Submicroscopic Changes of the Synapse After Nerve Section in the Acoustic Ganglion of the Guinea Pig. An Electron Microscope Study

Abstract

The degenerative changes of the synaptic regions after nerve section have been studied with the electron microscope in the interneuronal synapse of the ventral ganglion of the acoustic nerve of the guinea pig. Fixation with buffered osmic tetroxide was carried out 22, 44, and 48 hours after destruction of the cochlea on one side; the contralateral ganglion being used as control. The submicroscopic organization of normal axosomatic and axodendritic synapses is described. In the synaptic ending four morphological components are recognized: the membrane, the mitochondria, the synaptic vesicles (19, 20), and the cytoplasmic matrix. The intimate contact of glial processes with the endings and with the surface of the nerve cell is described. At the level of the synaptic junction there is a direct contact of the limiting membranes of the ending and of the cell body or dendrite. Both contacting membranes constitute the synaptic one with a total thickness of about 250 A. This membrane has regions of higher electron density where the synaptic vesicles come into intimate contact and fuse with it. Definite degenerative submicroscopic changes in the nerve endings were observed after 22 hours of destruction of the cochlea and were much more conspicuous after 44 and 48 hours. After 22 hours there is swelling of the ending and decreased electron density of the matrix. Most synaptic vesicles have disappeared or seem to undergo a process of clumping and dissolution. Some mitochondria also show signs of degeneration. After 44 hours the synaptic vesicles have practically disappeared; mitochondria are in different stages of lysis; the membrane of the ending becomes irregular in shape, and there is shrinkage and in some cases detachment of the ending. No changes in the postsynaptic cytoplasm were observed. These observations and particularly the rapid lysis of the synaptic vesicles are discussed in correlation with data from the literature indicating the early alteration of synaptic function and the biochemical changes occurring after section of the afferent nerve. The hypothesis that the synaptic vesicles may be carriers of acetylcholine or other active substances (19, 20) and that they may act as biochemical units in synaptic transmission is also discussed.2

Effects of cannabis sativa on ultrastructure of the synapse in monkey brain

“…Clumping of synaptic vesicles similar to that reported herein has been described subsequent to axonal sectioning by numerous investigators (De Robertis, 1956;Blackstad et al, 1965;Colonnier, 1964). Aggregation of vesicles is also produced by ischemia (Williams and Grossman, 1970) and by experimental allergic encephalomyelitis (Ross and Bornstein, 1969), as well as by toxins (triorthocresylphosphate and methionine sulfoximine -De Robertis et al, 1967b) and certain neuropathies (Alzheimer's disease - Gonatas et al, 1967).…”

The time courses of excitatory and inhibitory synaptic actions

“…Since the synaptic cleft between the presynaptic and subsynaptic membranes is now known to be only about 200 A, across (Palay, 1956;de Robertis, 1956), it might be supposed that a considerable time would be occupied in the clearing of this cleft by the outward diffusion of transmitter substance, and hence that the prolonged residuum of synaptic transmitter is satisfactorily accounted for. However, if the synaptic cleft is reasonably clear of diffusional barriers, and the transmitter molecules have a diffusion coefficient approximating to that of acetylcholine, it can be shown that synaptic clefts under synaptic knobs one or two microns in diameter are cleared by diffusion within a fraction of a millisecond (Eccles & Jaeger, 1958 (Eccles et at.…”

An emerging view of presynaptic structure from electron microscopic studies

“…This technique also allowed the discovery of synaptic vesicles (SVs), the clear vesicular structures of about 40 nm in diameter, accumulated at presynaptic terminals (De Robertis and Bennett 1954; Palade and Palay 1954). Synaptic vesicles were rapidly hypothesized to be containers for neurotransmitter quanta discovered during the same period (Del Castillo and Katz 1954, 1955; De Robertis and Bennett 1955; De Robertis 1956; Palay 1956; Robertson 1956). Some of the SVs are apposed (‘docked’) to the presynaptic plasma membrane at an area called the active zone (AZ; Palay 1956; Birks et al.…”