sec.

If the stimulus that is applied reaches the neuron threshold level, an action potential is initiated. Any stimulus above the threshold level also initiates an action potential, but if the stimulus intensity is below threshold (i.e., subthreshold) the membrane recovers from its transitory depolarization without initiating the action potential.

4. Conduction of the Action Potential:

Once the polarity at a given point on the nerve cell membrane has been reversed, current flows between this and the adjacent regions of the membrane. The flow of current to the neighboring region serves to open the Na⁺ gates there, reversing the polarity in that region. The cycle is repeated as the action poten­tial travels further and further along the nerve cell membrane.

The speed at which the impulse is propagated along the nerve fiber is directly dependent on the diameter of the axon (Fig. 24-24). An axon with a large diameter offers less electrical resistance than a smaller one and therefore depolarizes more readily and conducts faster. The rapid conduction speed observed in squid axons (25 m/sec) is due to the large axon diameter (1 mm or more!).

The rate of impulse conduction in mammalian nerve fibers exceeds that in the squid, but the increased speed is gained by a change in capaci­tance and not by an increase in axon diameter. The ca­pacitance is changed by the presence of myelin (a good insulator) in cells called Schwann cells, which are wrapped around the axon forming a sheath (Fig. 24- 25).

The outer surface of the axon membrane is ex­posed to the extracellular fluid only at the nodes of Ranvier (Figs. 24-21 and 24-24), which are about 2 mm apart. In effect, the impulse skips from node to node, a phenomenon called saltatory conduction, and travels considerably faster.

5. Synaptic Transmission:

Transmission of an impulse from one neuron to an­other or to an effector cell may be mediated electri­cally or chemically. Electrical transmission occurs when the axonal endings of the neuron form gap junc­tions with the next cell (i.e., the plasma membranes of the two cells are bridged by connexons).

In such an arrangement, the action potential passes directly and without delay from one cell to the next. More common is chemical transmission, which involves communication between cells that are sepa­rated by a narrow, fluid-filled space. When an impulse or action potential reaches the axonal endings of a neuron, neurotransmitters are released into this space (the synaptic cleft) and diffuse across the cleft to the next cell (e.g., the next neuron or an effector cell such as a muscle cell or gland cell).

The axon ter­minals, the synaptic cleft, and the specialized region of the cell responding to the neurotransmitter com­prise a synapse. The most common neurotransmitter is acetylcholine; others include norepinephrine, do­pamine, and seratonin. Neurotransmitters are synapse-specific, that is, they are released at some synapses but not at others. Moreover, certain neuro­transmitters act to stimulate the postsynaptic cell and others are inhibitory (some may even be stimulatory when released at one synapse and inhibitory at an­other).

Best understood are synapses at which acetylcho­line is the neurotransmitter. Until quite recently it was believed that acetylcholine is released into the synaptic cleft from acetylcholine-rich axoplasmic vesi­cles (called synaptic vesicles) that populate the neu­ron’s axonal endings. These vesicles were thought to fuse with the axolemma, thereby discharging their contents.

However, this now appears not to be the case and the synaptic vesicles play a different role (see be­low). Acetylcholine is released instead from the axo­plasm of the presynaptic cell through small channels formed in the membrane in response to the arrival of the action potential and the entry of calcium ions into the axoplasm from the synaptic cleft (Fig. 24-26). The released acetylcholine diffuses across the synaptic cleft and momentarily attaches to acetylcholine re­ceptors in the membrane of the postsynaptic cell, elic­iting a response by that cell (e.g., conduction of an­other action potential in nerve-nerve junctions).

All the acetylcholine released into the synaptic cleft by the presynaptic cell is broken down into choline and acetate by the enzyme acetylcholinesterase found on the surface of the postsynaptic cell and released into the cleft. New acetylcholine is synthesized in the presynaptic cell by the transfer of acetate from acetyl- CoA to choline by the cytoplasmic enzyme choline ace­tyltransferase (Fig. 24-27). Both the acetate and the choline produced in the synaptic cleft by the degrada­tion of acetylcholine may be transferred back into the cytoplasm of the presynaptic cell and recycled (Fig. 24-27).

What then is the role of the acetylcholine-rich syn­aptic vesicles? During prolonged stimulation of a nerve, rapidly diminishing axoplasmic acetylcholine is replaced by the release of needed neurotransmitter into the cytoplasm from the synaptic vesicles.

As de­picted in Figure 24-26, the release of acetylcholine is accompanied by the sequestering of the calcium ions that entered the cell from the synaptic cleft (i.e., actylcholine leaves the vesicles and Ca^{2 +} enters them). The calcium is then expelled into the synaptic cleft when the synaptic vesicles fuse with the axolemma. The synthesis of acetylcholine by the action of choline ace­tyltransferase is accompanied by the formation of new synaptic vesicles.