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Figure 12 Lesion volume and neuronal cell counts in quinolinic acid-lesioned rats. Control-implanted animals displayed a marked lesion volume (a, determined by Nissl staining) and a significant loss of multiple types of striatal cell types, including cholinergic (b), GABAergic (c), and diaphorase-positive neurons (d). The cholinergic and GABAergic neuronal losses were largely prevented in animals receiving CNTF implants, whereas the loss of diaphorase-positive neurons was not affected. In each case, data are presented as a percent loss of neurons on the lesioned/implanted side compared with intact contralateral side. Representative photomicrographs for cholinergic and GABAergic cells are shown for both control and CNTF-implanted animals. Note the appearance of numerous healthy appearing cholinergic and GABAergic neurons in the CNTF-treated animals. Scale bar in ChAT control is 500 um for ChAT control/CNTF, and scale bar in insert is 100 um for GAD control/CNTF and 17 um for insert [see (97) for additional details].

Figure 12 Lesion volume and neuronal cell counts in quinolinic acid-lesioned rats. Control-implanted animals displayed a marked lesion volume (a, determined by Nissl staining) and a significant loss of multiple types of striatal cell types, including cholinergic (b), GABAergic (c), and diaphorase-positive neurons (d). The cholinergic and GABAergic neuronal losses were largely prevented in animals receiving CNTF implants, whereas the loss of diaphorase-positive neurons was not affected. In each case, data are presented as a percent loss of neurons on the lesioned/implanted side compared with intact contralateral side. Representative photomicrographs for cholinergic and GABAergic cells are shown for both control and CNTF-implanted animals. Note the appearance of numerous healthy appearing cholinergic and GABAergic neurons in the CNTF-treated animals. Scale bar in ChAT control is 500 um for ChAT control/CNTF, and scale bar in insert is 100 um for GAD control/CNTF and 17 um for insert [see (97) for additional details].

the efficacy of this experimental therapeutic strategy (101). The complete lack of neuroprotection provided by intraven-tricular implants in monkeys should be considered more carefully in the ongoing clinical trials (38). If human trials are to yield clinically relevant positive effects, the means of CNTF delivery used in these studies needs to be improved. Whether this entails changing the site of implantation from the ventricle to the parenchyma, grafting more capsules, enhancing the CNTF delivery from the cells by changing the vector system or cell type employed, or changing the characteristics of the polymer membrane remains to be determined.

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