The nerve cell body contains nucleus and organelles just like any other cell of the body. It has a well-developed rough endoplasmic reticulum and Golgi apparatus. The axon is the conducting region of the nerve and the axon terminals are the secretory regions of the nerve. The axon terminal is also known as the synaptic knob or bouton. The dendrites are the receptive region of the nerve which gets input from nerve impulses. The branching helps to increase the surface area for reception. The myelin sheath covers the axon intermittently, with gaps called nodes of Ranvier.2 The purpose of myelin sheath is to speed up conduction by insulating the nerve in intervals. This type of insulation results in the generated action potential jumping from one node of Ranvier to the next. Schwann cells carry out the duty of making the myelin sheath in the peripheral nervous system by wrapping themselves around the axon. Oligodendrocytes are the central nervous system analogue of Schwann cells, in that it makes myelin sheath around axons of the central nervous system. Insulation of the axon is achieved by the myelin sheath.2 Insulation occurs in intervals, which causes action potential to jump from one node of Ranvier to the next. The myelin sheath is a good insulator because it is fatty and does not contain any channels. Action potential jumps from one node of Ranvier to the next and it is this jumping of action potential that speeds up conduction in the axon. A synapse is the site of impulse propagation between cells, causing conduction from one cell to another. The axodendritic synapse is the axon terminal of one neuron (presynaptic) that conducts to the dendrite of another neuron (postsynaptic). The axosomatic synpase is when the axon terminal of one neuron (presynaptic) conducts towards the cell body of another neuron (postsynaptic). An axoaxonic synapse, a rare type, is when the axon terminal of one neuron (presynaptic) conducts towards the axon hillock of another (postsynaptic).
Transmitter molecules are the neurotransmitters. The action potential is caused by the release of neurotransmitters by presynaptic axon terminal, which is picked up by the receptor of a postsynaptic neuron. The release of neurotransmitter is as a result of the exocytosis of vesicles containing neurotransmitters. This release mechanism is triggered by a calcium influx when action potential reaches axon terminal. Neurotransmitter reception results from the diffusion of neurotransmitter across the synaptic cleft, which binds to a receptor and opens up ion channels that causes a change in membrane potential of the postsynaptic neuron. If this graded potential is large enough, it will trigger a full-fledged, all-or-nothing action potential in the postsynaptic neuron. Neurotransmitters are quickly eliminated so that they don’t persistently stimulate the postsynaptic neuron. They are eliminated by enzymes, reuptake by presynaptic terminal, or they simply diffuse away. Neurotransmitter molecules include acetylcholine (ACh), norepinephrine (NE), dopamine, serotonin, histamine and ATP.2 The synaptic knob is another name for axon terminal and it contains vesicles of neurotransmitters waiting to be exocytosed. The action potential reaching the synaptic knob causes an influx of calcium, which signals the vesicles to fuse with cell membrane (exocytosis) to release the neurotransmitters into the synaptic cleft. Continuous synaptic activity will lead to the depletion of neurotransmitters which will cause fatigue. The action potential generated is an all-or-nothing response. As long as the neurotransmitters cause the postsynaptic cell to reach a certain threshold potential, the action potential induced is just as large as the presynaptic action potential. Since the postsynaptic action potential is as large as the presynaptic potential, propagation between the cells results in no resistance loss.
The resting membrane potential is an electric potential across the plasma membrane of approximately –70 millivolts (mV), with the interior of the cell negatively charged with respect to the exterior of the cell.2 Two primary membrane proteins are required to establish the resting membrane potential: the Na+/K+ ATPase and the potassium leak channels. The Na+/K+ ATPase pumps three sodium ions out of the cell and two potassium ions into the cell with the hydrolysis of one ATP molecule. The result is a sodium gradient with high sodium outside of the cell and a potassium gradient with high potassium inside the cell. Leak channels are channels that are open all the time, and that simply allow ions to leak across the membrane according to their gradient. Potassium leak channels allow potassium, but no other ions, to flow down their gradient out of the cell. The combined loss of many positive ions through Na+/K+ ATPases and the potassium leak channels leaves the interior of the cell with a net negative charge, approximately 70 mV more negative than the exterior of the cell; this difference is the resting membrane potential. It should be noted that there are very few sodium leak channels in the membrane, so the cell membrane is virtually impermeable to sodium. The fact that the resting membrane potential is –70 mV reflects both the differences in the equilibrium potentials for Na+ and K+, and also the relative numbers of leak channels for these two ions. If the cell were completely permeable to K+, the resting potential would be about –90 mV. The fact that the resting potential is very close to the K+ equilibrium potential indicates that there are a large number of K+ leak channels in the membrane; the cell at rest is almost completely permeable to potassium. However, the resting potential is slightly more positive than –90 mV, indicating that there are a few Na+ leak channels allowing Na+ in. Not very many Na+ leak channels, though, or the resting potential would be much more positive; closer to the Na+ equilibrium potential. This is in fact what we see when the cell does become completely permeable to Na+ at the beginning of the action potential; the membrane potential shoots upward to +35 mV.
Stages of an action potential are:
1) Resting: The cell is at rest, with the sodium-potassium pump maintaining a resting potential (-70 mV). Lots of sodium is outside the cell and lots of potassium inside. Ion channels are closed so the established ion gradient won’t leak.
2) Depolarization: The sodium channels open and positive sodium rushes inside. The membrane potential shoots up to +30 mV. There are now lots of sodium inside as well as lots of potassium inside.
3) Repolarization: The potassium channels open while the sodium channels close. This results in positive potassium rushing outside and the membrane potential drops back down. Lots of sodium found on the inside and lots of potassium found on the outside (opposite of the resting state).
4) Hyperpolarization: The potassium channels does not close fast enough, so the membrane potential actually drops below the resting potential for a very short period of time.
5) Refractory period: The sodium-potassium pump works to re-establish the original resting state (more potassium inside, sodium outside). Until this is done, the neuron cannot generate another action potential. Absolute refractory period is the period from depolarization to the cell having re-established the original resting state. Relative refractory period is the period after hyperpolarization till resting state re-established.
As mentioned above, the myelin sheath is formed by a type of glial cell called a Schwann cell. However, Schwann cells are not the only type of glial cell. Glial cells are specialized, non-neuronal cells that typically provide structural and metabolic support to neurons.3 Glia maintain a resting membrane potential but do not generate action potentials.
1) Dorland’s (2012). Dorland’s Illustrated Medical Dictionary (32nd ed.). Elsevier Saunders.
2) Black, J.A., Sontheimer, H., Oh, Y., and Waxman, S.G. (1995). In The Axon, S. Waxman, J. Kocsis, and P. Stys, eds. Oxford University Press, New York, pp. 116–143.
3) Jessen KR, Mirsky R (August 1980). “Glial cells in the enteric nervous system contain glial fibrillary acidic protein”. Nature. 736–7
4) Hille, Bertil (2001) . Ion Channels of Excitable Membranes (3rd ed.). Sunderland,
Mass: Sinauer Associates, Inc. p. 5.
5) NV, B. (2002). Medical Biochemistry. San Diego: Harcourt/Academic Press. (lipid)
6) Vander, Arthur (2008). Vander’s Human Physiology: the mechanisms of body function. Boston: McGraw-Hill Higher Education. pp. 345-347