No abstract available.
Animals ; Immunohistochemistry* ; Neurons* ; Rats* ; Substantia Nigra*

No abstract available.
Animals ; Neurons* ; Oxidopamine* ; Rats* ; Substantia Nigra*

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

OBJECTIVE: The purpose of this study is to investigate the effect of ipsilateral subthalamic nucleus(STN) lesioning on the spontaneous behavioral changes and the alteration of neuronal activities of deep cerebral nuclei in the rat parkinsonian model with 6-hydroxydopamine(6-OHDA). METHODS: To identify the spontaneous behavioral changes, apomorphine-induced rotational test and forepaw adjusting step were performed. We subsequently investigated the alteration of neuronal activities in the substantia nigra pars reticulata(SNpr) and globus pallidus(GP), in order to compare them with the behavioral changes in rat parkinsonian models. RESULTS: The STN lesioning in the rat parkinsonian model clearly improved behavioral changes. Compared to the normal control rats, rat PD models exhibited a significant increase in mean firing rates and the percentage of bursting neurons in the STN and SNpr. In the STN-lesioned rat PD models, mean firing rates and the percentage of bursting neurons in the SNpr were reduced and those in the GP increased. CONCLUSION: STN lesioning induced behavior improvement in rat parkinsonian models seems to be consistent with the surgical outcomes of the STN stimulation therapy in advanced Parkinsonn's disease(PD). The alteration of the neuronal activities in the SNpr and GP suggests that these sites are responsible for the improvement of parkinsonian motor symptoms observed following STN lesioning in rat parkinsonian models. The significance of bursting activity in the SNpr and GP remains obscure. Further study is necessary to elucidate the pathophysiological mechanism of PD.
Animals ; Fires ; Globus Pallidus ; Kainic Acid* ; Neurons* ; Oxidopamine* ; Parkinson Disease ; Rats* ; Substantia Nigra ; Subthalamic Nucleus

The aim of this study was to examine the effects of various concentrations of glutamate(10(-8), 10(-6) and 10(-4) M) on the circling movement induced by apomorphine in the unilateral substantia nigra-lesioned rats. Subcutaneous apomorphine(0.1 mg/kg) elicited contralateral circling movement(641.7+/-163.9/hr), Glutamate(10(-6)-10(-4) M) significantly reduced the numbers of apomorphine-induced circling movement. This reducing effect of glutamate was antagonized and/or reversed by 10(-7) M GABA antagonist bicuculline. These results suggest that glutamate reduces circling movement induced by apomorphine and this reducing effect of glutamate may be mediated by increased GABA concentration in striatum and substantia nigra.
Animals ; Apomorphine ; Bicuculline ; Dopamine ; GABA Antagonists ; gamma-Aminobutyric Acid ; Glutamic Acid* ; Rats* ; Substantia Nigra

BACKGROUND: Apomorphine-induced rotational behavior of unilateral 6-hydroxydopamine (OHDA) lesioned rat is widely used to develop anti-Parkinsonian treatments including drugs, neuroprotective therapy, and neural graft. Time course of changes in rotational behavior after lesioning, however, has not been fully elucidated. The aim of this study was to observe the chronological changes in the rotational response and to find the optimal period when this model is used for investigation of various therapies. METHODS: 6-OHDA was stereotaxically delivered to the unilateral substantia nigra in 13 rats. Rotational responses to apomorphine administrations were counted in the rotomotor on 2, 4, 8, 12, and 14 weeks after lesioning. RESULTS: The total turns for two hours increased continuously up to eight weeks, and then plateaued. CONCLUSIONS: Apomorphine-induced rotations increase until eight weeks after 6-OHDA lesioning. Therefore, this Parkinsonian model should be used at least eight weeks after lesioning. Even though priming was not excluded as an explanation in the experiment, we reason that progressive degeneration of dopaminergic neurons may explain the chronological changes in rotational behavior.
Animals ; Apomorphine* ; Dopaminergic Neurons ; Neuroprotective Agents ; Oxidopamine* ; Rats* ; Substantia Nigra ; Transplants

To determine whether toxic and trace elements may play -a role as ail etiologic factor in the development of Parkinson's disease (PD), we measured the levels of toxic and trace elements in the hair from 56 PD patients and 50 normal controls with atomic absorption spectrophotometer In the hair of PD, the zinc concentration showed a significantly lower amount (p=O. 0001) and the concentrations of lead, cad mium, and copper showed a significantly larger amount (Pb, Cd, Cu : p=0.0012, 0. 0444, 0.0286) compared with those of the normal controls. There were no significant differences between the two groups in concentrations of mercury, manganese, iron and aluminum. The levels of each of the toxic and trace elements measured had no significant relationship with Hoehn-Yahr stage, age or the duration of disease. Our data was inconsistent with previous results that analysed the levels of toxic and trace elements in substantia nigra of parkinsonian patients. Due to significant differences in the levels of zinc, copper, lead and cadmium between PD and normal control group, there may be a relationship between PD and those toxic and trace elements. Hair analysis can be so easily applied in clinical practice that a large scale study should be attempted to further evaluate the relationship between trace elements and PD.
Absorption ; Aluminum ; Cadmium ; Copper ; Hair* ; Humans ; Iron ; Manganese ; Parkinson Disease* ; Substantia Nigra ; Trace Elements ; Zinc

To clarify neuronal connection of the medial rectus muscle at brain stem, Bartha strain of the psecudorabies virus(PRV-Ba) and cholera toxin-horeserdish peroxidase(CT-HRP) was injected into medial rectus muscle of the rat. About 84 hours after PRV or CT-HRP injection, the brain was removed and processed immunohistochemical stain for PRV-Ba and neurohistochemical stain for CT-HRP using tetramethyl benzidine. The CT-HRP positive reaction was only present in ipsilateral oculomotor nucleus, contralateral abducence nucleus and bilaterally in rostral interstitial nucleus of medial longitudinal fasciculus, olivary pretectal nucleus, medial and superior vestibular nucleus, nucleus prepositus hypoglossi, prerubral field, nucleus Darkschewitsch, lateral substantia nigra, terminal nucleus of accessory nucleus, dorsal raphenucleus, locus ceruleus and pontime reticular formation. This study confirmed that both oculomotor nucleus and abducence nucleus were connected with each other through the medial longitudinal fasciculus, and neuronal connection of the medial rectus muscle in the rat brain stem.
Animals ; Brain Stem* ; Brain* ; Cholera ; Locus Coeruleus ; Neurons ; Rats* ; Reticular Formation ; Substantia Nigra

It is suggested that calbindin buffers the concentration of intracellular calcium as the calcium binding protein in the cell. In the neurodegerative disease such as Parkinsonian disease, Huntington 'disease, Alzheimer 'disease there is some change of calbindin. The calcium mediated neurotoxicity begins due to the decrease of calbindin gene in those disease. In this study the substantia nigra of the normal rat is immunostained with anti -calbindin antibody, the morphological characteristics and distribution of calbindin positive neurons are studied to confirm the suggestive neuroprotective role of calbindin in the Parkinsonian disease. In the substantia nigra tissues of rats, calbindin was immunostained in the cell body and cellular processes of the polygonal or ovoid neurons. The calbindin immumostained neurons were distributed mainly in the substantia nigra lateralis than substantia nigra compacta and have even distribution from cephalic section to caudal section. The degree of calbindin -immunostaining was similar from medial area to lateral area, from ventral area to dorsal area in the one section of substantia nigra. These results support the potentiative neuroprotective role of calbindin in the Parkinsonian disease.
Animals ; Buffers ; Calbindins* ; Calcium ; Carrier Proteins ; Immunohistochemistry ; Neurons* ; Rats* ; Substantia Nigra*

BACKGROUND: Many recent studies based on non-linearity have been performed to quantify the complex behavior of the brain in order to understand the pathophysiology of Parkinson's disease (PD). METHODS: We calculated the Fractal dimension (FD) and Lyapunov exponent (L1), the non-linear biologic signals, by digital EEG using 'CHASIM' program, non-linear times series signal simulator and then compared the UPDRS score with the degree of atrophy in the substantia nigra upon brain MRI and EEG data respectively. All subjects (N=20) showed definite hemiparkinsonism. RESULTS: Upon EEG analysis, a strong positive correlation was noted between FD of the left hemispheric electrodes (FP1,F3,T3,T5) and the UPDRS scores in left-sided symptomatic patients. Additionally, positive correlations were noted between the ipsilateral MRI index ratio in the right and left-sided symptomatic patients and respective UPDRS scores. CONCLUSIONS: These results suggested that thalamocortical drive is reduced in the contralateral hemisphere to parkinsonian symptoms and thalamocortical or corticothalamic glutaminergic projection in the ipsilateral hemisphere is increased in the early stage of Parkinson's disease. Additionally, hemiparkinsonim may primarilly cause anatomic and functional changes in the contralateral hemisphere and a compensatory effect in the ipsilateral hemisphere at the same time. We suggest that disease duration may be a compensating factor and of which require further investigation. We hope that our results will aid the understanding of the specific patterns of dysfunction and treatment effects by non-linear EEG measures and anatomic changes of the substantia nigra through continuous follow up of the patients. (J Korean Neurol Assoc 19(3):232~238, 2001)
Atrophy ; Brain ; Electrodes ; Electroencephalography* ; Fractals ; Hope ; Humans ; Magnetic Resonance Imaging ; Parkinson Disease* ; Substantia Nigra