Showing papers in "Experimental Neurology in 1993"

TL;DR: Data from in situ hybridization and intraocular transplantation support the concept that GDNF functions as a dopaminotrophic factor in vivo.

TL;DR: The results suggest blood-borne macromolecules, including those of the immune and complement systems, have potential widespread, extracellular distribution within the CNS and cerebrospinal fluid from sites deficient in a BBB.

TL;DR: A series of sensitive quantitative methods to assess the recovery of locomotor function in rats are designed, which are specific, are sensitive, and allow individual limb movements to be isolated.

TL;DR: A role for glial cell line-derived growth factor (GDNF) is suggested in both local and target-derived support of DA neurons, as well as potential involvement in the support of other neuronal populations in vivo.

TL;DR: Fetal spinal cord transplants promoted recovery of motor function in both newborn and adult operates, suggesting that the mechanisms underlying recovery of function must differ between the two groups.

TL;DR: Nerve growth factor (NGF), basic fibroblast growth factors (bFGF), and insulin-like growth factor II (IGF-II) prevented loss of both [Ca2+]i homeostasis and mitochondrial transmembrane potential, and protected hippocampal neurons against hypoglycemic injury, but did not prevent the hypoglycemia-induced reduction in ATP levels.

TL;DR: If similar dose-dependent neuronal necrosis proves to be a feature of other NMDA antagonists, such effects might raise concerns for the development and use of these compounds in human cerebrovascular diseases.

TL;DR: The results show that Mn may produce neuronal degeneration by an indirect excitotoxic process secondary to its ability to impair oxidative energy metabolism, similar to that found with two characterized mitochondrial toxins, aminooxyacetic acid, and 1-methyl-4-phenylpyridinium.

TL;DR: The results strongly indicate that stimuli other than neural degeneration initiated the activation of both microglial and astroglial cells, which then upon further activation by actual neuronal damage and degeneration adjust according to which neuronal structures were undergoing degeneration.

TL;DR: The present results provide an experimental primate model which closely resembles the neuropathologic and neurochemical features of Huntington's disease and strengthen the possibility that an NMDA receptor-mediated excitotoxic process plays a role in the pathogenesis of this disorder.

TL;DR: Observations from the present study suggest that early NOS expression seems to be associated with axonal sprouting and growth, and it is found that NOS is induced in a week of axonal injury in neurons that are normally NOS-negative.

TL;DR: In this review, recent advances in neurotrophin research are highlighted and their relevance to neurologic disease is discussed.

TL;DR: The alpha-ICAM antibody and tPA each effectively reduced neurological damage but the interaction was not significant, and combined therapy was no more effective than either substance alone.

TL;DR: Different neurotrophins in the regulation of neuronal survival and function are compared using dissociated embryonic cell cultures from two brain regions, the basal forebrain (BF) and locus coeruleus (LC).

TL;DR: The findings indicate that local injection of dopamine produces both post- and presynaptic damage to nigrostriatal structures, and support the contention that dopamine may act as a low-potency neurotoxin.

TL;DR: Brain macrophage/microglial cells produce TGF-beta 1 mRNA in the hippocampus in response to deafferentation and neurodegeneration.

TL;DR: The results suggest that sprouting of primary afferents within the spinal cord is one mechanism underlying the recovery of function after hemisection.

TL;DR: Clinical trials of recombinant human IGF-I have been initiated in patients with amyotrophic lateral sclerosis and are planned to begin soon in Patients with chemotherapy-induced peripheral neuropathies, together with evidence of safety in animals and man.

TL;DR: Results suggest that CSPG, in addition or as an alternative to beta-amyloid protein, could be responsible for the regression of neurites around senile plaques in Alzheimer's disease.

TL;DR: Recent developments in the biology of neurotrophic growth factors, especially members of the nerve growth factor-related neurotrophin family, are reviewed, which may point to their potential as therapeutic agents for the treatment of Parkinson's disease.

TL;DR: It is shown that beta-amyloid peptide when presented as an insoluble substrate which mimics its conformation in vivo can induce cortical glial cells in vitro and in vivo to locally deposit chondroitin sulfate containing proteoglycan.

TL;DR: The increase in blood flow noted in the Alzheimer patient suggests that data from clinical research may also generate a feedback to basic science, thus aiding in attempts to find new treatment strategies for neurodegenerative diseases.

TL;DR: The results provided quantitative data on the effects of specific 4-VO criteria and durations on selective, bilaterally symmetrical CA1 pyramidal cell damage, differential CA1-CA3 cell vulnerability, and prospect of a "therapeutic window" for pharmacological treatment of CA1 neuronal injury.

TL;DR: It is suggested that encapsulated genetically engineered cells can provide an efficient means for future applications involving delivery of neurotrophic factors.

TL;DR: The role of the septohippocampal pathway in the regulation of hippocampal field activity and behavior was assessed using the technique of intraseptal microinfusion ofcarbachol, atropine, and procaine, demonstrating that the frequency of carbachol-elicited type 2 theta can be modulated by the behavioral activation of type 1 theta.

TL;DR: The positive effects of NGF on neural regeneration and recovery of sensory function provide support for the potential use of N GF in treating peripheral nerve injuries.

TL;DR: A striking wave of enhanced cell death of 6- to 7-day-old neurons over the contralateral levels occurred ipsilaterally in both the 12-day and 7-week postbulbectomy animals.

TL;DR: It is concluded that transplanted NT2N cells represent a highly advantageous model system for studies of the developmental biology of neurons and their ability to establish molecular and structural polarity.