摘要:

ALPHA-SYNUCLEIN has been implicated in the pathogenesis of Parkinsonsis disease. To investigate the role of α-synuclein in the brain, the cDNA clone encoding the mouse cognate of the human α-synuclein was isolated from a mouse brain cDNA library. The open reading frame coded for 140 amino acids that share 95% identity with human α-synuclein. Northern blot analysis showed that α-synuclein mRNA was primarily expressed in brain and spleen of adult mouse.In situ hybridizationhistochemistry revealed the highest expression of α-synuclein mRNA in the hippocampal formation and neocortex of the adult mouse. α-synuclein mRNA expression in the brain was first observed in the hippocampus and neocortex on postnatal day 1. Levels of α-synuclein mRNA in these forebrain areas were nearly maximal at postnatal day 7 and remained relatively high until the adult stage. α-synuclein mRNA was expressed in the liver transiently during embryogenesis.

ISSN:0959-4965    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

β-AMYLOID has been shown to be neurotoxicin vivoandin vitro. Free radical production and subsequent lipid oxidation after β-amyloid application have been observedin vitroand are considered to be factors that contribute to the neurotoxicity. Field recordings in the area CA1 for 3 weeks showed a dose-dependent effect on amplitude after intracerebroventricular (i.c.v.) injections of 1, 5 or 10 nmol β-amyloid (25–35). The nitric oxide synthase inhibitors 7-nitro indazole (30 mg/kg, i.p.) and 1-(2–trifluoromethylphenyl)imidazole (150 nmol, i.c.v.) which preferentially inhibit the neuronal isoform prevented this β-amyloid-induced decay of synaptic transmission. The protective effect of these inhibitors was reversed by L-arginine (200 mg/kg, i.p.). The results support the theory that nitric oxide production contributes to β-amyloid-induced neuronal degeneration or reduction of neurotransmission.

ISSN:0959-4965    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

THE effects of a traumatic neocortical lesion, induced by transcranial cold injury, on brain metabolism and gene expression were examined. The surrounding of the lesions was characterized by increased glucose and lactate levels without major disturbances of protein synthesis or energy state. A transient pH decrease by 0.4 units was noticed 1 h post-injury, which shifted towards alkaline values by 3 h. The metabolic disturbances did not differ between injured animals with spontaneous spreading depressions (SD,n= 14) and those without SD (n= 7). In SD animals,c-fosmRNA was strongly elevated in the injury-remote cortex, buthsp72 mRNA was not enhanced. Thus, in contrast to focal ischemia, the metabolic dysfunction around traumatic cortical lesions is not aggravated by SD.

ISSN:0959-4965    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

VOLTAGE-ACTIVATED Ca2+channels represent a major pathway of Ca2+entry into neurones. The regulation of the expression of functional Ca2+channels thus plays a central role in neuronal differentiation. To study the influence of afferent innervation on Ca2+current expression, we compared HVA Ca2+currents in two categories of cultured neocortical neurones that showed pronounced differences in synaptic innervation density. Neurones strongly innervated by a presynaptic explant had a two-fold greater HVA Ca2+current density than neurones not innervated by explant fibres. Chronic blockade of synaptic activity did not affect HVA Ca2+current density in innervated neurones. Our results thus suggest an activity-independent regulation of HVA Ca2+current expression by afferent innervation.

ISSN:0959-4965    

出版商:OVID    

年代:1998

数据来源: OVID

ISSN:0959-4965    

出版商:OVID    

年代:1998

数据来源: OVID