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spines. This close anatomical localization of these two types of synapses suggests that
dopamine released from the nigrostriatal afferent terminals may have modulatory effects
on the excitatory signals generated from the cortex.
The importance of dopamine in normal striatal function is evidenced by the severe
disruption of behavior observed in Parkinson's disease and after chemical lesions of
nigral dopaminergic inputs to striatum. In recent years attention has been focused on
perforated synapses considering their possible involvement in synaptic plasticity in the
nervous system. 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 experimental situations. The aim of this chapter
was to analyze whether the dopamine depletion produces 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 present 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 excitatory, and in the
absence of the modulatory effects of dopamine, the neuron could die by excitotoxic
mechanisms. Thus, we can conclude that the presence of perforated synapses after striatal
dopamine depletion might be a form of negative synaptic plasticity.
I NTRODUCTION
Brain plasticity refers to the lifelong capacity for physical and functional brain change
enjoyed by humans and other animals and is inherently bidirectional: through the same
mechanisms and plasticity processes, brain function can either be strengthened or degraded,
depending on the circumstances. During normal aging, individuals typically undergo
physical, behavioral, and environmental changes that, in the aggregate, promote negative
plastic changes that degrade brain function. These root causes of functional decline involve a
complex interplay of physical brain deterioration, behavioral and environmental changes, and
brain plasticity processes (Mahncke et al., 2006).
One of the greatest challenges in neuroscience is understanding how the nervous system
acquires, stores, and utilizes information derived from the sensory world. With the
establishment of the “neuron doctrine” by Cajal (1894), which stated that the nervous system
is made up of discrete units (neurons), neuroscientists including Cajal proposed that
modifications might occur in the interaction between neurons. They suggested that certain
neuronal modifications might underlie developmental processes as well as processes
underlying learning and memory (Chen and Tonegawa, 1997).
In 1949, Hebb proposed a well-defined rule of synaptic plasticity: Coincident activity in
two connected neurons leads to strengthening of their connection. Hebb further postulated
that associative learning could be based on this synaptic modification. Today we know that
synaptic plasticity is expressed in many forms. Thus, Hebb's coincident rule can be applied
only to some forms of synaptic plasticity. Yet the notion that neural activity leads to synaptic
1 Laboratorio de Neuromorfología, UNAM FES Iztacala.Av. de los Barrios # 1 Los Reyes Iztacala. C.P. 54090
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