Synapse

Synapse

Originally two types of synapse were distinguished on ultra structural examination of the pyramidal cells of the cerebral cortex. The type I junction is usually extensive, the postsynaptic density prominent, rendering the synapse asymmetrical, and the wide synaptic cleft contains a dense plaque. In the type Ii synapse, in contrast, the postsynaptic density is less readily identifiable and the narrower cleft does not contain a dense plaque; the overall configuration is symmetrical. The presynaptic element in most cases is an axon, either at its end ( button terminal ) or along its course ( bout on en passant ): the axonal terminal can form a synapse with any part of another neuron and thus axo-dendritic, axo-somatic and axo­axonal synapses are distinguished. The presynaptic element, however, does not need to be an axonal terminal and synapses can be formed between any part of two neurons, providing a wide variety of synapses.

The presynaptic element contains the synaptic vesicles which, in turn, are filled with neuro­transmitters. The size, shape and content of the vesicles vary, depending upon the type of synapse. The most frequently Occurring vesicles are apparently clear, spherical and 40-50 nm in diameter. Elongated or flattened vesicles with clear centers are 20 nm wide and 50 nm long. There have been many attempts to correlate vesicular shape with functional activity: spherical vesicles occur in excitatory, type I synapses, whilst flattened vesicles are associated with inhibitory, type II synapses. Larger vesicles of up to 60nm in diameter with a dense core are encountered in areas of catecholamine activity and contain noradrenaline, dopamine or 5hydroxytryptamine. Another, larger dense-cored vesicle, up to lO nm with a spherical dense core of 50-70 nm in diameter, is most frequently seen in the presynaptic terminals of autonomic ganglia, but also occurs in various parts of the central nervous system intermingled with clear vesicles. The presynaptic element, particularly the axonal terminal, also contains other organelles, including mitochondria, neurofilaments, microtubules, smooth endoplasmic reticulum and glycogen.

The synaptic cleft, separating the presynaptic and postsynaptic membranes, is 20-30 nM wide and usually contains a dense plaque of intercellular material. In addition, filaments appear to traverse the cleft and contribute to the formation of the plaque.

The postsynaptic membrane is rendered conspicuous by an accumulation of dense material on its cytoplasmic surface. This post-synaptic density, composed of granular material and an occasional filamentous structure, is more pronounced in asymmetrical, type I, synapses. The existence of postsynaptic density is dependent upon the presence of the presynaptic element: if the presynaptic structures degenerate, the postsynaptic density will eventually disappear. The postsynaptic element so contains cisternac of the smooth endoplasmic reticulum and the spine apparatus, which is composed of 2-3 flattened cisternac, separated by plaques of dense material.

The morphological appearances of synapses reflect the functional dynamics of neuro­transmission. Accordingly, in chemical synapses the vesicles contain quanta of the neurotransmitter which is discharged into the synaptic cleft after the vesicle has fused with the presynaptic membrane. Thus, the uptake of calcium into the nerve terminal triggers off a chain of events leading to exocytosis: vesicular apposition, membrane fusion and fission. Although this vesicular or exocytotic hypothesis of neurotransmission provides a plausible explanation for the quintal nature of transmitter release, an increasing body of evidence now suggests that this not be the only mechanism by which chemical signals in the central nervous system are propagated. Chemical substances may be released from non-synaptic axon terminals and even from regions of nerve cells other than presynaptic axon.

A parasynaptic system is envisaged in which so called neuroactive or informational substances reach specific target cell receptors by diffusion from release points through the extracellular space. The mechanism of exocytosis itself remains poorly understood not only morpho­logically, but also neurochemistry, and various alternative biochemical mechanisms have been considered to explain the release of neurotransmitters.