synapse(redirected from adrenergic synapse)
Also found in: Dictionary, Thesaurus, Medical.
a specialized functional contact between excitable cells that transmits and transforms signals. The term “synapse” was introduced by the English physiologist C. Sherrington in 1897 to designate a contact between neurons. Contacts between neuronal axons and the cells of organs that perform particular functions are often defined as junctions, although they are a type of synapse. Synapses are the only pathways along which neurons can communicate with one another, and as such, they ensure all the principal manifestations of nervous-system activity and the integrative activity of the brain. A synapse includes a presynaptic portion (synaptic ending), a synaptic cleft, which separates two cells, and a postsynaptic portion, which is the part of a cell adjacent to a synaptic ending.
In most cases, interneuronal synapses are formed by the ax-onal endings of certain nerve cells and the body, dendrites, or axons of others. Accordingly, axosomatic, axodendritic, and axaxonic synapses are distinguished. Dendrite surfaces predominate, and consequently, axodendritic synapses are most commonly found. The number of synaptic contacts on different neurons of the central nervous system greatly varies. Hundreds or thousands of separate presynaptic fibers terminate on some cells, whereas other neurons have a single synapse. A large neuron of the reticular formation of the brain stem receives more than 4,000 synaptic contacts; on some cells the approximate number of synaptic contacts is more than 10,000–20,000. The density of synapses on the surface of a neuron may reach 15–20 per 100 square micrometers.
Synapses may be excitatory or inhibitory, depending on whether they activate or suppress the activity of a given cell. In either case, transmission through a synapse may be effected by means of a chemical or electrical mechanism. There are also mixed synapses, which combine chemical and electrical transmission mechanisms. Most commonly found are synapses with chemical mechanisms, in which signals are transmitted from presynaptic to postsynaptic membranes by means of mediators — chemical compounds whose molecules are capable of reacting with the specific receptors of a postsynaptic membrane. Mediators change the permeability of a postsynaptic membrane to ions, generating a local, nonregenerative potential. In an electrical synapse the current from an activated presynaptic membrane acts directly on a postsynaptic membrane.
Synapses with chemical and electrical transmission mechanisms are characterized by specific structural features. In synapses with the chemical transmission mechanisms the presynaptic ending includes synaptic vesicles, which contain high concentrations of a mediator. Presynaptic and postsynaptic membranes are separated by a synaptic cleft, which is usually 150–200 angstroms (Å) in width, although in some synapses the width reaches 1,000 Å or more. Synaptic vesicles have a tendency to become concentrated at the internal surface of a presynaptic membrane, opposite a synaptic cleft. They may emerge from a synapse’s presynaptic ending at breaks in the membrane, penetrate the synaptic cleft, and make contact with the postsynaptic membrane. The arrangement and number of synaptic vesicles vary as a result of nervous activity.
A postsynaptic membrane in a chemical synapse is characterized by swellings containing special active zones that are apparently associated with the membrane’s specialization as a chemoreceptor. In an electrical synapse the cleft between presynaptic and postsynaptic membranes is absent, and the complete coalescence of the membranes is sometimes observed. Both types of synapse are illustrated schematically in Figure 1,a. A chemical synapse’s presynaptic ending packed with presynaptic vesicles is shown in Figure 1,b.
Excitatory or inhibitory effects in a synapse with a chemical reaction are produced by a series of processes. The nerve impulse, upon arriving at a presynaptic ending, depolarizes the presynaptic membrane, whose permeability to calcium ions is increased. The entry of calcium ions into a synapse’s presynaptic ending releases a mediator, which diffuses through the synaptic cleft and reacts with the receptors of the postsynaptic membrane. This reaction usually results in an increase in the permeability of the postsynaptic membrane to one or more ions and to the generation of a postsynaptic potential. In excitatory synapses sodium conductivity increases, sometimes simultaneously with potassium conductivity, which leads to the depolarization and excitation of a postsynaptic cell. In inhibitory synapses the permeability of the postsynaptic membrane to chloride ions increases, sometimes simultaneously with potassium-ion permeability; this effect is usually accompanied by hyper-polarization.
The increase in the conductivity of a postsynaptic membrane, which shunts excitatory effects, is of the greatest significance in effecting synaptic inhibition. A mediator may also act on the metabolic processes of a postsynaptic neuron, producing prolonged postsynaptic potentials. In synapses with electrical mechanisms the currents of a presynaptic ending act directly on the postsynaptic cell without the participation of an intermediate chemical link because of the almost complete absence of a synaptic cleft; in such cases, the width of the cleft measures no more than 20 A. Thus, the shunting of the current flowing from a presynaptic cell to a postsynaptic cell is eliminated. The impulse generated in a presynaptic membrane is transmitted to a postsynaptic membrane passively and electrotonically, as if along cables (Figure 2).
In electrotonic synapses channels permit the molecules of low-molecular-weight compounds to pass from the cytoplasm of one cell to the cytoplasm of another. The channels do not communicate with the extracellular space and are absent in other areas of the membrane. Most neural activity can be effected by means of chemical and electrotonic synapses. Electrotonic synapses ensure the rapidity and stability of transmission and are less sensitive to fluctuations in temperature. A chemical mechanism more reliably ensures unidirectional conduction and makes it possible to change the effectiveness of a synapse as a result of preceding activity.
REFERENCESEccles, J. Fiziologiia sinapsov. Moscow, 1966 (Translated from English.)
Katz, B. Nerv, myshtsa i sinaps. Moscow, 1968. (Translated from English.)
Akert, K. “Sravnenie dvigatel’nykh kontsevykh plastinok i tsentral’-nykh sinapsov: Ul’trastrukturnoe issledovanie.” Zhurnal evoliutsion-noi biokhimii ifiziologii, 1975, vol. 11, no.2.
DeRobertis, E. D. Histophysiology of Synapses and Neurosecretion. Oxford, 1964.
Structure and Function of Synapses. Edited by G. D. Pappas and D. P. Purpura. New York, 1972.
Shapovalov, A. I. “Neuronal Organization and Synaptic Mechanisms of Supraspinal Motor Control in Vertebrates.” Rev. Physiol., Biochem., and Pharmacol., 1975, vol. 72.
A. I. SHAPOVALOV