What cellular elements sprout

In conclusion, the origin of TH ve neurons observed in the SNpc must remain a matter of speculation. They are likely to be a fruitful area for further study, providing insights into the process of neuronal repair in the brain, as well as for the deployment of stem cells for the repair of the nigra. 

if not all, dopamine terminals in the striatum are newly formed when the CPu is re-innervated following an SNpc lesion and the ultrastructure of these terminals is altered, suggesting they may produce, store and release more dopamine than normal terminals (Finkelstein et al., 2000 Stanic et al., 2003a). These changes include increased terminal 

Most animals with small lesions and many with intermediate lesions turned left or have only a modest tendency to turn toward the side of the lesion (right side). Only animals with large lesions persist in turning toward the lesioned side. Thus amphetamine induced turning provides a functional measure of the degree to which regenerated dopamine terminals can release dopamine. Amphetamine induced rotation is therefore a better measure of the degree of functional reinnervation rather than the size of a lesion. 

As synaptic contacts are being reestablished, it is likely that the high-affinity DAT is down regulated to maintain dopamine concentrations in the synaptic cleft. With time, and as the number of contacts normalize, normal transport may also be restored. This however, requires a lengthy process and would not be completed in animals with extensive lesions, even after 16 weeks. Blanchard et al. (1996) observed growth cones entering the striatum seven months after partial lesions, suggesting that 12 months or more may be required for normalization of synaptic function (Blanchard et al., 1996). 

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Knockout mice in understanding basal ganglia function and sprouting 2.4. WHAT CELLULAR ELEMENTS SPROUT ... 

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