Nerve Impulses and conduction of
Nerve Impulses and conduction of
In contrast to the endocrine system that achieves long-term control via chemical (hormonal) mechanisms, the nervous system relies on more rapid mechanisms of chemical and electrical transmission to propagate signals and commands. The rapid conduction of impulses is essential in allowing the nervous system to mediate short-term and near immediate communication and control between various body systems.
Nerve cells (neurons) are specialized so that at one end there is a flared structure termed the dendrite. At the dendrite, the neuron is able to process chemical signals from other neurons and endocrine hormones. If the signals received at the dendrite end of the neuron are of a sufficient strength, and properly timed, they are transformed into action potentials that sweep down the neural cell body (axon) from the dendrite end to the other end of the neuron, the presynaptic portion of the axon that ends at the next synapse (the extra cellular gap between neurons)in the neural pathway. The arrival of the action potential at the presynaptic terminus causes the release of ions and chemicals (neurotransmitters) that travel across the synapse, the gap or intercellular space between neurons, to act as the stimulus to create another action potential in the next neuron, and thus perpetuate the neural impulse.
Nerve impulses are transmitted through the synaptic gap via chemical signals in the form of a specialized group of chemicals termed neurotransmitters. Neurotransmitters can also pass the neural impulse on to glands and muscles. Except where the neural synapses terminates on a muscle (neuromuscular synapse) or a gland (neuroglandular synapse), the synaptic gap is bordered by a presynaptic terminal portion of one neuron and the dendrite of the postsynaptic neuron.
As the action potential sweeps into presynaptic region, there is a rapid influx of calcium from the extra cellular fluid into a specialized area of the pre-synaptic terminus termed the synaptic knob. Via the process of exocytosis, specific neurotransmitters are then released from synaptic vesicles into the synaptic gap. The neurotransmitters diffuse across the synaptic gap and specifically bind to specialized receptor sites on the dendrite of the postsynaptic neuron.
Neurotransmitters are capable of exciting (creating an action potential) or inhibiting, the postsynaptic neuron. Excitation results from neurotransmitter driven shifts in ion balance that results in a depolarization. Inhibitory neurotransmitters generally work by inducing a state of hyperpolarization.
Excitatory neurotransmitters work by causing changes in sodium ion balance that, if the stimulus is strong enough (i.e., sufficient neurotransmitter binds to dendrite receptors) results in the postsynaptic
neuron reaching threshold potential and the creation of an electrical action potential.
Excitation can also result from a summation of chemical neurotransmitters released from several pre-synaptic neurons that terminate on one postsynaptic neuron. In addition to such spatial control mechanisms, there are mechanisms that are time-dependent (temporal controls). Because neurotransmitters remain bound to their receptors for a time, excitation can also result from an increased rate of release of neurotransmitter from the presynaptic neuron.
Inhibitory neurotransmitters cause membrane changes that result in a movement of ions across the postsynaptic neural cell membrane that move the electrical potential away from the threshold potential.
Neural transmission across the synapse is, however, a result of a complex series of interactions that is far from the one-to-one presynaptic-postsynaptic neuron and many neurons can converge on a postsynaptic neuron.
Within the neuron, the mechanism of transmission is via the transmission of an electrical action potential that represents a change in electrical potential from the rest state the neuronal cell membrane. Electrical potentials are created by the separation of positive and negative ionic electrical charges that vary in distribution and strength on the inside and outside of the cell membrane. There are a greater number of negatively charged proteins on the inside of the cell, and an unequal distribution of positively charges cations both inside and outside the membrane.
The standing potential is maintained because, although there are both electrical and concentration gradients (a variation of high to low concentration) that induce the excess sodium cations to enter the cell and potassium cations to migrate out, the channels for such movements are normally closed so that the neural cell membrane remains impermeable or highly resistant to ion passage in the rest state.
The structure of the cell membrane and a physiological sodium-potassium pump maintain the neural cell resting membrane potential (RMP). Driven by an ATPase enzyme, a physiological sodium potassium pump moves three sodium cations from the inside of the cell for every two potassium cations that it moves back in. The ATPase is necessary because of this movement of cations against their respective resting concentration and electrical gradients.
Neural transmission, in the form of the creation of action potentials, results from sufficient electrical, chemical, or mechanical stimulus to the postsynaptic neuron that is greater than or equal to a threshold stimulus. The creation of an action potential is an “all or none” event and the level and form of stimulus must be sufficient and properly timed to create an action potential. When threshold stimulus is reached in the postsynaptic neuron, there is a rapid movement of ions and the resting membrane potential changes from-70mv to +30mv. This change of approximately 100mv is an action potential that travels down the neuron like a wave, altering the RMP in successively adjacent regions of neural cell membrane as it passes, until the action potential arrives at the presynaptic region of the axon to initiate the mechanisms of synaptic transmission.
Neural transmission is also subjected to refractory periods in which further excitation of the postsynaptic neuron is not possible. In addition, varying types of nerve fibers (e.g., myelinated or demyelinated) exhibit differences in how the action potential moved down the axon, or in the speed of transmission of the action potential.
Cooper, Geoffrey M. The Cell—A Molecular Approach. 3rd ed. Sunderland, MA: Sinauer Associates, Inc., 2003.
Guyton, Arthur C., and Hall, John E. Textbook of Medical Physiology. 11th ed. Philadelphia: W.B. Saunders Co., 2005.
Abbas L. “Synapse Formation: Let’s Stick Together.” Curr Biol. 8;13(1) (Jan. 2003):R25-7.
Izquierdo L.A, et al. “Molecular Pharmacological Dissection of Short- and Long-Term Memory.” Cell Mol Neurobiol. 22(3) (Jun 2002):269-87.
K. Lee Lerner