Biology Reference
In-Depth Information
Perforated synapses
The ipsilateral lesioned striatum exhibits a prominent increase in perforated synaptic
contacts from the 4th to the 120th day. Similar changes were distinguished in the contralateral
striatum from the 60th day after the lesion (figures 10D and 11-4). In contrast, the sham
lesioned striatum displayed a continuous discrete number of perforated synaptic contacts
(figure 10D).
The ultrastructural analysis of the ipsilateral and contralateral striatum neuropil
throughout the different stages of evolution after 6-OHDA lesion of the SNc of rats revealed
that this neurotoxin rapidly induces an important, and time dependent derangement of the
ipsilateral striatum neuropil, characterized by synaptic ending edema, alterations in the
postsynaptic target, and changes in the number of perforated synaptic contacts.
The contralateral striatum also exhibited statistically significant alterations in almost all
of the criteria evaluated in this study, however, not as dramatic as those observed in the
ipsilateral striatum.
Diameters of synaptic endings
The present analysis confirms previous observations referring to the fact that the
dopamine depletion of the nigrostriatal pathway induces cell alterations between 48-72 hrs
after the lesion (Zuch et al., 2000) and causes an increment in the size of the presynaptic
profile (Ingham et al., 1991; Pickel et al., 1992). We assume that this swelling is due to an
inherent degenerative process caused by 6-OHDA lesion; it seems that this nigrostriatal
denervation triggers a widely distributed edematous response in almost all striatum synaptic
endings. These observations are also confirmed with the analysis of the caudate nucleus
neuropil of PD patients (Machado-Salas et al., 1989; Zaja-Milatovic et al., 2005).
Postsynaptic target
It is known from previous ultrastructural studies that spines of medium-sized spiny
neurons receive mainly axospinous synaptic contacts (Bolam et al., 2000; Solis et al., 2007).
In accordance with other authors (Ingham et al., 1991; Pickel et al., 1992), we found that the
proportion of axospinous synapses was significantly reduced in the ipsilateral striatum of the
6-OHDA lesioned rats in all postlesion intervals. These findings are also confirmed by the
observations reported in PD patients (McNeill et al., 1988; Machado-Salas et al., 1989; Zaja-
Milatovic et al., 2005), where the synaptic contacts were predominantly of the axodendritic
type. It is established that the dopaminergic input to the striatum originates in the SNc.
Therefore, 6-OHDA lesion of the nigrostriatal pathway provokes a decrement of
dopaminergic axons and there upon of the dopaminergic buttons establishing synaptic contact
with the spines of the MSN of the striatum. The strongly lateralized effect of loss of the
axospinous synaptic contacts is explained in terms of the predominant ipsilateral projection of
the SN fibers (Yung et al., 1996). Ingham et al. (1998) suggest that the loss of spines may be
a random process. This would imply that dopamine subserves a neurotrophic function and
could play a role in the maintenance of spines (Arbuthnott et al., 2000). Indeed, the
