We have examined the development of rat striatum for evidence of cells dying in the process of physiological cell death. In present study we have indicated apoptotic cells in sections stained with cresyl violet (cell death characterized by pyknosis) or with DNA end labeling assay (TUNEL method). Our results demonstrated that cell loss during maturation of the rat striatum had the characteristics of apoptosis rather than necrosis. The greatest number of TUNEL - positive and pyknotic cells in the striatum were found during the first postnatal days; after 7th day of postnatal life a rapid decrease of its number was observed. After the second postnatal week no TUNEL-positive cells were observed in the striatum. Our analysis suggests that apoptotic cell death occurring during the development of striatal neuronal population takes place during the first week of postnatal life.
Two hundred fifty five medial prefrontal cortical (MPFC) and 187 caudate-putamen (CPu) sites were evaluated for intracranial self-stimulation in 67 animals using moveable electrodes and collecting trade-off functions between current and frequency. Eleven percent of the examined areas, located predominantly in the ventromedial aspects of MPFC and CPu, showed reliable self-stimulation and the average charge of 1.12 and 1.11 muC respectively, values that are in line with those reported for the Medial forebrain bundle. The distribution of charge, however, was greater than reported for the latter region, and ranged between 0.68 to 1.63 muC across sites. Some subjects were implanted with two electrodes, one aimed at the MPFC, and the other at the CPu, ventral tegmental area, or lateral hypothalamus. Only animals with CPu placements showed transference of self-stimulation to the MPFC, suggesting that these two regions might form part of the same reward substrate, a view that has anatomical, electrophysiological and recently behavioral support.
Using superfusion with albumin-containing medium of hippocampal and striatal slices of adult and developingrats at postnatal days(PND) 7-10, prelabelled with [3H]arachidonic acid ([3H]AA) we detected N-methyl-D-aspartate (NMDA) evoked release to the superfusion medium of radiolabelld material, 70% of which was associated with arachidonic acid (AA) and its metabolite.[3H[AA release was much more pronounced in PND 7-10 rats than in adults, and the response to NMDA in the hippocampal slices exceed the reactions in the striatal slices.The subsequent experiments, emplyoing only hippocampal slices of PND 7-10 rats, demonstrated that NMDA-stimulated [3H]AA release was dose-depended in the micromolar range,was sensitive to NMDA receptor antagonists, and wasinhibited in calcium-free medium and the presence of quinacrine.[3H]AA release induced by 100 ?M NMDA was not significantly inhibited by magnesium but was completly blocked by 7 Cl-kynurenic acid and ifenprodil (both antagonists 100 ?M).The sulfhydryl reducing reagent dithiothreitol induced [3H]AA release; this response was sensitive to NMDA receptor antagonists.These data indicate that the NMDA induced, calcium triggered, and phospholipides A2 depended AA release is highly pronounced in the developing rat hippocampus.NMDA receptors mediating AA release in the hippocampus of PND 7-10 rats are subject to glycine, polyamine and redox modulationn, but they show low sensitivity to Mg2+ inhibition.
Hepatic encephalopathy (HE) is characterized by motor symptoms associated with disturbed functions of the dopaminergic systems, but the underlying mechanisms are not clear. A previous study from our laboratories revealed that HE, induced in rats by repeated treatment with thioacetamide, enhanced the 50 mM potassium (KCl) -stimulated release of newly loaded [3H]dopamine in both striatal and frontal cerebral cortical slices in the presence of Ca2+. In the present study we compared the effects of HE on dopamine release in striatal and frontal cerebral cortical slices and synaptosomes in the presence and absence of Ca2+. HE enhanced the KCl-stimulated [3H]dopamine release from striatal and frontal cortical synaptosomes in the presence of Ca2+ to the same extent as in slices prepared from the respective brain regions. In the absence of Ca2+ a slight reduction in dopamine release was observed in frontal cortical synaptosomes from HE rats when compared to control rats, while no effect of HE on the release was discernible in frontal cortical and striatal slices and striatal synaptosomes. We conclude that in both brain regions studied HE stimulates dopamine exocytosis triggered by Ca2+ influx without affecting the release mediated by means of plasma membrane transporters or exocytosis involving intraterminal Ca2+.
Classical (chlorpromazine, haloperidol) and atypical (sulpiride and clozapine) neuroleptics applied for a period of 2 weeks diminished neuropeptide Y (NPY) levels in nucleus accumbens, but not in striatum. These changes were correlated with NPY mRNA level. However, the effect of these neuroleptics on the level of NPY in hypothalamus was different. It is suggested that changes in NPY levels caused by neuroleptics are mediated by dopaminergic D1/D2 receptors.
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