Nerve Cell

In the body's nervous system are many nerve cells are of the basic type illustrated above. Some kind of stimulus triggers an electric discharge of the cell which is analogous to the discharge of a capacitor. This produces an electrical pulse on the order of 50-70 millivolts called an action potential. The electrical impulse propagates down the fiber-like extension of the nerve cell (the axon). The speed of transmission depends upon the size of the fiber, but is on the order of tens of meters per second - not the speed of light transmission that occurs with electrical signals on wires. Once the signal reaches the axon terminal bundle, it may be transmitted to a neighboring nerve cell with the action of a chemical neurotransmitter.

The dendrites serve as the stimulus receptors for the neuron, but they respond to a number of different types of stimuli. The neurons in the optic nerve respond to electrical stimuli sent by the cells of the retina. Other types of receptors respond to chemical neurotransmitters.

The cell body contains the necessary structures for keeping the neuron functional. That includes the nucleus, mitochondria, and other organelles. Extending from the opposite side of the cell body is the long tubular extension called the axon. Surrounding the axon is the myelin sheath, which plays an important role in the rate of electrical transmission. At the terminal end of the axon is a branched structure with ends called synaptic knobs. From this structure chemical signals can be sent to neighboring neurons.

Contributing author: Ka Xiong Charand

Transmission of a nerve impulse along an axon

A nerve cell is like a receiver, transmitter and transmission line with the task of passing a signal along from its dendrites to the axon terminal bundle.

The stimulus triggers an action potential in the cell membrane of the nerve cell, and that action potential provides the stimulus for a neighboring segment of the cell membrane. When the propagating action potential reaches the axon, it proceeds down that "transmission line" by successive excitation of segments of the axon membrane.

Just the successive stimulation of action potentials would result in slow signal transmission down the axon. The propagation speed is considerably increased by the action of the myelin sheath.

The myelin sheath around the axon prevents the gates on that part of the axon from opening and exchanging their ions with the outside environment. There are gaps between the myelin sheath cells known as the Nodes of Ranvier. At those uncovered areas of the axon membrane, the ion exchange necessary for the production of an action potential can take place. The action potential at one node is sufficient to excite a response at the next node, so the nerve signal can propagate faster by these discrete jumps than by the continuous propagation of depolarization/repolarization along the membrane. This enhanced signal transmission is called saltatory conduction (from the Latin saltare, to jump or hop).

Tuzynski and Dixon offer some quantification of the sizes involved in these nerve cells. The axon is made up of connected segments of length about 2 mm and diameter typically 20 mm. This diameter compares to about 100 mm for the diameter of a human hair. Axon diameters may vary from 0.1 mm to 20 mm and may be up to a meter long. The much-studied squid has a giant axon of about a millimeter in diameter. The myelin sheaths are about 1mm in length. The action potential travels along the axon at speeds from 1 to 100 m/s.

Contributing author: Ka Xiong Charand

Neural Stimulation of a Muscle Fiber

Muscle fibers contract by the action of actin and myosin sliding past each other. The signal to initiate the contraction comes from the brain as a part of the somatic nervous system.

The illustration below is a schematic representation of the process from the arrival of a nerve signal to the terminal bundle of the nerve axon to the contration of a muscle fiber. The stimulation of muscle action is associated with the neurotransmitter chemical acetylcholine.

When the nerve signal from the somatic nerve system reaches the muscle cell, voltage-dependent calcium gates open to allow calcium to enter the axon terminal. This calcium moves the acetylcholine-containing miceles to fuse with the presynaptic membrane and release their acetylcholine into the synapse, where it is bound by acetylcholine receptors on the postsynaptic surface. The acetylcholine receptors are examples of ligand-gated ion channels: upon binding the acetylcholine molecule, they open up a channel for sodium and potassium ions to enter the cell. In this case acetylcholine is the "ligand" that opens the gate for sodium.

When the opening of the Na channels sends a rush of Na into the cell, which, if it is strong enough, causes nearby voltage-gated Na channels to open and produces an action potential. This action potential is not one in a nerve cell, but in the muscle cell.

The muscle fiber structure has lots of tubes called T-tubules or transverse tubules. When the action potential travels down these tubules, it eventually triggers the voltage-sensitive proteins that are linked to the calcium channels in the structure called the sarcoplasmic reticulum (Wiki) that surrounds the nerve fibers. This membrane-enclosed structure has similarities to the endoplasmic reticulum in other cells. In the rest state, the sarcoplasmic reticulum will have a reserved supply of calcium because its walls have many Ca pumps which use ATP energy to store calcium. With the stimulus of the action potential, calcium rushes into the cell and interacts with the actin. Associated with the actin are the troponin complex and the tropomyosin strand which block the binding of myosin. The supplied calcium ions bind to the troponin and pulls the "gaurding" troponin and tropomyosin strand away from the site where myosin can bind.

In order to bind to the actin, the myocin must have a supply of energy, which it obtains from ATP . Having absorbed energy from ATP, a unit of the myosin fiber will be in a stressed or high energy state, like a stretched spring. With the action of the calcium to withdraw the troponin and tropomyosin, the myosin structure can bind and use the energy to pull the actin fiber, shortening or contracting the muscle fiber.

While the contraction of a muscle can be repeated by following the above steps, there must be a pathway back to a rest state since you don't want your muscles to be in a permanently contracted state. Those mechanisms for return to rest are provided. The initial stimulus by the motor nerve which started the process is under conscious control, so you can decide to relax the muscle. The free acetylcholine in the synaptic gap is removed by another molecule, acetylcholinesterase. This is an essential function in neuromuscular junctions since the continued presence of acetylcholine could keep the muscle in extended contraction. In fact, the role of nerve poisons and the venom of some snakes is to block the action of acetylcholinesterase and force the muscles into a continuing contracted state. In normal operation the acetylcholinesterase works briefly and then ceases. The calcium pumps in the sarcoplasmic reticulum work to reclaim the calcium, and upon removal of the calcium from the receptors on the muscle, the "bodygaurd" troponin and tropomyocin move back to their blocking positions. The myosin and actin fibers return to their relaxed state.