Tyrosine hydroxylase (TH)-immunoreactive (ir) neurones are detected in the striatum of animals after dopamine depletion and also in human parkinsonian patients. Although there is extensive evidence for TH-ir neurones in the lesioned rodent striatum, there are few details regarding the molecular phenotype of these neurones, regulation of their TH expression after l-3,4-dihydroxyphenylalanine (L-DOPA) treatment and their function. In the present study, we examined the time-course of appearance of TH-ir neurones in the mouse striatum after 6-hydroxydopamine (6-OHDA) lesion and determined their molecular phenotype. We found that TH-ir neurones appeared in the striatum as early as 3 days after a 6-OHDA lesion. By 1 week after the lesion, the number of TH-ir neurones started to decrease and this decrease progressed significantly over time. Treatment with L-DOPA increased both the number of TH-ir neurones and the intensity of their immunolabelling. The TH-ir neurones that appear after the 6-OHDA lesion in the striatum are not newly generated cells as they did not incorporate 5-bromo-2-deoxyuridine. We found that the vast majority of TH-ir neurones colocalized with dynorphin and enkephalin, suggesting that they are projection neurones of the direct and indirect striatal output pathways. TH-ir neurones did not express the dopamine transporter but half of them expressed amino acid decarboxylase, an enzyme required for dopamine synthesis. Finally, striatal TH-ir neurones are functionally active, expressing the neuronal activation marker FosB in response to L-DOPA treatment. Promotion of these striatal TH-ir neurones may be beneficial in Parkinson's disease, particularly in the early stages when dopamine denervation is incomplete.

Object. The results of olfactory ensheathing cell (OEC) transplantation have raised great expectations as a potential treatment for spinal cord injury (SCI). Its capacity to promote functional neural repair, however, remains unclear. The authors studied axonal growth and locomotor recovery after C-7 contusion injury and OEC transplantation in adult rats. Methods. Twenty-four male Wistar rats underwent a mild C-7 contusion injury that completely disrupted the dorsal corticospinal tract (DCST). In 14 rats OECs were transplanted into the lesion, and 10 were used as controls. At 3 months postcontusion, the kinematics of locomotion were assessed, and the CST was traced by injecting dextran tetramethylrhodamine bilaterally into the cerebral cortex. The animals were killed 2 weeks after tracer injection, and their spinal cords were studied immunohistochemically. Although the survival of transplanted cells varied, they were present in all cases. The authors observed neither OEC migration nor DCST axon regeneration in any of the cell transplant—treated rats. Corticospinal axons ended in retraction bulbs at the proximal edge of the lesion or, exceptionally, a few micrometers inside the transplant. The results of neurofilament immunohistochemical analysis provided evidence of neurites from systems other than the DCST growing into the transplant, but in some cases these neurites formed loops of pathological appearance. Contusion injury of C-7 caused chronic locomotor deficits that did not improve after OEC transplants. Conclusions. The findings in this study indicate that OEC transplants alone are not sufficient for neural repair and functional recovery after SCI. In addition, OECs can induce abnormal axonal growth, making further studies necessary before considering their clinical use.