Brain Res 106:223–240Ĭhang HT, Wilson CJ, Kitai ST (1982) A Golgi study of rat neostriatal neurons: light microscopic analysis. Nature 347:768–770īutcher LL, Hodge GK (1976) Postnatal development of acetylcholinesterase in the caudate-putamen nucleus and substantia nigra of rats. Synapse 3:38–47īredt DS, Hwang PM, Snyder SH (1990) Localization of nitric oxide synthase indicating a neural role for nitric oxide. Brain Res 300:376–380īeal MF, Kowall NW, Swartz KJ, Ferrante RJ, Martin JB (1989) Differential sparing of somatostatin-neuropeptide Y and cholinergic neurons following striatal excitotoxin lesions. J Cell Biochem 27:415–422Īronin N, DiFiglia M, Graveland GA, Schwartz WJ, Wu JY (1984) Localization of immunoreactive enkephalins in GABA synthesizing neurons of the rat neostriatum. Brain Res 459:205–225Īrentsen R, Baldini F Jr, Davis LG, Higgins GA, Lin Y, Manning RW, Wolfson B (1985) In situ hybridization of putative somatostatin mRNA within hypothalamus of the cat using synthetic oligonucleotide probes. Trends Neurosci 12:366–375Īoki C, Pickel VM (1988) Neuropeptide Y-containing neurons in the rat striatum: ultrastructure and cellular relations with tyrosine hydroxylase-containing terminals and with astrocytes. Anat Rec 94:239–247Īlbin RL, Young AB, Penney JB (1989) The functional anatomy of basal ganglia disorders. The peptides are also suggested to be differentially regulated at the level of transcription because the number of somatostatin mRNA-containing neurons increased significantly in the slice cultures compared with in vivo, while the number of neuropetide Y mRNA-containing neurons was unchanged.Ībercrombie M (1946) Estimation of the nuclear population from microtome sections. From the finding that the number of neuropeptide Y mRNA-containing neurons both in vitro and in vivo was significantly higher than the number of neuropeptide Y-immunoreactive neurons - unlike the number of somatostatin mRNA containing neurons - it is suggested that somatostatin and neuropeptide Y are differentially regulated at the level of translation. The relative loss of projection neurons and preservation of interneurons in single slice cultures of striatal tissue apparently mimick some of the neurodegenerative changes of Huntington's disease. In contrast, the enkephalin mRNA-containing neurons, which in vivo are projection neurons, were significantly fewer in the cultures. Comparison of cell numbers per unit volume showed that, in the cultures, the number of presumed interneurons, with the exception of NPY mRNA-containing neurons, significantly exceeded that in vivo.
This implies that the mutual distribution of presumed interneurons and projection neurons was preserved in the slice cultures. Both in the slice cultures and in the brain, the number of enkephalin mRNA-containing neurons significantly exceeded that of neuropeptide Y- and somatostatin mRNA-containing neurons. From quantitative estimates we found the same mutual rank order of the numbers of neuropeptide Y- and somatostatin-immunoreactive neurons and NADPH-diaphorase positive neurons in vivo and in vitro. This pattern may represent an intermediate stage between the patch-matrix distribution in the newborn and the homogeneous staining in the adult rat striatum. In the striatal slices the distribution of the NADPH-diaphorase staining stayed uneven after 3–5 weeks in culture, with areas almost devoid of staining alternating with more heavily stained areas. In the newborn rats, included as controls, a patch-matrix distribution of the NADPH-diaphorase staining is described for the first time. Similar basic morphologies of the presumed interneurons and double staining of NADPH-diaphorase positive and somatostatin immunoreactive neurons suggest that the two neuropeptides and NADPH-diaphorase are extensively colocalized in the cultures, as in vivo. We focused on (1) the medium-sized, aspiny interneurons, which in vivo express the neuropeptides somatostatin and neuropeptide Y and the nitric oxide synthesizing enzyme nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase, and which are spared in Huntington's disease and (2) the enkephalinergic, medium-sized projection neurons, which are particularly vulnerable in Huntington's disease. The presence of specific cell markers was shown by immunocytochemistry, histochemistry and in situ hybridization with alkaline-phosphatase-labeled oligonucleotide probes. The striatal cultures were grown for 12–39 days in the absence of any other brain tissue. In order to establish an in vitro model of Huntington's disease, we prepared slice cultures of striatal tissue from newborn rats.
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