| 1. |
- Dunnett, S. B, et al.
(author)
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Preface
- 2017
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In: Functional Neural Transplantation IV Translation to Clinical Application, Part B. - 0079-6123. - 9780128138793 ; 231
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Book chapter (other academic/artistic)
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| 2. |
- Kokaia, Z., et al.
(author)
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Transplantation of reprogrammed neurons for improved recovery after stroke
- 2017
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In: Functional Neural Transplantation IV Translation to Clinical Application, Part B. - : Elsevier. - 0079-6123. - 9780128138793 ; 231, s. 245-263
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Book chapter (peer-reviewed)abstract
- Somatic cells such as fibroblasts, reprogrammed to induced pluripotent stem cells, can be used to generate neural stem/progenitor cells or neuroblasts for transplantation. In this review, we summarize recent studies demonstrating that when grafted intracerebrally in animal models of stroke, reprogrammed neurons improve function, probably by several different mechanisms, e.g., trophic actions, modulation of inflammation, promotion of angiogenesis, cellular and synaptic plasticity, and neuroprotection. In our own work, we have shown that human skin-derived reprogrammed neurons, fated to cortical progeny, integrate in stroke-injured neuronal network and form functional afferent synapses with host neurons, responding to peripheral sensory stimulation. However, whether neuronal replacement plays a role for the improvement of sensory, motor, and cognitive deficits after transplantation of reprogrammed neurons is still unclear. We conclude that further preclinical studies are needed to understand the therapeutic potential of grafted reprogrammed neurons and to define a road map for their clinical translation in stroke.
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| 3. |
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| 4. |
- Björklund, A, et al.
(author)
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Reafferentation of the subcortically denervated hippocampus as a model for transplant-induced functional recovery in the CNS
- 1990
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In: Progress in Brain Research. - 0079-6123. ; 83, s. 411-426
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Research review (peer-reviewed)abstract
- Subcortical deafferentation of the hippocampal formation is known to induce profound behavioural deficits. Transplants of fetal septal or brainstem tissue are capable of restoring some aspects of normal physiological and behavioural function in subcortically deafferented (i.e. fimbria-fornix or septal lesioned) rats. Such grafts have been shown to re-establish extensive new afferent inputs to the denervated hippocampal formation. As shown for grafted cholinergic and noradrenergic neurons, the ingrowing axons form laminar innervation patterns which closely mimic those of the normal cholinergic and noradrenergic innervations. The ingrowth appears to be very precisely regulated by the denervated target: each neuron type produces distinctly different innervation patterns; the growth is inhibited by the presence of an intact innervation of the same type; and it is stimulated by additional denervating lesions. Both ultrastructually and electrophysiologically the graft-derived fibres have been seen to form extensive functional synaptic contacts. Biochemically, cholinergic septal grafts and noradrenergic locus coeruleus grafts restore transmitter synthesis and turnover in the reinnervated hippocampus. Intracerebral microdialysis has revealed that acetylcholine and noradrenaline release is restored to normal or supranormal levels in the graft-reinnervated hippocampus, and that the grafted neurons can be activated in a normal way from the host through behavioural activation induced by sensory stimulation or electrical stimulation of the lateral habenula. These results indicate that the grafted monoaminergic neurons can restore tonic regulatory neurotransmission at previously denervated synaptic sites even when they are implanted into the ectopic brain sites. Such functional reafferentation may be sufficient for at least partial restoration of function in the subcortically deafferented hippocampus.
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| 5. |
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| 6. |
- Dunnett, S., et al.
(author)
-
Preface
- 2017
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In: Functional Neural Transplantation IV Translation to Clinical Application, Part A. - 0079-6123. ; 230
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Book chapter (other academic/artistic)
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| 7. |
- Ekerot, Carl-Fredrik, et al.
(author)
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Chapter 24 The control of forelimb movements by intermediate cerebellum
- 1997
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In: Progress in brain research. - 0079-6123. - 0444801049 ; 114, s. 423-429
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Book chapter (other academic/artistic)abstract
- In a series of studies, the functional organization of cerebellar regions contributing to the control of forelimb movements via the rubro- and corticospinal tracts has been characterized in the cat. The system consists of the cerebellar cortical C1, C3 and Y zones and their efferent intracerebellar nucleus, the interpositus anterior. Based on analyses of cutaneous and muscle afferent climbing fibre input, of corticonuclear connections and of limb movements controlled, a modular organization of this cerebellar control system is proposed. Each module consists of a number of cortical microzones, defined by their homogeneous climbing fibre input, and a group of neurones in nucleus interpositus anterior on which these microzones converge. The input to climbing fibres is multi-modal and originates from cutaneous A beta (tactile), A delta and C (nociceptive) fibres and from muscle afferents. The cutaneous receptive fields have spatial characteristics suggestive of a relation to elemental movements. For most climbing fibres, the spatial relationship between cutaneous and muscle afferent input is such that the muscle afferent input originates from muscles that, if activated, would tend to move the cutaneous receptive field of the climbing fibre towards a stimulus applied to the skin. By contrast, the limb movement controlled by the module often has the opposite direction, and would thus tend to move the cutaneous receptive field away from a stimulus applied to the skin. Functional implications of this organization for the involvement of these regions in acute and adaptive motor control of limb movements are discussed.
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| 8. |
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| 9. |
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| 10. |
- 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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