PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 6153279

A new hypothesis for synaptic modification: an interactive process between postsynaptic competition and presynaptic regulation.

Y Hirai
View original source ↗Export metadata ↓

Abstract

Based on recent physiological observations, a new hypothesis for the algorithm for synaptic modification is proposed: an interactive process between postsynaptic competition and presynaptic regulation controls the synaptic modification, and both functions obey the same competitive rule. A fundamental algorithm for the competitive rule is proposed and analysed. The interactive process is deomposed into two procedures. The first one is a postsynaptic competition, in which all synapses making contact with the same postsynaptic cell compete for their terminal sites, and the postsynaptic cell makes demands for synaptic modification upon the presynaptic cells. The second one is a presynaptic regulation, in which the presynaptic cell regulates the postsynaptic demands and determines the net amount of the modification for each snyapse originating from it. The performance of the alforithm has been simulated on a digital computer. The initial structure of the simulated neural network consists of randomly-connected presynaptic and postsynaptic cells, with no other structures assumed. After repetitive presentations of a uniform stimulus, the basic configurations of neural connections (one-to-one, one-to-many, many-to-one and many-to-many connections) are organized in dependence on the parameters of the algorithm.

Explore related subjects

Axonal TransportAxonsHumansModels, NeurologicalNerve NetSynapsesSynaptic TransmissionJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Y Hirai. 1980. A new hypothesis for synaptic modification: an interactive process between postsynaptic competition and presynaptic regulation.. https://doi.org/10.1007/bf00337021

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1995

Retinal distortion and cotton-wool spots associated with epiretinal membrane contraction.

PURPOSE AND BACKGROUND: Several articles on surgery for macular pucker have noted the presence of intraretinal white spots, presumably cotton-wool spots, associated with epiretinal membranes. It was proposed that membrane contraction and resultant nerve fiber layer distortion might lead to blockage of axoplasmic flow and thus a cotton-wool spot. To see whether the observations supported this concept, the authors studied patients with epiretinal membranes associated with intraretinal white spots involving the center of the fovea, where there are normally no retinal vessels and the only axons are in Henle fiber layer. METHODS: Four patients with epiretinal membranes associated with prominent areas of intraretinal whitening involving the center of the fovea were examined before and after surgery. Observations and measurements were made from projected fundus photographs. RESULTS: The intraretinal white spots, which appeared preoperatively to lie in the center of the fovea, proved to have been pulled in from more peripheral retina by the epiretinal membrane. These white areas were associated with surprisingly great distortion of the inner retina. Stretching of the inner retina seemed to play a larger role in the retinal distortion than full-thickness retinal folding. CONCLUSION: The appearance and time course of these intraretinal white lesions were consistent with cotton-wool spots caused by mechanical disruption of axonal flow. The marked retinal stretching and distortion of the innermost layers of the retina were the most striking findings in this study and also seemed consistent with the concept that membrane contraction and resultant nerve fiber layer distortion might lead to blockage of axoplasmic flow and thus a cotton-wool spot.

Axonal Transport↗
PubMed1995

Are the pathobiological changes evoked by traumatic brain injury immediate and irreversible?

Traumatic brain injury has long been thought to evoke immediate and irreversible damage to the brain parenchyma and its intrinsic vasculature. In this review, we call into question the correctness of this assumption by citing two traumatically related brain parenchymal abnormalities that are the result of a progressive, traumatically induced perturbation. In this context, we first consider the pathogenesis of traumatically induced axonal damage to show that it is not the immediate consequence of traumatic tissue tearing. Rather, we illustrate that it is a delayed consequence of complex axolemmal and/or cytoskeletal changes evoked by the traumatic episode which then lead to cytoskeletal collapse and impairment of axoplasmic transport, ultimately progressing to axonal swelling and disconnection. Second, we consider the traumatized brain's increased neuronal sensitivity to secondary ischemic insult by showing that even after mild traumatic brain injury, CA1 neuronal cell loss can be precipitated by the induction of sublethal ischemic insult within 24 hrs of injury. In demonstrating this increased sensitivity to secondary insult, evidence is provided that it is triggered by the neurotransmitter storm evoked by traumatic brain injury, allowing for sublethal neuro-excitation. In relation to this phenomenon, the protective effect of receptor antagonists are discussed, as well as the concept that this relatively prolonged posttraumatic brain hypersensitivity offers a potential window for therapeutic intervention. Collectively, it is felt that both examples of the brain parenchyma's response to traumatic brain injury show that the resulting pathobiology is much more complex and progressive than previously envisioned, and as such, rejects many of the previous beliefs regarding the pathobiology of traumatic brain injury.

Axonal Transport↗