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focused on the development and plasticity of the nigrostriatal pathway (Murrin and Ferrer
1984; Voom et al., 1988; Weihmuller and Bruno 1989; Zigmond and Striker 1989).
Figure 8. Electron micrograph from the striatum neuropil. At the center of the micrograph lies a typical
dendritic spine, which contains an evident spine apparatus (*) receiving three synaptic contacts: two
asymmetric, probably glutamatergic (arrows) on the head of the spine (Sh) and one symmetric (arrow
head), probably dopaminergic (DA) with the neck of the spine (Sn). Along the micrograph it can be
distinguish various synaptic contacts between presynaptic buttons (B) establishing asymmetric contacts
(arrow) with the head of a dendritic spine (Sh) and two more symmetric (arrow heads) with dendrites
(D).
There have been relatively few studies on ultrastructural changes within the striatum
following dopamine (DA) deafferentation. Ingham et al. (1991) first reported that the size of
enkephalin-immunoreactive terminals and length of the synaptic specialization was larger up
to 13 months post-lesion. They later reported that there was also an increase in the length of
the synaptic specialization associated with asymmetric synapses (Ingham et al., 1993). This
later observation would suggest changes in striatal glutamate synapses.
Although this anatomical configuration suggests that DA has a direct modulatory effect
on cortical signaling (Arbuthnott et al., 1998), the role of DA in presynaptic modification of
corticostriatal afferents has been controversial because of the extraordinary complexity of
MSN innervation (Akopian and Walsh, 2002) and the challenges inherent in using
postsynaptic recordings to determine alterations in presynaptic activity (Van der Kloot, 1991;
Sulzer and Pothos, 2000; Reynolds and Wickens, 2002). Electron microscopy (Fisher et al.,
1994; Sesack et al., 1994; Wang and Pickel, 2002) and electrophysiology (Calabresi et al.,
1993; O'Donnell and Grace, 1994; Hsu et al., 1995; Flores-Hernandez et al., 1997; Cepeda et
al., 2001; Tang et al., 2001; West and Grace, 2002; Bamford et al., 2004) studies, however,
have supported the concept that DA directly regulates glutamate release from corticostriatal
terminals by stimulating D2 receptors located on a subpopulation of cortical afferents,
