No abstract available.
Dopaminergic Neurons* ; Retina* ; Rodentia*

No abstract available.
Dopaminergic Neurons* ; Retina*

No abstract available.
Animals ; Dopaminergic Neurons* ; Parkinson Disease ; Rats* ; Transplantation

Parkinson disease (PD) is a neurodegenerative disease characterized by the selective loss of dopaminergic neurons from the substantia nigra pars compacta leading to the impairment of motor functions. Recent genetic studies have uncovered several genes involved in inherited forms of the disease. These gene products are likely to be implicated in the biochemical pathways underlying the etiology of sporadic PD. Our review discusses the pathogenetic mechanisms of the mutated genes.
Dopaminergic Neurons ; Genetics ; Neurodegenerative Diseases ; Parkinson Disease* ; Substantia Nigra

A growing body of evidence suggests that glial cells play an important role in neural development, neural survival, nerve repair and regeneration, synaptic transmission and immune inflammation. As the highest number of cells in the central nervous system, the role of glial cells in Parkinson's disease (PD) has attracted more and more attention. It has been confirmed that nigral iron accumulation contributes to the death of dopamine (DA) neurons in PD. Until now, most researches on nigral iron deposition in PD are focusing on DA neurons, but in fact glial cells in the central nervous system also play an important role in the regulation of iron homeostasis. Therefore, this review describes the role of iron metabolism of glial cells in death of DA neurons in PD, which could provide evidence to reveal the mechanisms underlying nigral iron accumulation of DA neurons in PD and provide the basis for discovering new potential therapeutic targets for PD.
Dopaminergic Neurons ; Humans ; Iron ; Nerve Degeneration ; Neuroglia ; Parkinson Disease

Induced neural precursor cells (iNPCs) are one source of transplantable dopaminergic neurons used in cell therapy for Parkinson's disease. In the present study, we demonstrate that iNPCs can be generated by transducing Brn2, Ascl1, Myt1L and Bcl-xL in a culture supplemented with several mitogens and subsequently can be differentiated to dopaminergic neurons (DA). However, studies have shown that iDA and/or iNPC-derived DA neurons using various conversion protocols have low efficiency. Here, we show that early exposure of FGF8 to fibroblasts efficiently improves differentiation of DA neurons. So our study demonstrates that FGF8 is a critical factor for generation of iNPC-derived DA neurons.
Cell- and Tissue-Based Therapy ; Dopaminergic Neurons* ; Fibroblasts ; Mitogens ; Neurons ; Parkinson Disease

We describe 7 patients with sleep related periodic leg movements(SRPLM) associated with variable neurological diseases, including focal thoracic cord lesions(4 cases), idiopathic Parkinson's diseased case), recurrent aseptic meningitis(1 case), and subacute sensory polyneuropathy(l case). Four patients with SRPLM associated with thoracic cord lesions also had paraparesis, suggesting involvement of pyramidal tract in the genesis of SRPLM. All the other three patients had dysesthesia, and at least two of them had restless legs syndrome. SRPLM of a patient with a thoracic schwannoma disappeared completely after surgical removal of tumor. One patient with intramedullary thoracic cord lesion and one asociated with Parkinson's disease showed marked improvement of SRPLM after levodopa treatment. Damage to the pyramidal tract or abnormal sensory inputs seem to activate lumbosacral generator selectively. Such neuronal systems are suspected to be modulated by. The dopaminergic neuronal system and the neuronal structures related to sleep.
Dopaminergic Neurons ; Humans ; Leg* ; Levodopa ; Neurilemmoma ; Neurons ; Paraparesis ; Paresthesia ; Parkinson Disease ; Pyramidal Tracts ; Restless Legs Syndrome

Protein O-GlcNAcylation is a post-translational modification that links environmental stimuli with changes in intracellular signal pathways, and its disturbance has been found in neurodegenerative diseases and metabolic disorders. However, its role in the mesolimbic dopamine (DA) system, especially in the ventral tegmental area (VTA), needs to be elucidated. Here, we found that injection of Thiamet G, an O-GlcNAcase (OGA) inhibitor, in the VTA and nucleus accumbens (NAc) of mice, facilitated neuronal O-GlcNAcylation and decreased the operant response to sucrose as well as the latency to fall in rotarod test. Mice with DAergic neuron-specific knockout of O-GlcNAc transferase (OGT) displayed severe metabolic abnormalities and died within 4-8 weeks after birth. Furthermore, mice specifically overexpressing OGT in DAergic neurons in the VTA had learning defects in the operant response to sucrose, and impaired motor learning in the rotarod test. Instead, overexpression of OGT in GABAergic neurons in the VTA had no effect on these behaviors. These results suggest that protein O-GlcNAcylation of DAergic neurons in the VTA plays an important role in regulating the response to natural reward and motor learning in mice.
Animals ; Dopaminergic Neurons/physiology* ; GABAergic Neurons/physiology* ; Mice ; Nucleus Accumbens/metabolism* ; Reward ; Ventral Tegmental Area/metabolism*

It has been suggested that transition metal ions such as iron can produce an oxidative injuries to nigrostriatal dopaminergic neurons, like Parkinson's disease (PD) and subsequent compensative increase of tetrahydrobiopterin (BH4) during the disease progression induces the aggravation of dopaminergic neurodegeneration in striatum. It had been established that the direct administration of BH4 into neuron would induce the neuronal toxicity in vitro. To elucidate a role of BH4 in pathogenesis in the PD in vivo, we assessed the changes of dopamine (DA) and BH4 at striatum in unilateral intranigral iron infused PD rat model. The ipsistriatal DA and BH4 levels were significantly increased at 0.5 to 1 d and were continually depleting during 2 to 7 d after intranigral iron infusion. The turnover rate of BH4 was higher than that of DA in early phase. However, the expression level of GTP-cyclohydrolase I mRNA in striatum was steadily increased after iron administration. These results suggest that the accumulation of intranigral iron leads to generation of oxidative stress which damage to dopaminergic neurons and causes increased release of BH4 in the dopaminergic neuron. The degenerating dopaminergic neurons decrease the synthesis and release of both BH4 and DA in vivo that are relevance to the progression of PD. Based on these data, we propose that the increase of BH4 can deteriorate the disease progression in early phase of PD, and the inhibition of BH4 increase could be a strategy for PD treatment.
Disease Progression ; Dopamine ; Dopaminergic Neurons ; Ions ; Iron ; Models, Animal ; Neurons ; Oxidative Stress ; Parkinson Disease* ; RNA, Messenger

Fetal dopaminergic or nondopaminergic cortical tissues were implanted directly into the denervated striatum of partial lesioned rat parkinsonian models. After transplantation, at rats were behaviourally tested with apomorphine and sacrificed for tyrosine hydroxylase immunohistochemical stain. The results of this study are summarized as follows : 1) Of 45 rats partially lesioned with 6-hydroxydopamine, 17 rats(37.8%) met a criteria(a minimum of 4 times/min to apomorphine-induced rotation test) of the rat parkinsonian model. 2) Eight weeks after transplantation of the fetal dopaminergic tissues into the striatum of the rat parkinsonian model, transplanted dopaminergic cells were found to be alive. Also reinnervated dopaminergic fibers were found in the previously denervated striatum. And the behavioural study suggested that the transplantation of the fetal dopaminergic neurons had influenced on the apomorphine-induced rotation. 3) Eight weeks after transplantation of the fetal nondopaminergic tissues into the striatum of the rat parkinsonian model, dopaminergic cells were not found in the previously denervated striatum. However, reinnervation of the dopaminergic fibers were found in the preciously denervated striatum. However, reinnervation of the dopaminergic fibers were found in the previously denervated striatum as well as the reduction of the apomorphine-induced rotation compared to the pregraft state. The major finding of this study support a trophic hypothesis for the mechanism of recovery in response to fetal dopaminergic or nondopaminergic tissue. The author conclude that fetal nondopaminergic tissue also had some beneficial effect in reducing apomorphine-induced rotational asymmetry probably by promoting recovery or sprouting of remaining dopaminergic fibers at the previously denervated striatum of the rat parkinsonian model.
Animals ; Apomorphine ; Dopaminergic Neurons ; Oxidopamine ; Rats* ; Tissue Transplantation* ; Transplantation ; Transplants* ; Tyrosine 3-Monooxygenase