Synapses on dendritic shafts exhibit a perforated postsynaptic density

doi:10.1016/0006-8993(87)90943-7

Brain Research

Volume 422, Issue 2, 6 October 1987, Pages 352-356

https://doi.org/10.1016/0006-8993(87)90943-7 Get rights and content

Abstract

Synapses on dendritic shafts were examined in electron micrographs of serial sections obtained from the molecular layer of the rat dentage gyrus. Some of these synapses have been found to exhibit profiles of a discontinuous postsynaptic density (PSD). PSD reconstructions from serial sections were performed in a plane perpendicular to that of the sections. The results obtained indicate that profiles of discontinuous PSDs observed in random sections of dendritic shaft synapses are generated by sectioning of PSD plates that contain 1–3 holes or perforations. Earlier serial studies of osmicated material have demonstrated that a proportion of axospinous synapses also exhibit a perforated PSD. It appears, therefore, that the presence of PSD perforations is a general phenomenon shared by subpopulations of different types of synapses, both those involving dendritic shafts and those involving dendritic spines.

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Citation Excerpt :
In the central nervous system, the majority of excitatory synapses are formed on dendritic spines (Gray, 1959; Yuste and Bonhoeffer, 2001; Muller et al., 2002). Asymmetric synapses can be further divided into perforated and non-perforated synapses based on the configuration of the PSD (Geinisman et al., 1987; Jones et al., 1991). Perforated synapses have a discontinuity or perforation in the PSD, whereas non-perforated synapses have continuous PSD profiles.
Synapses are essential to neuronal functions. Synaptic changes occur under physiological and pathological conditions. Here we report the remodeling of synapses in the CA1 area of the hippocampus after transient global ischemia using electron microscopy. Much electron-dense material appeared in the cytoplasm of dendrites at 24 h after ischemia. Many dark axons or terminals were found in the CA1 neuropil; some of which were phagocytized by dendrites. Interestingly autophagosomes appeared in many axons or dendrites at 48 h after ischemia. In addition, postsynaptic density (PSD) – like structures or synaptic – like structures were found inside spines and dendrites. Statistical analysis demonstrated that the thickness of PSDs in the CA1 neuropil increased from 12 to 48 h after ischemia. The frequency of autophagosomes appeared to escalate from 12 to 48 h after ischemia. The frequency of asymmetric synapses was significantly increased at 12 h and 24 h after ischemia in stratum oriens, proximal and distal stratum radiatum. Among asymmetric synapses, the number of perforated synapses consistently increased and reached a peak (approximately 10-fold increase) at 48 h after ischemia. On the other hand, the number of multiple synaptic boutons decreased after ischemia reaching a two to fourfold decrease at 48 h after ischemia. These results have shown that ischemia induces an increase of asymmetric synapses as well as synaptic autophagy, which may contribute to the neuronal death in the CA1 area after transient global ischemia.
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Synapses on dendritic shafts exhibit a perforated postsynaptic density

Abstract

Brain Research

Dev. Brain Res.

Brain Research

A serial-section study of perforated synapses in rat neocortex

Cell Tissue Res.

Plasticity in the central nervous system: do synapses divide?

Form of the postsynaptic density. Serial section study

J. Cell Biol.

Loss of perforated synapses in the dentate gyrus: morphological substrate of memory deficit in aged rats