摘要:

AbstractThe ontogeny of oligodendrocytes in the myelin deficient (md) rat mutant and in control rats was explored immunohistochemically using an antiserum against the oligodendrocyte specific enzyme, glycerol phosphate dehydrogenase (GPDH), and the avidin‐biotin complex technique. In control rats, GPDH was demonstrated to be expressed relatively early in oligodendrocyte differentiation, prior to either myelin basic protein or proteolipid protein expression. With development, oligodendrocytes containing GPDH increased in number, apparent staining intensity, cell soma area and process elaboration. Fewer GPDH+oligodendrocytes were observed in the brain of mutant rats than in unaffected littermates at all developmental ages, and major developmental increases in oligodendrocyte density were delayed. The density of GPDH+oligodendrocytes was reduced by about 40% in both the corpus callosum and in the cingulate cortex of P22–25 md mutants compared with control rats. The oligodendrocyte cell soma area was not influenced by the md condition, and increased 2‐fold with development in rats of both genotypes. The area of coronal sections occupied by the corpus callosum increased about 2.5‐fold with development, and was 30% smaller in mutant rats late in their lifespan than in unaffected littermates. The reductions in oligodendrocyte density reported here are of insufficient magnitude to fully account for biochemically measured reductions in oligodendrocyte gene expression accompanying the md trait, indicating that gene expression per oligodendrocyte is also impaired. Cell counts in control rats also revealed that oligodendrocytes are overproduced during development. Cell density and the total number of corpus callosum GPDH+oligodendrocytes per section were maximal at P22–25 and then decreased to adult values. These results suggest that glial cells, like neurons, may be generated in excessive numbers, and some subsequently die, as a normal concomitant of development.

ISSN:0736-5748    

DOI:10.1016/0736-5748(92)90013-P

出版商:Wiley    

年代:2003

数据来源: WILEY

摘要:

AbstractThe neurotransmitter serotonin has been shown to regulate neurite outgrowth in many embryonic and adultHelisomaneurons. To determine whether intracellular calcium concentration is also regulated by serotonin in large numbers of neurons, the calcium indicator Fura 2 was used to measure intracellular calcium in mass‐dissociated cultures of embryonic and adult neurons. Comparisons between embryonic and adult neurons revealed that embryonic neurons have a narrow population distribution of rest intracellular calcium levels around relatively low values. In contrast, the population distribution for adult neurons covered a much wider range of rest calcium concentrations. In both embryonic and adult cultures, serotonin induced a shift in the population distribution of calcium concentrations to higher levels, and increased the mean and median calcium concentrations. Analysis of individual adult neurons prior to and following the addition of serotonin revealed that approximately 50% of the neurons responded with an increase in calcium concentration. In contrast, there was no evidence of a serotonin‐induced decrease in calcium concentration in any neurons. Since the percentage of neurons responding to serotonin in this study is very similar to the percentage that responded in previous studies on neurite outgrowth, these data support the hypothesis that an increase in intracellular calcium is a common intermediate step in the regulation of neurite outgrowth by serotonin throughout theHelisomanervous system.

ISSN:0736-5748    

DOI:10.1016/0736-5748(92)90014-Q

出版商:Wiley    

年代:2003

数据来源: WILEY

摘要:

AbstractThe age‐dependent modifications of synaptosomal plasma membrane protein composition in three different rat brain regions (cerebral cortex, cerebellum and striatum) at various ages (4,12 and 24 months) were studied. The proteins were separated by gel‐electrophoresis and the quantity of the different polypeptides was determined densitometrically from the stained gels.In the three brain regions examined several age‐related modifications in the amount of the synaptosomal plasma membrane proteins were observed. In particular a significant decrease in the content of some synaptosomal plasma membrane proteins at 24 months of age was found. The agerelated modifications in the protein composition of synaptosomal plasma membrane may cause changes in many brain functions, such as neurotransmission, ionic transport and enzyme activities.Particularly interesting is the decrease of a protein with 18 kDa mol. wt. This protein has been identified as calmodulin by immunoblotting assay. The decrease in the amount of this protein may be correlated to the impairment of several Ca2+‐ requiring processes in the aging brain.

ISSN:0736-5748    

DOI:10.1016/0736-5748(92)90015-R

出版商:Wiley    

年代:2003

数据来源: WILEY

摘要:

AbstractVital staining and routine histological analyses of mouse embryos 12 h after acute maternal ethanol administration (2.9 g/kg) illustrated that selected neuronal cell populations are killed. At the time of treatment, embryos had 5–15 somite pairs, corresponding to the developmental stages occurring in humans during the fourth week of post‐fertilization; i.e. when neural folds are present and neural tube fusion begins. Affected cell populations in embryos having 6–26 somite pairs (up to the stage of anterior neuropore closure) were in discrete locations in the alar and basal plates of the rhombencephalon, in the otic placode/vesicle, and in the regions of the epibranchial placodes, olfactory placodes and trigeminal ganglion. The potential basis for the vulnerability of these cell populations to ethanol‐induced cell death is discussed. Our understanding of the scope of ethanol‐induced CNS damage is dependent upon further defining ethanol‐sensitive cell populations at all stages of CNS development.

ISSN:0736-5748    

DOI:10.1016/0736-5748(92)90016-S

出版商:Wiley    

年代:2003

数据来源: WILEY

摘要:

AbstractInsulin function in the nervous system is still poorly understood. Possible roles as a neuromodulator and as a growth factor have been proposed (Baskinet al., 1987,Ann. Rev. Physiol.49, 335–347). Stable cell lines may provide an appropriate experimental system for the analysis of insulin action on the various cellular components of the central nervous system.We report here a study to investigate the presence and the properties of insulin specific binding sites in the murine neuroblastoma line, N18TG2, together with insulin action on cell growth and metabolism. Also, receptor internalization has been studied. Binding experiments, carried out in standard conditions at 20°C, enabled us to demonstrate that these cells bind insulin in a specific manner, thus confirming previous findings on other cell lines. Saturation curves showed the presence of two binding sites with Kd 0.3 and 9.7 nM. Competition experiments with porcine and bovine insulin showed an IC50 of 1 and 10 nM, respectively. Competition did not occur in the presence of the unrelated hormones ACTH and FSH. Dissociation experiments indicated the existence of an internalization process of the ligandreceptor complex; this was confirmed by an ultrastructural study using gold conjugated insulin. As far as the insulin action in N18TG2 cells is concerned, physiological concentrations stimulate cell proliferation, whereas no stimulation of glucose uptake was observed, indicating that insulin action in these cells is not mediated by general metabolic effects.On the basis of these data, N18TG2 line appears to be a very suitable model for further studies of the neuronal type insulin receptors, and possibly insulin specific action on the nervous system.

ISSN:0736-5748    

DOI:10.1016/0736-5748(92)90017-T

出版商:Wiley    

年代:2003

数据来源: WILEY

摘要:

AbstractGlial hyaluronate‐binding protein (GHAP) and a large aggregating chondroitin sulfate proteoglycan (Ag‐Pg) similar to a fibroblast proteoglycan (versican) were localized in bovine, dog and cat central nervous system (CNS) gray matter by indirect immunofluorescence. The distribution of the two hyaluronate‐binding proteins was identical with that of hyaluronate, an extracellular glycosaminoglycan. All substances formed a finely reticulated mesh in the neuropil with a condensation of the stain around large neurons. It is concluded that in gray matter, as in white matter, the extracellular matrix (ECM) contains hyaluronate‐protein aggregates. We suggest that the hyaluronate‐protein aggregates correspond to the pericellular network first described by Golgi.

ISSN:0736-5748    

DOI:10.1016/0736-5748(92)90018-U

出版商:Wiley    

年代:2003

数据来源: WILEY

摘要:

AbstractLevels of dopamine and norepinephrine were measured in seven brain areas after 60 min of sustained seizure activity induced by intraperitoneal repetitive timed administrations of pentylenetetrazol in rats at 10, 14, 17 and 21 days of postnatal life. The tissue levels of norepinephrine were markedly reduced in the majority of brain structures, except for striatum at 10 and 14 days. Conversely, dopamine concentrations increased in many areas and at various ages, except in cerebral cortex at 10 and 14 days and in midbrain between 14 and 21 days. PTZ seizures induced marked increases over control levels in the rates of glucose utilization, measured by the quantitative autoradiographic [14C]2‐deoxyglucose method, in all dopamine‐ and norepinephrine‐innervated areas studied at 10 and 14 days, except in cerebellar cortex at both ages and in frontal cortex and anteroventral thalamus at 14 days. At 17 and 21 days, glucose utilization remained increased over control levels in some areas, mainly in catecholaminergic cell groupings such as substantia nigra, ventral tegmental area and locus coeruleus, but was significantly reduced in cortex, caudate nucleus and thalamus, and similar to control rates in other regions.The present results suggest that pentylenetetrazol‐induced seizures lead to a simultaneous increase in functional activity of norepinephrine neurons and an inhibition of dopaminergic‐mediated neurons. They also confirm the maturation of connections, of metabolic activity and of neurotransmitter interaction within the brain, occurring mainly during the third week of postnatal life, paralleled by an increased selective vulnerability of some regions to this kind of insult.

ISSN:0736-5748    

DOI:10.1016/0736-5748(92)90019-V

出版商:Wiley    

年代:2003

数据来源: WILEY

摘要:

AbstractKainic acid‐induced seizure activity in adult rats produces an impairment of long‐term potentiation induction in hippocampal slices. As the consequences of seizure activity are different in adult and juvenile rats, we tested the ability of hippocampal slices prepared from kainate‐treated juvenile rats to exhibit long‐term potentiation. Long‐term potentiation was induced by theta‐burst stimulation and was not significantly different in slices prepared from control or kainate‐injected juvenile rats (16–18 postnatal days). Short‐term potentiation, however, was reduced in the kainate‐treated juveniles. Calpain inhibitor I has been shown to prevent long‐term potentiation formation in adult hippocampal slices, and we evaluated its effect on long‐term potentiation in hippocampal slices from juvenile rats. Calpain inhibitor I produced a significant reduction in the degree of long‐term potentiation induced by theta‐burst stimulation in hippocampal slices prepared from 14–20 postnatal day‐old animals. The results are consistent with the notion that, although similar mechanisms participate in the formation of long‐term potentiation in juvenile and adult animals, juvenile animals are much more resistant than adult animals to the consequences of seizure activity.

ISSN:0736-5748    

DOI:10.1016/0736-5748(92)90020-Z

出版商:Wiley    

年代:2003

数据来源: WILEY

摘要:

AbstractIn vitroneuronal preparations are used to study the action mechanism of substances which are active in normal and pathological brain aging. One major concern within vitroassays is that the use of embryonic or adult neurons may hamper an appreciation of the relevance of these substances on aged nervous tissue. In the present study for the first time cultures of aged dorsal root ganglia from 24‐months‐old rats were maintainedin vitroup to 2 weeks. This model was used to investigate the neurotrophic/ neuroprotective action of nerve growth factor and acetyl‐l‐carnitine. A large population of aged dorsal root ganglia neurons was responsive to nerve growth factor (100 ng/ml). Nerve growth factor induced an increase of initial rate of axonal regeneration and influenced the survival time of these neurons. Acetyl‐l‐carnitine (250 μM) did not affect the axonal regeneration but substantially attenuated the rate of neuronal mortality. A significant difference was evident between the acetyl‐l‐carnitine‐treated and the untreated neurons from the first cell counting (day 3 in culture). After 2 weeks the number of aged neurons treated with acetyl‐l‐carnitine was almost double that of the controls. The effects of acetyl‐l‐carnitine on aged DRG neurons potentially explain the positive effects in clinical andin vivoexperimental studies.

ISSN:0736-5748    

DOI:10.1016/0736-5748(92)90021-Q

出版商:Wiley    

年代:2003

数据来源: WILEY

摘要:

AbstractSeveral ontogenetic studies performed in different species suggest a developmental role for 5‐HT neurons. The 5‐HT system interconnecting the CNS and the tentacular sensory organs in pulmonates is a suitable model for studying the postulated developmental role of 5‐HT neurons. In this paper we describe the behavior of the 5‐HT fibers during the early stages of blastema reinnervation, primordium formation and differentiation of regenerating tentacular sensory organs in the pulmonate snailCryptomphalus aspersa. Our results show that the regeneration process allows the development of a normal pattern of 5‐HT innervation of the regenerated sensory organs and suggest that 5‐HT could be involved in reciprocal developmental interactions with regenerating tentacular tissues.

ISSN:0736-5748    

DOI:10.1016/0736-5748(92)90022-R

出版商:Wiley    

年代:2003

数据来源: WILEY