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- Jankowska, Elzbieta
(author)
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A neuronal system of movement control via muscle spindle secondaries
- 1989
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In: Progress in Brain Research. - 0079-6123 .- 1875-7855. ; 80, s. 299-303
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Research review (peer-reviewed)abstract
- A recently discovered spinal interneuronal system of movement control is briefly described. It includes a population of midlumbar interneurones with a predominant monosynaptic input from secondary muscle spindle afferents but supplied with information via several other afferent and descending neuronal systems as well. The neurones are in direct contact with both motoneurones and other interneurones. The evidence in favour for their involvement in locomotion is briefly summarized. © 1989, Elsevier B.V.
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| 3. |
- Wieloch, Tadeusz
(author)
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Neurochemical Correlates to Selective Neuronal Vulnerability
- 1985. - C
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In: Molecular Mechanisms of Ischemic Brain Damage. - 0079-6123. - 0444806547 ; 63, s. 69-85
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Book chapter (peer-reviewed)abstract
- This chapter describes some of the special neurochemical features of the areas of the brain selectively vulnerable to ischemic and hypoglycemic insults. The chapter focuses on the neuronal connections to the vulnerable brain areas, on the distribution of receptors and transmitter content in the vulnerable areas, and on some current hypothesis of neuronal damage. Emphasis will be placed on a possible imbalance between excitation and inhibition of neurons as a factor in the development of neuronal necrosis, in particular the importance of excitatory transmitters, suggested to mediate ischemic and hypoglycemic brain damage. The amino acids glutamate and aspartate are major excitatory transmitters in the central neurons system. When present in high concentration they are neurotoxic and can play a role in the pathogenesis of several neurological diseases, such as temporal lobe epilepsy, Huntington's disease, and olivopontocerebellar dystrophy.
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| 4. |
- Janson, A M, et al.
(author)
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Protective effects of chronic nicotine treatment on lesioned nigrostriatal dopamine neurons in the male rat
- 1989
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In: Progress in Brain Research. - 1875-7855. ; 79, s. 257-265
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Journal article (peer-reviewed)abstract
- The present results demonstrate that chronic nicotine treatment can in part protect against mechanically-induced and neurotoxin-induced degeneration of nigrostriatal DA neurons. These results indicate that in sufficient doses chronic treatment with nicotine may be considered in the pharmacological treatment of Parkinson's disease. It remains to be demonstrated whether these protective actions can be extended to include also other injured neurons such as the cholinergic neurons, known to be severely affected in Alzheimer's disease.
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| 5. |
- Owman, Christer, et al.
(author)
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Studies of protective actions of nicotine on neuronal and vascular functions in the brain of rats: comparison between sympathetic noradrenergic and mesostriatal dopaminergic fiber systems, and the effect of a dopamine agonist
- 1989
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In: Progress in Brain Research. - 1875-7855. ; 79, s. 267-276
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Journal article (peer-reviewed)abstract
- Neuroprotective and possible trophic actions of nicotine were studied in two types of experimental models: (1) one in which the meso-striatal dopamine system was subjected to partial hemitransection, and regional glucose utilization (using 2-[3H]deoxyglucose) and blood flow (using [14C]iodoantipyrine) were measured by computer-assisted quantitative autoradiography based on a double-isotope technique; and (2) another where the sympathetic cranial nervous system supplying the brain vasculature was subjected to decentralization, axotomy, and partial or complete ganglionectomy, and the neuronal survival and fiber regeneration were elucidated by fluorescence histochemistry of noradrenaline, tyrosine hydroxylase, and neuropeptide Y. Continuous nicotine infusion for 4 weeks failed to significantly affect the neuronal response to the surgical interference of the sympathetic noradrenergic system. The same nicotine treatment for 2 weeks significantly improved glucose utilization and blood flow in caudate-putamen on the side in which the meso-striatal dopamine system had been transected, thus eliminating the 16% side-to-side asymmetry in the metabolism caused by the axotomy. The dopamine agonist, EMD 23,448, was without significant effect on this asymmetry. The hemitransection produced marked reduction in metabolism and flow also in the ventro-lateral thalamus. In substantia nigra, glucose utilization was markedly elevated--perhaps as a consequence of a regenerative increase in protein synthesis--opposite to a considerable reduction in nigral blood flow. Little or no effect of the hemitransection was seen in hippocampus or nucleus accumbens. In neither of these four regions did nicotine (or EMD 23,448) have any overt influence on glucose metabolism or blood flow. It is concluded that nicotine, mainly through its protective action on the meso-striatal dopaminergic system, is able to improve striatal glucose utilization and associated blood flow, probably reflecting a tendency to amelioration of neurotransmission function of surviving terminals belonging to the nigro-striatal dopamine neurons.
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