The primary pathology of PD is degeneration of dopaminergic neurons in the substantia nigra pars compacta, resulting in loss of the nigrostriatal pathway and a reduction of dopamine contents in the striatum. 
To test the hypothesis whether the methylation state of the TNF-alpha promoter contributes to increased expression of TNF-alpha in PD we compared DNA from different brain regions (substantia nigra pars compacta (SNpc) and cortex) of PD patients and neurologically healthy, age and sex matched controls by bisulfite sequencing of the TNF-alpha promoter region.
PD results primarily from a severe and selective devastation of dopaminergic neurons in substantia nigra pars compacta.
Neuromelanin-sensitive magnetic resonance imaging can detect signal alterations in the substantia nigra pars compacta and/or locus ceruleus that occur in Parkinson's disease and psychiatric disorders such as depression and schizophrenia.
Parkinson's disease (PD) is neurodegenerative diseases caused by the loss of dopaminergic neurons in the substantia nigra pars compacta.
Parkinson's disease (PD) is a movement disorder caused by the loss of dopaminergic neurons in the substantia nigra pars compacta, leading to nigrostriatal degeneration.
Clinical and pathological studies have shown that the disease extends beyond the substantia nigra pars compacta and involves various non-dopaminergic neurotransmitter systems that mediate both motor and non-motor symptoms that characterise PD.
6-OHDA with or without galantamine and/or nicotine were injected into unilateral substantia nigra pars compacta (SNpc) of rats.
We analyzed recordings from three BG locations: the external part of the globus pallidus (GPe), the substantia nigra pars reticulata (SNr), and dopaminergic neurons from the substantia nigra pars compacta (SNc) during performance of a probabilistic visuo-motor task.
The progressive debilitation of motor functions in Parkinson's Disease (PD) results from degeneration of dopaminergic neurons within the substantia nigra pars compacta of the midbrain.
Here, we performed the selective gene rescue of functional beta2*-nAChRs in either the substantia nigra pars compacta (SNpc) or the ventral tegmental area (VTA) of beta2KO mice.
Recently, dopamine (DA) neurons of the substantia nigra pars compacta (SNc) were found to exhibit sustained responses related to reward uncertainty, in addition to the phasic responses related to reward-prediction errors (RPEs).
The lesion decreased the number of TH (+) cells of the pars compacta of substantia nigra by 33%, without modifying the number of TH (+) cells in ventral tegmental area.
After substantia nigra pars compacta-lesion, the percentage of presumed non-cholinergic neurons exhibiting irregular pattern increased significantly compared to normal rats, while having no significant change in the firing pattern of presumed cholinergic neurons.
The aim of the present study was to investigate changes in the firing activity of thalamic parafascicular nucleus (PF) neurons at different time periods after 6-hydroxydopamine (6-OHDA) lesions of the substantia nigra pars compacta (SNc) and the role of the pedunculopontine nucleus (PPN) in these changes.
Bilateral infusion of 6-OHDA in the striatum of rats caused early (1 week) damage of dopaminergic terminals in striatum and in cell bodies in substantia nigra pars compacta.
Parkinson's disease (PD) is characterized by progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc) caused by an abnormal rate of apoptosis.
Parkinson's disease is a progressive neurodegenerative disorder, associated with the selective loss of dopaminergic neurons in the substantia nigra pars compacta.
Activity of complex I (the point of entry for most electrons that traverse the mitochondrial electron transport chain) has been found to be impaired in the substantia nigra pars compacta and also in other brain tissues in PD patients. The dramatic effect of aging on PD risk may be explained in part by the fact that mitochondrial DNA deletions are abundant and cause functional impairment in aged human substantia nigra pars compacta neurons.
Parkinson disease is characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta. These results indicate that JNK is involved in proteasome inhibition-induced dopaminergic neuron degeneration through caspase-3-mediated apoptotic pathways, suggesting that this kinase may be a therapeutic target for the prevention of substantia nigra pars compacta degeneration in Parkinson disease patients..
We assessed the presence of degenerating neurons in the substantia nigra pars compacta (SNpc) and ventral tegmental area (VTA) of parkinsonian monkeys.
RESULTS: T2 relaxation time was significantly higher in patients than in controls in the substantia nigra pars compacta.
This study explores whether melatonin neuroprotects dopaminergic cells of the substantia nigra pars compacta (SNc) from degeneration in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice (well-known animal model of Parkinson disease).
The present study demonstrates that GSTpi is actively expressed in both substantia nigra pars compacta and striatum of C57BL/6 mice brain, mostly in oligodendrocytes and astrocytes.
We will discuss the complicated relationships between the genetically defined cases and the two key pathological events seen in PD, namely loss of dopaminergic neurons in the substantia nigra pars compacta and the formation of protein inclusions, Lewy bodies, in the neurons that survive to the end stage of the disease course.
Parkinson's disease (PD) is a chronic and progressive neurodegenerative disorder of largely unknown etiology caused by a pathological cascade resulting in the degeneration of midbrain dopaminergic neurons of the substantia nigra pars compacta (SNpc) projecting to the nucleus striatum, the main input station of the basal ganglia neuronal circuit.
Of particular note is the compartmentalization of the iron-enrichment in this region; the pars reticulata contains higher levels of stainable iron as compared to the pars compacta.
On the other hand, DA cells in the ventral tegmental area (VTA) and the substantia nigra pars compacta (SNc) do not change their mean firing rate across the sleep-wake cycle.
The main control seems to be inhibitory, this effect being more marked in the ventral tegmental area (VTA) as compared to the substantia nigra pars compacta (SNc).
With antibodies raised against the N-terminal mouse EAAT4 sequence, the highest protein expression levels were observed in the substantia nigra pars compacta, ventral tegmental area, paranigral nucleus, habenulo-interpeduncular system, supraoptic nucleus, lateral posterior thalamic nucleus, subiculum, and superficial layers of the superior colliculus.
In the present work, we studied the effect of the selective cyclooxygenase-2 (COX-2) inhibitors, compound 11 g, celecoxib and selective COX-1 inhibitor SC-560 (intraperitoneally and acutely) on striatal glutamatergic and dopaminergic neurotransmission in normal and substantia nigra pars compacta (SNc)-lesioned rats using the microdialysis technique.
Parkinson's disease (PD) is a neurodegenerative disease that mainly affects dopaminergic (DA-ergic) neurons in the substantia nigra pars compacta (SNc).
A refinement in the analysis is introduced, the Spin-Lattice Distribution Index (SI), which is an automated measure of MRI signal in the substantia nigra pars compacta (SN(C)).
We report here, for the first time, a dose-related: increase in NTN protein expression within the striatum and substantia nigra (SN) pars compacta of nonhuman primates; increase in nigrostriatal tyrosine hydroxylase (TH), (the rate-limited enzyme for dopamine); and activation of phosphorylated signal-regulated kinase (a common neurotrophic signaling event).
In normal pups from P5 to P15, only 1-2% of neurons containing TH mRNA in the ventral tegmental area (VTA) and substantia nigra, pars compacta, also displayed VGLUT2 mRNA.
Here we showed that the multiple dosing scheme (with a higher cumulative dose) triggered a severe gliosis not only in the striatum and substantia nigra pars compacta (SNpc), but also in hippocampus and cerebellum when examined by noninvasive in vivo imaging and by immunohistochemistry (IHC), respectively, in the PD5 to PD7 mice.
The factors contributing to substantia nigra pars compacta (SNc) dopamine (DA) neuron death and striatal DA depletion in Parkinson's disease (PD) are still poorly understood.
Astrocyte activation observed in the MPTP mouse model and Parkinson's disease patients participates in the cascade of deleterious events that ultimately leads to death of dopaminergic neurons in the substantia nigra pars compacta (SNpc).
Apomorphine-induced rotations and the number of Nissl-stained neurons in the substantia nigra pars compacta (SNC) were counted after 2 weeks.
We report an anatomical abnormality of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and ventral tegmental area (VTA) in different strains of inbred and outbred mice, one mouse strain (C57BL/6, B6) from different commercial suppliers, and in B6J mice bred internally.
Parkinson's disease (PD) is characterized by loss of dopaminergic (DAergic) neurons in the substantia nigra pars compacta (SNc).
Age-associated specific loss of DA neurons particularly in the midbrain region substantia nigra pars compacta (SNpc) causes Parkinson disease (PD), an incurable condition characterized by rigidity, involuntary and slowed movement affecting about 1% of people over the age of 60 years.
Characteristic features of PD include dopaminergic neuron death in the substantia nigra (SN) pars compacta, accumulation of alpha-synuclein inclusions known as Lewy bodies in the SN, and brain iron accumulation beyond that observed in non-PD brains of a similar age.
Parkinson's disease is a chronic neurological disease characterized by dopaminergic neuron degeneration in the substantia nigra pars compacta.
Excitatory inputs from the pedunculopontine nucleus interact with timed inhibitory inputs from model striosomes in the ventral striatum to regulate dopamine burst and dip responses from cells in the substantia nigra pars compacta and ventral tegmental area.
Tyrosine hydroxylase (TH) staining of the striatum and substantia nigra pars compacta revealed that edaravone might exert neuroprotective effects on nigrostriatal dopaminergic systems.
HR/RET double-labeled neurons were abundantly distributed in the substantia nigra pars compacta ipsilateral to the caudate-putamen stereotaxically injected with HRP.
In a second study, we evaluated the NMDA activation profile in a rat model of Parkinson's Disease (PD) which was created by a unilateral injection of 6-OHDA into the rostral substantia nigra pars compacta.
MPTP administration resulted in a significant decrease in striatal dopamine levels and tyrosine hydroxylase immunostaining in the striatum and substantia nigra pars compacta. Mice receiving EGb761 had significantly attenuated MPTP-induced loss of striatal dopamine levels and tyrosine hydroxylase immunostaining in the striatum and substantia nigra pars compacta.
A hallmark of Parkinson's disease (PD) is the progressive loss of the A9 midbrain dopaminergic (mDA) neurons in the substantia nigra pars compacta.
The mechanism by which the dopamine neurons of the substantia nigra pars compacta degenerate in Parkinson's disease, is partly unknown.
Parkinson's disease (PD) is a progressive neurodegenerative disorder associated with selective loss of dopaminergic neurons in substantia nigra pars compacta.
In the current study, we investigated the neuroprotective properties of several COX inhibitors against 1-methyl-4-phenylpyridinium (MPP+) in neuroblastoma Neuro 2A (N-2A) cells in vitro and the protection against degeneration of substantia nigra pars compacta (SNc) dopaminergic (DA) neurons after the administration of 1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine (MPTP) in C57/BL6 male mice.
Dopamine (DA) neurons release DA not only from axon terminals at the striatum, but from their somata and dendrites at the substantia nigra pars compacta (SNc).
Dysfunction of mitochondrial complex I leads to degeneration of dopaminergic neurons of the substantia nigra pars compacta, as seen in Parkinson's disease, through activation of mitochondria-dependent programmed cell death pathways.
Injections of anterograde tracer into the PPN led to intense fiber labeling in the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA).
The present study examined whether in rats the communication between the substantia nigra pars compacta (SNc) and CeA is critical only at the time of surprise, for example to detect prediction error information, or is also needed to maintain and later express that information as enhanced learning.
Administration of rotenone can induce biochemical and histological alterations similar to those of Parkinson's disease in rats, leading to the selective loss of dopaminergic neurons in the substantia nigra pars compacta.
However, little is known about the effects of ghrelin on the substantia nigra pars compacta (SNpc) neurons in which ghrelin's receptor, growth hormone secretagogue receptor (GHSR)-1a, is highly expressed.
The results indicate a higher prevalence of pathological features in depressed compared to non-depressed PD patients, particularly in catecholamine areas of the brain; the locus coeruleus (neuronal loss: odds ratio=7.2, p=08; gliosis: odds ratio=18.0, p=008); dorsal vagus nerve (gliosis: odds ratio=7.63, p<0.05), and substantia nigra pars compacta (gliosis: odds ratio=2.85, ns).
Microtubule disruption caused by unilateral injection of COL blocked the retrograde axonal transport of fluorogold previously injected into striatum and induced substantial death of striatal and DA neurons in substantia nigra pars compacta.
Administration with 6-OHDA into the SN pars compacta of ovariectomized rats caused more decrease in the number of TH(+) cells as well as more damage to the function of sensory gating in SN.
Compared with late-stage PD animals, postmortem analysis demonstrated that more dopaminergic neurons remained in the substantia nigra pars compacta, and more fibers were found in the striatum.
Pathologically, it is not until 70-80% of the dopaminergic neurons from the substantia nigra pars compacta are lost before clinical symptoms are observed.
Glial cell line-derived neurotrophic factor (GDNF) can exert neuroprotective effects on the substantia nigra pars compacta (SNc) dopaminergic (DA) neurons that are undergoing degeneration in Parkinson's disease (PD).
Parkinson's disease (PD) is characterized not only by a progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNc) but also by a degeneration of locus coeruleus (LC) noradrenergic neurons.
In the midbrain, numerous Lmx1b-expressing neurons were present in the substantia nigra pars compacta and ventral tegmental area.
Good response to levodopa or dopamine agonists, reduced dopamine uptake in the corpus striatum and neuronal loss of the substantia nigra pars compacta have been documented in a few cases.
Since these carriers are selectively inhibited by 2-aminobicyclo[ 2.2.1]heptane-2-carboxylic acid (BCH), we have applied this compound to electrophysiologically recorded dopaminergic neurons of the rat substantia nigra pars compacta to examine the possible modulation of the effects of L-dopa by System L.
The number and morphology of tyrosine hydroxylase-positive cells in the substantia nigra pars compacta and ventral tegmental area were determined stereologically. The number of tyrosine hydroxylase-positive cells in rats fed the n-3 PUFA-deficient diet was 33.9% lower in the substantia nigra pars compacta and 33.7% lower in the ventral tegmental area than in those fed the control diet (P<0.05); however, the volume of tyrosine hydroxylase-positive cell bodies was not different between diet groups in either brain region.
To elucidate the functional relationship between serotonin neurons and dopamine neurons, we performed single-unit recording in the dorsal raphe nucleus (DRN), a major source of serotonin, and the substantia nigra pars compacta, a major source of dopamine, while monkeys performed saccade tasks in which the position of the target indicated the size of an upcoming reward.
By in situ hybridization, we detected cellular expression of CRF-BP mRNA in the VTA; no such expression was seen in neighboring substantia nigra pars compacta (SNC) or substantia nigra pars reticulata.
The pathogenesis of Parkinson's disease (PD) involves ongoing apoptotic loss of dopaminergic neurons in the substantia nigra pars compacta.
Parkinson's disease (PD) is a degenerative neurological disorder characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) of the brain.
We investigated in the rat the relative effects of selective bilateral partial lesions of substantia nigra pars compacta (SNc) or ventral tegmental area (VTA) which did not affect locomotion, on fine motor, motivational and cognitive behaviors.
Rats with unilateral 6-hydroxydopamine lesions of the substantia nigra pars compacta and medial forebrain bundle were administered histaminergic agents, and apomorphine-induced turning behavior was tested on Days 7 and 14 post-lesion.
Nitrogen pressure exposure in rats results in decreased dopamine (DA) release at the striatal terminals of the substantia nigra pars compacta (SNc) dopaminergic neurons, demonstrating the narcotic potency of nitrogen.
BACKGROUND: We investigated alterations in the substantia nigra pars compacta (SNc) and locus ceruleus (LC) in schizophrenic and depressive patients by using a neuromelanin-sensitive magnetic resonance imaging (MRI) technique that enables direct visualization of these nuclei and examined whether this technique could distinguish between these disorders and healthy subjects.
Idiopathic Parkinson disease (PD) is traditionally considered a movement disorder with hallmark lesions located in the substantia nigra pars compacta (SNpc).
Parkinson's disease is a common progressive neurodegenerative disorder characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta.
In this review, we compare characteristics that regulate extracellular DA behavior in substantia nigra pars compacta (SNc) and striatum, including regional differences in structure (a 40% greater extracellular volume fraction in SNc vs.
In the present study, extracellular recording was used to examine the neuronal activity of the basolateral nucleus (BL) of the amygdala and the effects of systemic administration of the selective 5-HT(1A) receptor antagonist WAY-100635 on the neuronal activity in the normal rats and rats with 6-hydroxydopamine (6-OHDA)-produced lesions in the substantia nigra pars compacta (SNc).
TH-positive cells and GFAP-positive cells in substantia nigra pars compacta (SN(C)) and striatum were counted using design-based stereology.
We found that the zebra finch LSt projects to the GP, substantia nigra pars reticulata (SNr) and pars compacta (SNc), but not the thalamus.
Neurons in midbrain dopamine centers, the substantia nigra pars compacta (SNc) and ventral tegmental area (VTA), densely innervate Area X and show singing-related changes in firing rate.
Interestingly, severe inflammation in the substantia nigra pars compacta (SNpc) accelerates the onset and progression of Parkinson's disease.
Emerging evidence indicate the modulating effects of estrogen on dopaminergic neurons in the substantia nigra pars compacta (SNpc).
In substantia nigra pars compacta 29% of cells were glutamic acid decarboxylase mRNA-positive, 58% in the retrorubral field and 35% in the ventral tegmental area.
The aim of this study was to study, under normobaric conditions, possible alterations of NMDA receptor activity in the substantia nigra pars compacta (SNc) induced by repetitive exposures to nitrogen pressure.
Rats with unilateral lesion of the substantia nigra pars compacta (SNpc) have been used as a model of Parkinson's disease.
We now describe and characterize such a model, which is based on the stereotaxic injection into rat right substantia nigra pars compacta of the A30P mutated form of alpha-syn fused to a protein transduction domain (TAT).
The nigrostriatal pathway of rats was lesioned by unilateral infusion of 6-OHDA into either the striatum or substantia nigra pars compacta (SNpc).
The aim of the present study was to investigate whether cyclooxygenase-2 (COX-2) expression is involved in the pathogenesis of neurodegeneration in dementia with Lewy bodies (DLB) by measuring COX-2 mRNA and protein expression in frontal cortex and substantia nigra pars compacta of DLB and control human brains.
Recently, using the medial forebrain bundle (MFB) 6-hydroxydopmaine (6-OHDA) lesion rat model of Parkinson's disease (PD), we have demonstrated that blockade of central IGF-1 receptors (IGF-1R) attenuated estrogen neuroprotection of substantia nigra pars compacta (SNpc) DA neurons, but exacerbated 6-OHDA lesions in IGF-1 only treated rats (Quesada and Micevych [ 2004]: J Neurosci Res 75:107-116).
A reduction in DA neurotransmission in the substantia nigra pars compacta (SNpc), for example, could impair activation of the basal ganglia and reduce stimulation of the motor cortex leading to central fatigue.
An important feature of Parkinson's disease is the degeneration of dopaminergic neurons in the substantia nigra pars compacta.
Excitotoxic lesions of posterior, but not anterior pedunculopontine tegmental nucleus (PPTg) change nicotine self-administration, consistent with the belief that the anterior PPTg (aPPTg) projects to substantia nigra pars compacta (SNC) and posterior PPTg (pPPTg) to the ventral tegmental area (VTA).
Studies involving estrogen treatment of ovariectomized rats or mice have attributed to this hormone a neuroprotective effect on the substantia nigra pars compacta (SNpc) neurons.
Parkinson's disease (PD) is a progressive, neurodegenerative disorder which involves the loss of dopaminergic neurons of the substantia nigra pars compacta.
Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta.
In this study, we used immunohistochemistry to investigate the topographical localization of HRD1 in the brain and demonstrated that HRD1 immunoreactivity was expressed widely in the substantia nigra pars compacta (SNC) containing dopaminergic neurons and was expressed in the cerebral cortex, hippocampus, dentate gyrus, striatum, globus pallidus, and Purkinje cells of the cerebellar cortex.
In contrast, ethanol decreased proenk mRNA expression in the substantia nigra pars compacta and pars reticulata 2 h after drug exposure.
Immunohistochemistry and histology showed significant reduction of 3-NP-induced neuronal loss in striatum, substantia nigra pars compacta, cerebellar cortex, pontine nuclei and inferior olives of MSA mice receiving 2.5 mg/kg rasagiline.
Pitx3 deficiency in mice causes a dramatic loss of dopaminergic neurones located in the substantia nigra pars compacta during development.
Activation of microglia along with the release of inflammatory cytokines and oxidative factors often accompanies toxin-induced degeneration of substantia nigra pars compacta (SNc) dopamine (DA) neurons.
In vivo, the systemic application of cell-permeable Hsp70 protected DA neurons of the substantia nigra pars compacta against subacute toxicity of MPTP.
Rats were injected with rAAV2/5 vectors in the substantia nigra pars compacta (SNc) on one side of the brain; the other side remained as a nontransduced control.
However, most neurologists now link severe loss of nigral cells in the ventrolateral tier of the pars compacta of the substantia nigra with bradykinesia and the presence of Lewy bodies in a number of discrete brain stem and cortical regions with Parkinson's disease.
BACKGROUND: Parkinson disease (PD) is a progressive neurodegenerative disorder in which the major pathologic substrate is a loss of dopaminergic neurons from the lateral substantia nigra pars compacta (SNc). CONCLUSIONS: High field strength MRI demonstrates lateral substantia nigra pars compacta abnormalities in early Parkinson disease (PD) consistent with increased iron content and corresponding to the known distribution of neuronal loss occurring in this disorder.
The present study sought to determine the mechanisms underlying the effect of Delta(9)-tetrahydrocannabinol (Delta(9)-THC) on neurons in the substantia nigra pars compacta (SNpc) using single-unit extracellular recordings in anesthetized rats.
Parkinson's disease is a neurodegenerative disorder characterized by the progressive loss of the dopaminergic neurons in the substantia nigra pars compacta, which project to the striatum. After in vivo MRS acquisitions, mice were killed; successful lesion verified by tyrosine hydroxylase immunolabeling on the substantia nigra pars compacta and in vitro MRS acquisitions performed on perchloric extracts of anterior part of mice brains.
In situ hybridization revealed that ADX counteracted the elevated FGF-2 mRNA levels in putative glial cells of the ipsilateral pars compacta of the substantia nigra and in the ventral tegmental area. The ADX also counteracted the increased density and intensity of the astroglial FGF-2 immunoreactive profiles within the lesioned pars compacta of the substantia nigra and the ventral tegmental area as determined by stereology.
Numerous double-labeled HRP/c-RET neurons were found in the substantia nigra pars compacta with predominate distribution ipsilateral to the injected striatum. Taken together with previous observations on glial cell line-derived neurotrophic factor in the basal ganglia, this study provides evidence that the c-RET protein may mediate biological activity of GDNF family ligands in most of projecting neurons in the substantia nigra pars compacta where the dopaminergic neurons are numerously distributed.
The SN comprises two major regions, the SN pars compacta (SNc) consisting of dopaminergic projection neurons, and the SN pars reticulata (SNr) consisting of GABAergic parvalbumin-positive projection neurons. These results show marked GABA(A)R subunit hetereogeneity in the SN, suggesting that GABA exerts quite different effects on pars compacta and pars reticulata neurons in the human SN via GABA(A) receptors of different subunit configurations..
However, most neurologists now link severe loss of nigral cells in the ventrolateral tier of the pars compacta of the substantia nigra with bradykinesia and the presence of Lewy bodies in a number of discrete brain stem and cortical regions with Parkinson's disease.
Parkinson's disease is an environmentally influenced, neurodegenerative disease of unknown origin that is characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta of the brain.
Tyrosine hydroxylase immunoreactive (TH-IR) staining of dopamine neurons of the substantia nigra pars compacta confirmed that modafinil was able to partially prevent the MPTP-induced neuronal damage.
As well as the typical neuropathological findings of ALS (marked upper and lower motor neuron loss), post-mortem examination showed prominent neuronal loss and gliosis in the subthalamus, and in the internal globus pallidus, substantia nigra pars compacta, and red nucleus.
RESULTS: 6-OHDA lesion of the substantia nigra pars compacta (SNc) significantly increased the firing rate with no change in the firing pattern of neurons of the ventral mPFC in rats.
The gonadal steroid E(2) is a critical survival, neurotrophic and neuroprotective factor for dopaminergic neurons of the substantia nigra pars compacta (SNpc), the cells that degenerate in Parkinson's disease (PD).
Ablation of Ret did not modify the MPTP-induced loss of dopaminergic neurons in the substantia nigra pars compacta and the dopaminergic innervation of the striatum at 14 days.
Paraquat (PQ) causes selective degeneration of dopaminergic neurons in the substantia nigra pars compacta, reproducing an important pathological feature of Parkinson disease. Finally, we tested the sensitivity of Bak-deficient mice and found them to be resistant to PQ treatments that depleted tyrosine hydroxylase immuno-positive neurons in the substantia nigra pars compacta of wild-type mice..
MPTP-challenge with genistein or estrogen pretreatment demonstrated reduced neurotoxicity, with tyrosine hydroxylase-immunoreactive (TH-IR) neurons in the substantia nigra pars compacta (SNpc) affected to a significantly lesser extent as compared to the MPTP treated control.
Although the cause of Parkinson's disease is unknown, the pathologic manifestation involves the loss or dysfunction of dopaminergic neurons in the substantia nigra pars compacta.
Parkinson's disease is one of the most common neurodegenerative diseases caused by the loss of dopaminergic neurons in the substantia nigra pars compacta.
The neuropathology is characterized by the loss of dopamine neurons in the substantia nigra pars compacta.
We have investigated the developmental profile of functional synaptic NMDA receptor subunits in dopaminergic neurones of the substantia nigra pars compacta (SNc).
The authors previously demonstrated that isoflurane, a widely used volatile anesthetic, induced depolarization and increased the frequency of spontaneous action potentials in principal dopamine neurons in rat substantia nigra pars compacta. These results demonstrate that isoflurane accelerated the inactivation and delayed the recovery from inactivation of A-type K channels in principal neurons in rat substantia nigra pars compacta without affecting delayed rectifier K channels.
We have explored the survival of dopaminergic cells of the substantia nigra pars compacta (SNc) in 6 hydroxydopamine (6OHDA)-lesioned rats with prior cortical removal.
An abnormal accumulation of cytosolic dopamine resulting in reactive oxygen species and dopamine-quinone products may play an important role in the rather selective degeneration of substantia nigra pars compacta (SNc) dopaminergic neurons in Parkinson's disease.
First, we found that NF-kappaB was activated within the substantia nigra pars compacta of PD patients and MPTP-intoxicated mice.
Furthermore, its systemic application in aged mice protected dopaminergic neurons following administration of MPTP as revealed by counting of tyrosine hydroxylase-immunoreactive neurons in the substantia nigra pars compacta.
Catecholaminergic neurons of the primate substantia nigra (SN) pars compacta (SNc) and the locus coeruleus contain neuromelanin (NM) granules as characteristic structures underlying the pigmentation of these brain areas.
Parkinson's disease (PD) is characterized by the death of dopaminergic neurons and the presence of Lewy bodies in the substantia nigra pars compacta.
We found neuroprotective effects against DA depletion, loss of tyrosine hydroxylase neurons and induction of alpha-synuclein inclusions in the substantia nigra pars compacta.
Compared with that in wild-type mice, glucose utilization in STOP-KO mice was significantly increased in the olfactory cortex, ventromedial and anterolateral hypothalamus, ventral tegmental area, and substantia nigra pars compacta.
Experiments were performed in anaesthetized naive rats and rats selectively lesioned in the substantia nigra pars compacta (SNc) or VTA.
Fas, a member of the tumor necrosis factor receptor family with proapoptotic functions, was reported to be elevated within the striatum and substantia nigra pars compacta (SNc) of Parkinson's disease (PD) patients.
Like humans with Parkinson's disease (PD), the ak mouse lacks the majority of the substantia nigra pars compacta (SNc) and experiences striatal denervation.
Midbrain dopamine (DA) neurons are found in two nuclei, the substantia nigra pars compacta (SNc) and ventral tegmental area (VTA).
Parkinson's disease (PD) is a chronic and progressive neurological disorder characterized by selective degeneration of dopaminergic neurons in the substantia nigra pars compacta.
In parallel, (TH) protein expression in the substantia nigra pars compacta (SNpc) revealed to be a sensitive target for MPTP, once it was found to be down-regulated immediately after the 1st MPTP exposure until the last time-point.
Parkinson's disease (PD) is a chronic neurodegenerative disorder characterized by the death of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and the subsequent decrease of dopamine levels in the striatum.
In vivo, 14-26 suppressed both oxidative stress and ER stress and prevented neuronal death in the substantia nigra pars compacta (SNpc) after injection of 6-OHDA in mice.
Autoradiography experiments revealed enhanced nociceptin opioid receptor (NOP) binding in medial amygdala (22-26%), frontal (21-23%) and entorhinal (27-32%) cortices, and reduced binding in the substantia nigra pars compacta (28%) and medial central gray (29%) of rats with PS.
Seven days post-lesion, the number of dopaminergic cells in the substantia nigra pars compacta and the levels of dopamine and its metabolites 3, 4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in the striata were quantified and compared with the vehicle-treated groups.
Parkinson's disease (PD) is a progressive neurodegenerative disease with typical motor symptoms due to the preferential loss of midbrain dopaminergic (mDA) neurons in the substantia nigra pars compacta.
Nitrogen pressure exposure, in rats, resulted in a decreased dopamine (DA) level by the striatal terminals of the substantia nigra pars compacta (SNc) dopaminergic neurons, due to the narcotic potency of nitrogen.
We thus observed the influence of deficiency of complement 3 (C3), the key component of complement system, on the death of dopaminergic neurons in substantia nigra pars compacta (SNpc) and the loss of dopaminergic fibers in striatum induced by acute or chronic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).
Syn130m mice showed significant loss of DAergic neurons in the substantia nigra pars compacta.
This system could be at fault in Parkinson's disease which is characterized by an increased level of iron in the substantia nigra pars compacta and an impaired storage of dopamine due to the disruption of vesicular trafficking.
The dopamine (DA) system of the dorsal striatal pathway projecting from the substantia nigra pars compacta (A9) to the dorsal part of the striatum (motor striatum) functions in the control of speed and dexterity of movement.
Although there are signs of pathology in many brain regions, the core symptoms of Parkinson's disease are attributable to the selective degeneration of dopaminergic neurons in the substantia nigra pars compacta.
They demonstrate a consistent pattern characterized by damage to the globus pallidus (particularly the internal segment) with sparing of the substantia nigra pars compacta and the absence of Lewy bodies. This finding contrasts with what is seen in PD, in which there is preferential degeneration of dopamine neurons in the substantia nigra pars compacta coupled with Lewy bodies and preservation of the pallidum.
Degeneration of dopamine neurons in the substantia nigra pars compacta (SNc) plays an important role in the pathophysiology of neurodegenerative diseases like Parkinsonism and vascular dementia.
Gene expression profiling was performed in the laser capture microdissected substantia nigra pars compacta (SNc) after a single administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in common marmosets. RNA from substantia nigra pars compacta tissue underwent a double linear amplification and was then applied to a whole human genome oligo microarray.
The effect of paraquat on catecholaminergic neurons was reminiscent of that of Parkinson's disease, with preferential loss of dopaminergic neurons in the ventral tier of the substantia nigra pars compacta and loss of tyrosine hydroxylase staining in the locus coeruleus.
The results are explained on the basis of dextromethorphan (15-75 mg/kg)-induced blockade of NMDA receptors in striatum and substantia nigra pars compacta.
In a prior study, we showed that the few striatal projection neurons that contain both substance P (SP) and enkephalin (ENK) in rats may preferentially project to the substantia nigra pars compacta. Since striatal neurons that project to the pars compacta are thought to preferentially reside in the striosomal compartment, we investigated if striatal neurons that contain both SP and ENK are preferentially localized to the patch compartment. These results are consistent with the notion that SP/ENK colocalizing neurons preferentially project to pars compacta, and these and our prior results additionally raise the possibility that neurons of this type in the striatal matrix may also project to the pars compacta..
Our findings demonstrate early progressive microglial activation in substantia nigra pars compacta (SNc) associated with increased expression of iNOS and correlating with dopaminergic neuronal loss.
Insulin-associated changes in c-Fos(+) cell numbers were evident in the arcuate nucleus, bed nucleus of the stria terminalis and substantia nigra pars compacta, concomitant with elevated leptin levels and reduced chow intake.
To understand contribution of microglia and blood inflammatory cells to brain inflammation, the behavior of microglia, neutrophils, and monocytes was investigated in LPS (lipopolysaccharide)-injected substantia nigra pars compacta, cortex, and hippocampus of normal and/or leukopenic rats using specific markers of neutrophils (myeloperoxidase, MPO), and microglia and monocytes (ionized calcium binding adaptor molecule-1, Iba-1), as well as a general marker for these inflammatory cells (CD11b).
Selective delivery of antioxidants to the substantia nigra pars compacta (SNpc) during Parkinson's disease (PD) can potentially attenuate oxidative stress and as such increase survival of dopaminergic neurons.
In guinea pig brain slices, talnetant antagonized NKB-induced increases in neuronal firing in the medial habenula (pKB = 7.9) and senktide-induced increases in neuronal firing in the substantia nigra pars compacta (pKB = 7.7) with no diminution of maximal agonist efficacy, suggesting competitive antagonism at native NK3 receptors.
injection, the survival ratios of tyrosine hydroxylase-immunoreactive (TH-IR) neurons in the substantia nigra pars compacta and TH-IR fibres in the striatum were only 59 and 13%, respectively, compared with the normal controls.
Evidence suggests that increased glutamatergic input to the substantia nigra pars compacta as a result of hyperactivity of subthalalmic nucleus output pathways may contribute to the progressive degeneration of nigral dopaminergic neurones in Parkinson's disease (PD), a debilitating neurodegenerative disorder which affects approximately 1% of people aged over 65.
Results show that bilateral 6-OHDA infusion significantly decreased (70%) the number of dopaminergic cells in the substantia nigra pars compacta (SNc).
We will review the protective role of DJ-1 to prevent dopaminergic neurons in the substantia nigra pars compacta (SNpc) from degeneration and how its dysfunction would lead to neurodegeneration..
Rats were lesioned in the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA) and assigned to subgroups with respect to the stereologically verified extent of the nigral and/or VTA degeneration.
Progressive loss of dopaminergic neurons in the substantia nigra pars compacta and their terminal connections in the striatum are central features in Parkinson's disease (PD).
Although the midbrain dopaminergic system dominates reward pathways, chronic nicotine does not change alpha4* receptor levels in dopaminergic neurons of ventral tegmental area (VTA) or substantia nigra pars compacta.
Furthermore, we observed an increase in alpha-synuclein immunoreactivity and accumulation and neurodegeneration in the substantia nigra pars compacta in aged VMAT2 LO mice.
Parkinson's disease (PD) is a progressive movement disorder caused by the selective and massive loss of dopaminergic neurons (DA) in the substantia nigra pars compacta (SNc).
In Parkinson's disease, the progressive loss of dopaminergic neurons in the pars compacta of the substantia nigra leads to debilitating motor dysfunction.
The expression of the proapoptotic protein bax and the antiapoptotic proteins bcl-2 and bcl-xL was investigated by Western blot in the pars compacta of the substantia nigra of pure and common DLB forms.
The brains were collected on day 11 and quantitative immunohistochemistry was used to assess the number of NT-, SOD1- and SOD2-immunoreactive (IR) cells in the substantia nigra pars compacta (SNpc).
Sections of substantia nigra from elderly subjects (N = 15; mean 81.3; SD 7.0) and younger subjects (N = 7; mean 30.3; SD = 8.7), all of which had no specific neurologically or neuropathologically defined disorders, were stained immunohistochemically for MHC Class II and the area occupied by microglia was quantified in substantia nigra pars compacta.
The major symptoms are related to the progressive loss of dopaminergic neurons in the substantia nigra pars compacta.
The M5 muscarinic receptor (M5R) is expressed in dopamine-containing neurones of the substantia nigra pars compacta and ventral tegmental area, and regulates the release of mesolimbic dopamine.
We also report that PAR1 is expressed in human substantia nigra pars compacta glia as well as tyrosine hydroxylase-positive neurons.
In the substantia nigra, immunoreactivities for TRPC3 and TRPC7 were prominent in the cell bodies and several processes in the pars compacta and pars reticulata.
Using extracellular unitary recordings in anaesthetized rats, this study examined the implication of the serotonin 7 (5-HT(7)) receptors in the inhibitory effect of amphetamine on ventral tegmental area and substantia nigra pars compacta dopamine neuronal activity. Interestingly, this antagonist prevented significantly the inhibition of dopamine neuronal firing activity induced by amphetamine (1 mg/kg, i.v.) in the ventral tegmental area, but not in the substantia nigra pars compacta.
In the present study, an attempt was made to confirm the assumptions in Parkinsonian rats, which were produced by unilateral injections of 6-hydroxydopamine (6-OHDA) into the substantia nigra pars compacta (SNC).
For instance, the cardinal symptoms of Parkinson's disease, such as tremor, rigidity and bradykinesia, are caused by the selective degeneration of dopaminergic neurons originating in the substantia nigra pars compacta, which modulate the activity of MSNs in the dorsal striatum.
Our results showed that there were significantly more (20-24%) dopaminergic cells in the substantia nigra pars compacta (SNc) of the MPTP-treated monkeys that had STN alteration, either with kainic acid lesion or DBS, compared to the non-MPTP-treated monkeys (intact animals).
Generation and survival of midbrain dopaminergic (DA) neurons were investigated using tyrosine hydroxylase (TH) immunocytochemistry combined with tritiated thymidine autoradiography at appropriate anatomical levels throughout the anteroposterior (A/P) axes of the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA).
Degeneration of dopaminergic neurons of the substantia nigra pars compacta is a cardinal feature of Parkinson's disease (PD).
It is well known that the death of dopaminergic neurons of the substantia nigra pars compacta (SNc) is the pathological hallmark of Parkinson's disease (PD), the second most common and disabling condition in the expanding elderly population.
In situ hybridization data and a direct comparison of SN neurons expressing tyrosine hydroxylase (TH) and/or the beta-gal marker for EphB1 revealed that EphB1 is not expressed in TH+ neurons of pars compacta (SNc), but is restricted to neurons in pars reticulata (SNr).
Why dopamine-containing neurons of the brain's substantia nigra pars compacta die in Parkinson's disease has been an enduring mystery. The reliance on these channels increases with age, as juvenile dopamine-containing neurons in the substantia nigra pars compacta use pacemaking mechanisms common to neurons not affected in Parkinson's disease.
As social interactions are dependent on brain motivation systems, here we test the hypothesis that the midbrain ventral tegmental area-substantia nigra pars compacta (VTA-SNc) complex, which provides a strong dopaminergic input to LAreaX, is a source of this modulation.
We demonstrated that a 50% lesion of the substantia nigra pars compacta (SNpc) suffices to produce disruptions of several parameters in the sleep-wake pattern of rats.
The dopaminergic cells in the substantia nigra pars compacta were unaffected by METH or haloperidol alone or the combination of METH and haloperidol.
The mechanisms responsible for the progressive degeneration of dopaminergic neurons and pathologic iron deposition in the substantia nigra pars compacta of patients with Parkinson's disease (PD) remain unclear.
A marked increase in the extent of lipid peroxidation, superoxide dismutase (SOD) and g-glutamyl transpeptidase (g-GTP) was seen, while a significant decrease in the levels of glutathione (GSH), total thiols and glutathione peroxidase (GPx) activity was observed in the substantia nigra pars compacta (SNpc) of MPTP treated animals.
In situ hybridization and immunohistochemical analysis demonstrate the expression and localization of LRRK2 to various neuronal populations in brain regions implicated in Parkinson's disease (PD) including the cerebral cortex, caudate-putamen and substantia nigra pars compacta.
Parkinson's disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic neurons within the substantia nigra pars compacta.
The stimulatory effect of nicotine on DA release most probably results from its ability to excite the neuronal firing rate and to increase the bursting activity of DA neurons in the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA), and from its stimulatory action on DA terminals in the corpus striatum and the nucleus accumbens.
substantia nigra pars compacta dopaminergic neurons project predominantly to the striatum and regulate striatal functions.
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