The presence of perforated synapses in the striatum after dopamine depletion, is this a sign of maladaptive brain plasticity?

Synaptic plasticity is the process by which long-lasting changes take place at synaptic connections. The phenomenon itself is complex and can involve many levels of organization. Some authors separate forms into adaptations that have positive or negative consequences for the individual. It has been...

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Bibliographic Details
Published in:Microscopy 2014-12, Vol.63 (6), p.427-435
Main Authors: Anaya-Martínez, Verónica, Gutierrez-Valdez, Ana Luisa, Ordoñez-Librado, Jose Luis, Montiel-Flores, Enrique, Sánchez-Betancourt, Javier, Sánchez Vázquez del Mercado, César, Reynoso-Erazo, Leonardo, Tron-Alvarez, Rocío, Avila-Costa, Maria Rosa
Format: Article
Language:English
Subjects:
Animals
Corpus Striatum - drug effects
Corpus Striatum - physiology
Corpus Striatum - ultrastructure
Dopamine - deficiency
Dopamine - physiology
Male
Microscopy, Electron
Neuronal Plasticity - physiology
Oxidopamine - pharmacology
Rats
Rats, Wistar
Synapses - drug effects
Synapses - physiology
Synapses - ultrastructure
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Summary:Synaptic plasticity is the process by which long-lasting changes take place at synaptic connections. The phenomenon itself is complex and can involve many levels of organization. Some authors separate forms into adaptations that have positive or negative consequences for the individual. It has been hypothesized that an increase in the number of synapses may represent a structural basis for the enduring expression of synaptic plasticity during some events that involve memory and learning; also, it has been suggested that perforated synapses increase in number after some diseases and experimental situations. The aim of this study was to analyze whether dopamine depletion induces changes in the synaptology of the corpus striatum of rats after the unilateral injection of 6-OHDA. The findings suggest that after the lesion, both contralateral and ipsilateral striata exhibit an increased length of the synaptic ending in ipsilateral (since third day) and contralateral striatum (since Day 20), loss of axospinous synapses in ipsilateral striatum and a significant increment in the number of perforated synapses, suggesting brain plasticity that might be deleterious for the spines, because this type of synaptic contacts are presumably excitatory, and in the absence of the modulatory effects of dopamine, the neuron could die through excitotoxic mechanisms. Thus, we can conclude that the presence of perforated synapses after striatal dopamine depletion might be a form of maladaptive synaptic plasticity.
ISSN:2050-5701
DOI:10.1093/jmicro/dfu032