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

Abstract Synaptic plasticity is the process by which long-lasting changes take place at synapticconnections. The phenomenon itself is complex and can involve many levels of organiza-tion. Some authors separate forms into adaptations that have positive or negative conse-quences for the individual. It has been hypothesized that an increase in the number ofsynapses may represent a structural basis for the enduring expression of synaptic plasti-city during some events that involve memory and learning; also, it has been suggestedthat perforated synapses increase in number after some diseases and experimental situa-tions. The aim of this study was to analyze whether dopamine depletion induces changesin 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 exhibitan increased length of the synaptic ending in ipsilateral (since third day) and contralateralstriatum (since Day 20), loss of axospinous synapses in ipsilateral striatum and a signifi-cant increment in the number of perforated synapses, suggesting brain plasticity thatmightbe deleterious for thespines, becausethistypeofsynapticcontacts arepresumablyexcitatory, and in the absence of the modulatory effects of dopamine, the neuron coulddie through excitotoxic mechanisms. Thus, we can conclude that the presence of perfo-rated synapses after striatal dopamine depletion might be a form of maladaptive synapticplasticity.