Efferent synaptic connections of dopaminergic neurons grafted into the caudate nucleus of experimentally induced parkinsonian monkeys are different from those of control animals

1998 ◽  
Vol 123 (3) ◽  
pp. 323-333 ◽  
Author(s):  
C. Leranth ◽  
John R. Sladek Jr. ◽  
Robert H. Roth ◽  
D. Eugene Redmond Jr.
Keyword(s):  
Caudate Nucleus ◽  
Dopaminergic Neurons ◽  
Synaptic Connections ◽  
Experimentally Induced

Intrastriatal implantation of interleukin-1

1994 ◽  
Vol 80 (3) ◽  
pp. 484-490 ◽  
Author(s):  
Jin Wang ◽  
Krzysztof S. Bankiewicz ◽  
Robert J. Plunkett ◽  
Edward H. Oldfield
Keyword(s):  
Substantia Nigra ◽  
Caudate Nucleus ◽  
Ventral Tegmental Area ◽  
Dopaminergic Neurons ◽  
Interleukin 1 ◽  
Behavioral Recovery ◽  
Content Type ◽  
Median Forebrain Bundle ◽  
Ventral Tegmental ◽  
Fine Print

✓ Intrastriatal implantation with dopaminergic or nondopaminergic tissue can elicit behavioral recovery in parkinsonian animals. Because in these animals, especially in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned monkeys, there are still considerable numbers of dopaminergic neurons left in the mesencephalon, implantation-induced trophic effects on host residual dopaminergic neurons have been suggested as a mechanism underlying the behavioral recovery. Gliosis around the graft is a universal finding in any implantation procedure and is probably mediated by interleukin-1 (IL-1); in addition, activated astrocytes secrete several neurotrophic factors in vitro. Therefore, the authors postulated that trophic effects from IL-1-induced gliosis may be a “final common pathway” for recovery in parkinsonian animals after implantation. Hemiparkinsonism was induced in rats by injection of 6-hydroxydopamine either directly into the substantia nigra or into the median forebrain bundle. The substantia nigra-lesioned rats showed complete depletion of dopaminergic neurons in the substantia nigra but sparing of those in the ventral tegmental area, whereas the median forebrain bundle-lesioned animals had depletion of dopaminergic cells in the substantia nigra and the ventral tegmental area. Polymer pellets containing either slow-released IL-1 alpha and beta or placebo pellets were implanted in the caudate nucleus on the lesioned side in both groups. The rats' rotational response to amphetamine was tested weekly for 8 weeks. Selective substantia nigra-lesioned rats with implantation of IL-1 pellets had a 45% reduction in amphetamine-induced rotation, whereas placebo-implanted substantia nigra-lesioned rats had a 14% reduction in rotation. In the median forebrain bundle-lesioned group, neither IL-1 nor placebo implantation elicited any effect on turning. Immunohistochemical staining for glial fibrillary acidic protein was markedly increased surrounding the IL-1 pellets compared to the placebo pellets. In the selective substantia nigra-lesioned rats with IL-1 pellets implanted in the caudate nucleus, a considerable number of tyrosine hydroxylase immunoreactive (TH-IR) fibers were observed in the medial and middle portions of the caudate nucleus. Fewer TH-IR fibers were seen in the rats with placebo-bearing pellets. These results suggest that neurotrophic activities mediated by IL-1 and reactive astrocytes might be a common path through which tissue trauma and some tissue transplants exert their beneficial effects in parkinsonian animals. Furthermore, most of the sprouted dopaminergic fibers induced by IL-1 in the caudate nucleus come from dopaminergic neurons in the ventral tegmental area.

Dopamine (DA) cell transplant in rat caudate nucleus and motor recovery: Growth and synaptic connections

1986 ◽  
Vol 3 ◽  
pp. S30
Author(s):  
Hitoo Nishino ◽  
Taketoshi Ono ◽  
Masaji Fukuda ◽  
Jiro Takahashi ◽  
Ryoko Shibata ◽  
...  
Keyword(s):  
Caudate Nucleus ◽  
Motor Recovery ◽  
Cell Transplant ◽  
Synaptic Connections

scholarly journals Glutamatergic Control of Striatal Dopamine Release in Normal Rats and 6-OHDA Rats with Intrastriatal Grafts

1992 ◽  
Vol 3 (4) ◽  
pp. 225-226
Author(s):  
T. Kondoh ◽  
W. C. Low
Keyword(s):  
Dopaminergic Neurons ◽  
Animal Experiments ◽  
Target Cells ◽  
Synaptic Connections ◽  
Dynamic Regulation ◽  
Afferent Inputs ◽  
Da Release ◽  
Host Brain

Recent animal experiments suggest that transplanted neurons become integrated with the host brain. Neuroanatomical studies have shown that transplanted dopaminergic neurons can form synaptic connections on target cells in the host striatum. Other studies also have shown that grafted neurons not only innervate the host striatum but also receive afferent inputs from neurons of the host. However, little is known about the dynamic regulation of graft-derived dopamine (DA) release by the host brain. In normal animals, cortical neuronal input to the striatum is carried mainly via glutamate (Glu) neurons. Interactions between DA and Glu in the striatum are shown byin vivoandin vitrostudies. Usingin vivomicrodialysis, the present study was carried out in order to elucidate the effects of glutamatergic agonists and Glu blockade on DA release in the normal striatum and in the striatum of 6-OHDA rats with dopamine grafts.

scholarly journals The Neurotoxicity of 1-Methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine in the Monkey and Man

1984 ◽  
Vol 11 (S1) ◽  
pp. 166-168 ◽  
Author(s):  
R. Stanley Burns ◽  
Sanford P. Markey ◽  
Jere M. Phillips ◽  
Chuang C. Chiueh
Keyword(s):  
Substantia Nigra ◽  
Caudate Nucleus ◽  
Dopaminergic Neurons ◽  
Cell Injury ◽  
Biochemical Property ◽  
Nerve Cells ◽  
Axoplasmic Flow ◽  
Retrograde Degeneration

ABSTRACTl-Methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) selectively destroys dopaminergic neurons in the pars compacta of the substantia nigra (A8 and A9 cells). MPTP or its metabolite enters nerve cells at the level of their terminals in the caudate nucleus and putamen leading to a disturbance in axoplasmic flow and retrograde degeneration. The species-dependent neurotoxicity of MPTP (primate vs. rodent) suggests that a biochemical property of the cell related to neuromelanin may be important in the mechanism of cell injury.

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