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Journal articles on the topic 'Substanita nigra'

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Published: 10 December 2022

Last updated: 28 January 2023

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1

Bannon, Michael J., and Christopher J. Whitty. "Neurokinin receptor gene expression in substantia nigra: localization, regulation, and potential physiological significance." Canadian Journal of Physiology and Pharmacology 73, no. 7 (July 1, 1995): 866–70. http://dx.doi.org/10.1139/y95-119.

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Neurokinin receptor gene expression within the rat and human substantia nigra was examined in detail. In the rat, the relative abundances of nigral neurokinin receptor mRNAs were neurokinin 3 > neurokinin 1 [Formula: see text] neurokinin 2. High levels of neurokinin 3 mRNA were localized to dopamine neurons, as determined by dopamine cell lesions and colocalization with tyrosine hydroxylase mRNA. Stimulation of nigral neurokinin 3 receptors activated dopamine cells, as evidenced by increases in striatal dopamine metabolism and in a postsynaptic measure of dopamine neurotransmission (i.e., striatal substance P encoding mRNA). These and other anatomical and physiological data suggest that in the rat, substance P (released from striatonigral neurons) may act on nigral nondopamine cells through neurokinin 1 receptors, while the substance P cotransmitter neurokinin A may act preferentially on nigral dopamine neurons through neurokinin 3 receptors. Interestingly, high levels of neurokinin 1 (but not neurokinin 3) receptor mRNA are seen within human substantia nigra dopamine cells. Thus drugs interacting with neurokinin receptors may prove to be of value in the treatment of various neuropsychiatric disorders.Key words: neurokinin receptor, mRNA, dopamine, substantia nigra, human.

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2

Quijano, Aloia, Carmen Diaz-Ruiz, Andrea Lopez-Lopez, Begoña Villar-Cheda, Ana Muñoz, Ana I. Rodriguez-Perez, and Jose L. Labandeira-Garcia. "Angiotensin Type-1 Receptor Inhibition Reduces NLRP3 Inflammasome Upregulation Induced by Aging and Neurodegeneration in the Substantia Nigra of Male Rodents and Primary Mesencephalic Cultures." Antioxidants 11, no. 2 (February 8, 2022): 329. http://dx.doi.org/10.3390/antiox11020329.

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The tissue renin–angiotensin system (RAS) has been shown to be involved in prooxidative and proinflammatory changes observed in aging and aging-related diseases such as dopaminergic degeneration in Parkinson’s disease (PD). We studied the activation of the NLRP3 inflammasome in the substantia nigra with aging and early stages of dopaminergic degeneration in PD models and, particularly, if the brain RAS, via its prooxidative proinflammatory angiotensin II (AngII) type 1 (AT1) receptors, mediates the inflammasome activation. Nigras from aged rats and mice and 6-hydroxydopamine PD models showed upregulation in transcription of inflammasome-related components (NLRP3, pro-IL1β and pro-IL18) and IL1β and IL18 protein levels, which was inhibited by the AT1 receptor antagonist candesartan. The role of the AngII/AT1 axis in inflammasome activation was further confirmed in rats intraventricularly injected with AngII, and in primary mesencephalic cultures treated with 6-hydroxydopamine, which showed inflammasome activation that was blocked by candesartan. Observations in the nigra of young and aged AT1 and AT2 knockout mice confirmed the major role of AT1 receptors in nigral inflammasome activation. In conclusion, the inflammasome is upregulated by aging and dopaminergic degeneration in the substantia nigra, possibly related with a decrease in dopamine levels, and it is mediated by the AngII/AT1 axis.

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3

Wala, Elzbieta P., Jewell W. Sloan, and Xin Jing. "Substantia Nigra." Pharmacology Biochemistry and Behavior 64, no. 3 (November 1999): 611–23. http://dx.doi.org/10.1016/s0091-3057(99)00125-2.

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4

Garant, Douglas S., and Karen Gale. "Substantia nigra-mediated anticonvulsant actions: Role of nigral output pathways." Experimental Neurology 97, no. 1 (July 1987): 143–59. http://dx.doi.org/10.1016/0014-4886(87)90289-5.

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5

Biondetti, Emma, Rahul Gaurav, Lydia Yahia-Cherif, Graziella Mangone, Nadya Pyatigorskaya, Romain Valabrègue, Claire Ewenczyk, et al. "Spatiotemporal changes in substantia nigra neuromelanin content in Parkinson’s disease." Brain 143, no. 9 (August 28, 2020): 2757–70. http://dx.doi.org/10.1093/brain/awaa216.

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Abstract This study aimed to investigate the spatiotemporal changes in neuromelanin-sensitive MRI signal in the substantia nigra and their relation to clinical scores of disease severity in patients with early or progressing Parkinson’s disease and patients with idiopathic rapid eye movement sleep behaviour disorder (iRBD) exempt of Parkinsonian signs compared to healthy control subjects. Longitudinal T1-weighted anatomical and neuromelanin-sensitive MRI was performed in two cohorts, including patients with iRBD, patients with early or progressing Parkinson’s disease, and control subjects. Based on the aligned substantia nigra segmentations using a study-specific brain anatomical template, parametric maps of the probability of a voxel belonging to the substantia nigra were calculated for patients with various degrees of disease severity and controls. For each voxel in the substantia nigra, probability map of controls, correlations between signal-to-noise ratios on neuromelanin-sensitive MRI in patients with iRBD and Parkinson’s disease and clinical scores of motor disability, cognition and mood/behaviour were calculated. Our results showed that in patients, compared to the healthy control subjects, the volume of the substantia nigra was progressively reduced for increasing disease severity. The neuromelanin signal changes appeared to start in the posterolateral motor areas of the substantia nigra and then progressed to more medial areas of this region. The ratio between the volume of the substantia nigra in patients with Parkinson’s disease relative to the controls was best fitted by a mono-exponential decay. Based on this model, the pre-symptomatic phase of the disease started at 5.3 years before disease diagnosis, and 23.1% of the substantia nigra volume was lost at the time of diagnosis, which was in line with previous findings using post-mortem histology of the human substantia nigra and radiotracer studies of the human striatum. Voxel-wise patterns of correlation between neuromelanin-sensitive MRI signal-to-noise ratio and motor, cognitive and mood/behavioural clinical scores were localized in distinct regions of the substantia nigra. This localization reflected the functional organization of the nigrostriatal system observed in histological and electrophysiological studies in non-human primates (motor, cognitive and mood/behavioural domains). In conclusion, neuromelanin-sensitive MRI enabled us to assess voxel-wise modifications of substantia nigra’s morphology in vivo in humans, including healthy controls, patients with iRBD and patients with Parkinson’s disease, and identify their correlation with nigral function across all motor, cognitive and behavioural domains. This insight could help assess disease progression in drug trials of disease modification.

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6

Lersy, François, and Hamid Merdji. "Substantia Nigra Involvement." Neurology 97, no. 8 (May 26, 2021): 391–92. http://dx.doi.org/10.1212/wnl.0000000000012277.

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7

Toomsoo, Toomas, Inga Liepelt-Scarfone, Riina Kerner, Liis Kadastik-Eerme, Toomas Asser, Inna Rubanovits, Daniela Berg, and Pille Taba. "Substantia Nigra Hyperechogenicity." Journal of Ultrasound in Medicine 35, no. 1 (January 2016): 17–23. http://dx.doi.org/10.7863/ultra.14.12069.

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8

Tanibuchi, Ikuo, Hiroyuki Kitano, and Kohnosuke Jinnai. "Substantia Nigra Output to Prefrontal Cortex Via Thalamus in Monkeys. I. Electrophysiological Identification of Thalamic Relay Neurons." Journal of Neurophysiology 102, no. 5 (November 2009): 2933–45. http://dx.doi.org/10.1152/jn.91287.2008.

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A few studies have been performed in primate basal ganglia–thalamo–prefrontal pathways. Nevertheless, their electrophysiological properties and anatomical arrangements remain obscure. This study examined them in nigro-thalamo-cortical pathways from the substantia nigra pars reticulata (SNr) to the frontal cortex (FRC) via the mediodorsal (MD) and ventral anterior (VA) thalamus in monkeys. First, single thalamocortical neurons with SNr input were identified by antidromic responses to FRC stimulation and by inhibitory orthodromic responses with short latencies (<5 ms) to SNr stimulation. Second, single nigrothalamic neurons were found by antidromic responses to stimulation of the portions of the MD and VA where the thalamocortical neurons were recorded. The inhibitory orthodromic responses in the thalamocortical neurons were considered to be monosynaptically induced by nigral stimulation because the latency distribution of the orthodromic responses in the thalamocortical neurons was similar to that of the antidromic responses in the nigrothalamic neurons. Almost all relay neurons in the rostrolateral MD received inhibitory afferents from the caudolateral SNr and projected to the prefrontal area ventral to the principal sulcus, which constituted the densest nigro-thalamo-cortical projections. Meanwhile, neurons in the VA received inhibitory signals from the whole rostrocaudal extent of the SNr and projected to wide regions of the FRC; neurons in its pars magnocellularis mostly projected to different prefrontal areas, while those in its pars parvocellularis projected to motor areas. This report substantiated the topography of thalamocortical neurons monosynaptically receiving inhibitory SNr input and projecting to the FRC in the primate MD and VA at the single-neuron level.

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9

Simmons, DeNard V., Matthew H. Higgs, Sharmon Lebby, and Charles J. Wilson. "Indirect pathway control of firing rate and pattern in the substantia nigra pars reticulata." Journal of Neurophysiology 123, no. 2 (February 1, 2020): 800–814. http://dx.doi.org/10.1152/jn.00678.2019.

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Unitary pallido-nigral synaptic currents were measured using optogenetic stimulation, which activated up to three unitary synaptic inputs to each substantia nigra pars reticulata (SNr) cell. Episodic barrages of synaptic conductances were generated based on in vivo firing patterns of globus pallidus pars externa (GPe) cells and applied to SNr cells using conductance clamp. Barrage inputs were compared to continuous step conductances with the same mean. Barrage inputs and steps both slowed SNr neuron firing and produced disinhibition responses seen in peristimulus histograms. Barrages were less effective than steps at producing inhibition and disinhibition responses. Barrages, but not steps, produced irregular firing during the inhibitory response. Phase models of SNr neurons were constructed from their phase-resetting curves. The phase models reproduced the inhibition and disinhibition responses to the same inputs applied to the neurons. The disinhibition response did not require rebound currents but arose from reset of the cells’ oscillation. The differences in firing rate and irregularity in response to barrage and step inhibition resulted from the high sensitivity of SNr neurons to inhibition at late phases in their intrinsic oscillation. During step inhibition, cells continued rhythmic firing at a reduced rate. During barrages, brief bouts of intense inhibition stalled the cells’ phase evolution late in their cycle, close to firing, and even very brief respites from inhibition rapidly released single action potentials. The SNr cell firing pattern reflected the fine structure of the synaptic barrage from GPe, as well as its onset and offset. NEW & NOTEWORTHY The pallido-nigral pathway connects the striatum to spontaneously active basal ganglia output neurons in the substantia nigra. Each substantia nigra neuron receives powerful inhibitory synaptic connections from a small group of globus pallidus cells and may fire during pauses in pallidal activity. Despite lacking any hyperpolarization-activated rebound currents, they fire quickly to even brief pauses in the pallido-nigral inhibition. The mechanism of their rapid disinhibitory response is explained by features of their phase-resetting curves.

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10

Iribe, Yuji, Kevin Moore, Kevin C. H. Pang, and James M. Tepper. "Subthalamic Stimulation-Induced Synaptic Responses in Substantia Nigra Pars Compacta Dopaminergic Neurons In Vitro." Journal of Neurophysiology 82, no. 2 (August 1, 1999): 925–33. http://dx.doi.org/10.1152/jn.1999.82.2.925.

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The subthalamic nucleus (STN) is one of the principal sources of excitatory glutamatergic input to dopaminergic neurons of the substantia nigra, yet stimulation of the STN produces both excitatory and inhibitory effects on nigral dopaminergic neurons recorded extracellularly in vivo. The present experiments were designed to determine the sources of the excitatory and inhibitory effects. Synaptic potentials were recorded intracellularly from substantia nigra pars compacta dopaminergic neurons in parasagittal slices in response to stimulation of the STN. Synaptic potentials were analyzed for onset latency, amplitude, duration, and reversal potential in the presence and absence of GABA and glutamate receptor antagonists. STN-evoked depolarizing synaptic responses in dopaminergic neurons reversed at approximately −31 mV, intermediate between the expected reversal potential for an excitatory and an inhibitory postsynaptic potential (EPSP and IPSP). Blockade of GABAA receptors with bicuculline caused a positive shift in the reversal potential to near 0 mV, suggesting that STN stimulation evoked a near simultaneous EPSP and IPSP. Both synaptic responses were blocked by application of the glutamate receptor antagonist, 6-cyano-7-nitroquinoxalene-2,3-dione. The confounding influence of inhibitory fibers of passage from globus pallidus and/or striatum by STN stimulation was eliminated by unilaterally transecting striatonigral and pallidonigral fibers 3 days before recording. The reversal potential of STN-evoked synaptic responses in dopaminergic neurons in slices from transected animals was approximately −30 mV. Bath application of bicuculline shifted the reversal potential to ∼5 mV as it did in intact animals, suggesting that the source of the IPSP was within substantia nigra. These data indicate that electrical stimulation of the STN elicits a mixed EPSP-IPSP in nigral dopaminergic neurons due to the coactivation of an excitatory monosynaptic and an inhibitory polysynaptic connection between the STN and the dopaminergic neurons of substantia nigra pars compacta. The EPSP arises from a direct monosynaptic excitatory glutamatergic input from the STN. The IPSP arises polysynaptically, most likely through STN-evoked excitation of GABAergic neurons in substantia nigra pars reticulata, which produces feed-forward GABAA-mediated inhibition of dopaminergic neurons through inhibitory intranigral axon collaterals.

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11

Nikonenko, A. G. "Spatial clustering of substantia nigra astrocytes analyzed in rotenone model of hemiparkinsonism." Fiziolohichnyĭ zhurnal 68, no. 5 (September 13, 2022): 10–15. http://dx.doi.org/10.15407/fz68.05.010.

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This paper addresses spatial aspects of reactive astrogliosis in the substantia nigra pars compacta (SNc) of the rat brain observed 40 and 70 days after the intracerebral 12 µg rotenone infusion. The infusion was shown to cause a marked increase in astrocyte density at both analyzed time points. Minimal spanning tree (MST) analysis was applied to analyze spatial patterns formed by nigral astrocytes. Spatial clusters of these cells, identified as disjoint MST subgraphs, were more numerous in the infused SNc tissue as compared with the control one. Size and density of clusters were significantly different between the infused and control areas 40 and 70 days after the infusion. In conclusion, the data suggests that rotenone-related astrogliosis in the substantia nigra includes changes in spatial patterns of astrocytes as well as transient spatial clustering of these cells.

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12

Ponzoni, Silvia, Luis Carlos J. Gaziri, Luiz R. G. Britto, Wagner J. Barreto, and David Blum. "Clearance of manganese from the rat substantia nigra following intra-nigral microinjections." Neuroscience Letters 328, no. 2 (August 2002): 170–74. http://dx.doi.org/10.1016/s0304-3940(02)00464-0.

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13

Parent, Martin, and André Parent. "Substantia Nigra and Parkinson's Disease: A Brief History of Their Long and Intimate Relationship." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 37, no. 3 (May 2010): 313–19. http://dx.doi.org/10.1017/s0317167100010209.

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The substantia nigra was discovered in 1786 by Félix Vicq d'Azyr, but it took more than a century before Paul Blocq and Georges Marinesco alluded to a possible link between this structure and Parkinson's disease. The insight came from the study of a tuberculosis patient admitted in Charcot's neurology ward at la Salpêtrière because he was suffering from unilateral parkinsonian tremor. At autopsy, Blocq and Marinesco discovered an encapsulated tumor confined to the substantia nigra, contralateral to the affected side, and concluded that tremor in that particular case resulted from a midbrain lesion. This pioneering work, published in 1893, led Edouard Brissaud to formulate, in 1895, the hypothesis that the substantia nigra is the major pathological site in Parkinson's disease. Brissaud's hypothesis was validated in 1919 by Constantin Trétiakoff in a remarkable thesis summarizing a post-mortem study of the substantia nigra conducted in Marinesco's laboratory. Despite highly convincing evidence of nigral cell losses in idiopathic and post-encephalitic Parkinsonism, Trétiakoff's work raised considerable doubts among his colleagues, who believed that the striatum and pallidum were the preferential targets of parkinsonian degeneration. Trétiakoff's results were nevertheless confirmed by detailed neuropathological studies undertaken in the 1930s and by the discovery, in the 1960s, of the dopaminergic nature of the nigrostriatal neurons that degenerate in Parkinson's disease. These findings have strengthened the link between the substantia nigra and Parkinson's disease, but modern research has uncovered the multifaceted nature of this neurodegenerative disorder by identifying other brain structures and chemospecifc systems involved in its pathogenesis.

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14

Eyer, Gian-Carlo, Stefano Di Santo, Ekkehard Hewer, Lukas Andereggen, Stefanie Seiler, and Hans Rudolf Widmer. "Co-Expression of Nogo-A in Dopaminergic Neurons of the Human Substantia Nigra Pars Compacta Is Reduced in Parkinson’s Disease." Cells 10, no. 12 (November 30, 2021): 3368. http://dx.doi.org/10.3390/cells10123368.

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Parkinson’s disease is mainly characterized by a progressive loss of dopaminergic neurons in the substantia nigra pars compacta. Together with the small number, the high vulnerability of the dopaminergic neurons is a major pathogenic culprit of Parkinson’s disease. Our previous findings of a higher survival of dopaminergic neurons in the substantia nigra co-expressing Nogo-A in an animal model of Parkinson’s disease suggested that Nogo-A may be associated with dopaminergic neurons resilience against Parkinson’s disease neurodegeneration. In the present study, we have addressed the expression of Nogo-A in the dopaminergic neurons in the substantia nigra in postmortem specimens of diseased and non-diseased subjects of different ages. For this purpose, in a collaborative effort we developed a tissue micro array (TMA) that allows for simultaneous staining of many samples in a single run. Interestingly, and in contrast to the observations gathered during normal aging and in the animal model of Parkinson’s disease, increasing age was significantly associated with a lower co-expression of Nogo-A in nigral dopaminergic neurons of patients with Parkinson’s disease. In sum, while Nogo-A expression in dopaminergic neurons is higher with increasing age, the opposite is the case in Parkinson’s disease. These observations suggest that Nogo-A might play a substantial role in the vulnerability of dopaminergic neurons in Parkinson’s disease.

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15

FREED, WILLIAM J., H. ELEANOR SPOOR, RENAUD BEAUREPAIRE, JEFFREY A. GREENBERG, and SAUL S. SCHWARZ. "Embryonic Substantia Nigra Grafts." Annals of the New York Academy of Sciences 495, no. 1 Cell and Tiss (June 1987): 581–94. http://dx.doi.org/10.1111/j.1749-6632.1987.tb23701.x.

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16

Mahamed, Safraaz, Tiffany J. Garrison, Joel Shires, and Michele A. Basso. "Stimulation of the substantia nigra influences the specification of memory-guided saccades." Journal of Neurophysiology 111, no. 4 (February 15, 2014): 804–16. http://dx.doi.org/10.1152/jn.00002.2013.

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In the absence of sensory information, we rely on past experience or memories to guide our actions. Because previous experimental and clinical reports implicate basal ganglia nuclei in the generation of movement in the absence of sensory stimuli, we ask here whether one output nucleus of the basal ganglia, the substantia nigra pars reticulata (nigra), influences the specification of an eye movement in the absence of sensory information to guide the movement. We manipulated the level of activity of neurons in the nigra by introducing electrical stimulation to the nigra at different time intervals while monkeys made saccades to different locations in two conditions: one in which the target location remained visible and a second in which the target location appeared only briefly, requiring information stored in memory to specify the movement. Electrical manipulation of the nigra occurring during the delay period of the task, when information about the target was maintained in memory, altered the direction and the occurrence of subsequent saccades. Stimulation during other intervals of the memory task or during the delay period of the visually guided saccade task had less effect on eye movements. On stimulated trials, and only when the visual stimulus was absent, monkeys occasionally (∼20% of the time) failed to make saccades. When monkeys made saccades in the absence of a visual stimulus, stimulation of the nigra resulted in a rotation of the endpoints ipsilaterally (∼2°) and increased the reaction time of contralaterally directed saccades. When the visual stimulus was present, stimulation of the nigra resulted in no significant rotation and decreased the reaction time of contralaterally directed saccades slightly. Based on these measurements, stimulation during the delay period of the memory-guided saccade task influenced the metrics of saccades much more than did stimulation during the same period of the visually guided saccade task. Because these effects occurred with manipulation of nigral activity well before the initiation of saccades and in trials in which the visual stimulus was absent, we conclude that information from the basal ganglia influences the specification of an action as it is evolving primarily during performance of memory-guided saccades. When visual information is available to guide the specification of the saccade, as occurs during visually guided saccades, basal ganglia information is less influential.

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17

Ma, Shuang Y., Frank M. Longo, Matias Röyttä, and Yrjö Collan. "MODERN STEREOLOGICAL EVALUATION IN THE AGING HUMAN SUBSTANTIA NIGRA." Image Analysis & Stereology 22, no. 2 (May 3, 2011): 73. http://dx.doi.org/10.5566/ias.v22.p73-80.

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Quantitative estimation of neuronal numbers in the human substantia nigra (SN) can be achieved by a conventional single section (SS) count or by the more modern stereological disector (DS) count. However, counting results from SS counts are potentially biased and might not accurately reflect the total neuronal number in the SN or the changes in the total number of neurons occurring during aging or with neurodegenerative disease. Potential sources of bias include the lack of linearity between cell number per area of section and cell number per volume; the variation in the counting level and orientation of tissue sections; and shrinkage of tissue. Modern stereological DS counting overcomes these problems and has played a crucial role in many recent studies in neuropathology, neuroanatomy, neuropharmacology and neurogenetics. Over the past decades, four stereology based counting methods including physical DS, physical fractionator, optical DS and optical fractionator, have been established for quantitative measurement. Recently, stereological estimates have revealed a linear reduction rate of total nigral neuronal numbers with age of about 10% per decade. These findings suggest that the surviving nigral neurons undergo a degenerative change leading to neuronal dysfunction with aging. Furthermore, as an advanced quantitative tool, modern stereological evaluation may provide new insights into the aging of the human SN thereby enabling us to better understand the pathophysiological processes in aging brain.

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18

Rodríguez-Sánchez, Escartín-Pérez, Leyva-Gómez, Avalos-Fuentes, Paz-Bermúdez, Loya-López, Aceves, Erlij, Cortés, and Florán. "Blockade of Intranigral and Systemic D3 Receptors Stimulates Motor Activity in the Rat Promoting a Reciprocal Interaction Among Glutamate, Dopamine, and GABA." Biomolecules 9, no. 10 (September 20, 2019): 511. http://dx.doi.org/10.3390/biom9100511.

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In vivo activation of dopamine D3 receptors (D3Rs) depresses motor activity. D3Rs are widely expressed in subthalamic, striatal, and dendritic dopaminergic inputs into the substantia nigra pars reticulata (SNr). In vitro studies showed that nigral D3Rs modulate their neurotransmitter release; thus, it could be that these changes in neurotransmitter levels modify the discharge of nigro-thalamic neurons and, therefore, motor behavior. To determine how the in vitro responses correspond to the in vivo responses, we examined the effect of intra-nigral and systemic blockade of D3Rs in the interstitial content of glutamate, dopamine, and GABA within the SNr using microdialysis coupled to motor activity determinations in freely moving rats. Intranigral unilateral blockade of D3R with GR 103,691 increased glutamate, dopamine, and GABA. Increments correlated with increased ambulatory distance, non-ambulatory activity, and induced contralateral turning. Concomitant blockade of D3R with D1R by perfusion of SCH 23390 reduced the increase of glutamate; prevented the increment of GABA, but not of dopamine; and abolished behavioral effects. Glutamate stimulates dopamine release by NMDA receptors, while blockade with kynurenic acid prevented the increase in dopamine and, in turn, of GABA and glutamate. Finally, systemic administration of D3R selective antagonist U 99194A increased glutamate, dopamine, and GABA in SNr and stimulated motor activity. Blockade of intra-nigral D1R with SCH 23390 prior to systemic U 99194A diminished increases in neurotransmitter levels and locomotor activity. These data highlight the pivotal role of presynaptic nigral D3 and D1R in the control of motor activity and help to explain part of the effects of the in vivo administration of D3R agents.

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19

Gorbatyuk, Oleg S., Shoudong Li, Frederic Nha Nguyen, Fredric P. Manfredsson, Galina Kondrikova, Layla F. Sullivan, Craig Meyers, Weijun Chen, Ronald J. Mandel, and Nicholas Muzyczka. "α-Synuclein Expression in Rat Substantia Nigra Suppresses Phospholipase D2 Toxicity and Nigral Neurodegeneration." Molecular Therapy 18, no. 10 (October 2010): 1758–68. http://dx.doi.org/10.1038/mt.2010.137.

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20

Jones, S. A., B. G. M. Dickie, A. Klegeris, and S. A. Greenfield. "The subthalamo-nigral pathway regulates movement and concomitant acetylcholinesterase release from the substantia nigra." Journal of Neural Transmission 98, no. 1 (February 1994): 23–37. http://dx.doi.org/10.1007/bf01277592.

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21

Kee, Samantha. "Cerebellar modulation of substantia nigra." Intrinsic Activity 4, Suppl. 2 (August 29, 2016): A18.83. http://dx.doi.org/10.25006/ia.4.s2-a18.83.

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22

Gibb, W. R. G. "Neuropathology of the Substantia nigra." European Neurology 31, no. 1 (1991): 48–59. http://dx.doi.org/10.1159/000116721.

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23

Heller, Adam, and Sheryl S. Coffman. "Crystals in the Substantia Nigra." ACS Chemical Neuroscience 10, no. 8 (June 30, 2019): 3415–18. http://dx.doi.org/10.1021/acschemneuro.9b00318.

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24

Misgeld, Ulrich. "Innervation of the substantia nigra." Cell and Tissue Research 318, no. 1 (August 24, 2004): 107–14. http://dx.doi.org/10.1007/s00441-004-0918-2.

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25

Studer, Lorenz. "Culture of Substantia Nigra Neurons." Current Protocols in Neuroscience 00, no. 1 (September 1997): 3.3.1–3.3.12. http://dx.doi.org/10.1002/0471142301.ns0303s00.

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26

Berg, Daniela, Wolfgang Roggendorf, Ute Schröder, Rüdiger Klein, Thomas Tatschner, Peter Benz, Oliver Tucha, et al. "Echogenicity of the Substantia Nigra." Archives of Neurology 59, no. 6 (June 1, 2002): 999. http://dx.doi.org/10.1001/archneur.59.6.999.

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27

Heckers, Stephan, and Christine Konradi. "Substantia Nigra Hyperactivity in Schizophrenia." Biological Psychiatry 74, no. 2 (July 2013): 82–83. http://dx.doi.org/10.1016/j.biopsych.2013.04.017.

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28

Chu, Yaping, Raymond T. Bartus, Fredric P. Manfredsson, C. Warren Olanow, and Jeffrey H. Kordower. "Long-term post-mortem studies following neurturin gene therapy in patients with advanced Parkinson’s disease." Brain 143, no. 3 (March 1, 2020): 960–75. http://dx.doi.org/10.1093/brain/awaa020.

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Abstract We performed post-mortem studies on two patients with advanced Parkinson’s disease 8 and10 years following AAV2-neurturin (CERE120) gene therapy, the longest post-mortem trophic factor gene therapy cases reported to date. CERE120 was delivered to the putamen bilaterally in one case (10 years post-surgery), and to the putamen plus the substantia nigra bilaterally in the second (8 years post-surgery). In both patients there was persistent, albeit limited, neurturin expression in the putamen covering ∼3–12% of the putamen. In the putamen, dense staining of tyrosine hydroxylase-positive fibres was observed in areas that contained detectable neurturin expression. In the substantia nigra, neurturin expression was detected in 9.8–18.95% and 22.02–39% of remaining melanin-containing neurons in the patient with putamenal and combined putamenal and nigral gene delivery, respectively. Melanized neurons displayed intense tyrosine hydroxylase and RET proto-oncogene expression in nigral neurons in the patient where CERE120 was directly delivered to the nigra. There was no difference in the degree of Lewy pathology in comparison to untreated control patients with Parkinson’s disease, and α-synuclein aggregates were detected in neurons that also stained for neurturin, RET, and tyrosine hydroxylase. These changes were not associated with antiparkinsonian benefits likely due to the limited neurturin expression. This study provides the longest term evidence of persistent transgene expression following gene delivery to the CNS and the first human results when targeting both the terminal fields in the putamen as well as the originating nigral neurons.

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Sanderson, P., R. Mavoungou, and D. Albe-Fessard. "Changes in substantia nigra pars reticulata activity following lesions of the substantia nigra pars compacta." Neuroscience Letters 67, no. 1 (June 1986): 25–30. http://dx.doi.org/10.1016/0304-3940(86)90202-8.

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Corda, M. G., A. Concas, M. L. Porceddu, E. Sanna, and G. Biggio. "Striato-nigral denervation increases type II benzodiazepine receptors in the substantia nigra of the rat." Neuropharmacology 25, no. 1 (January 1986): 59–62. http://dx.doi.org/10.1016/0028-3908(86)90059-6.

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Yelnik, Jerome, Chantal François, Gerard Percheron, and Simone Heyner. "Golgi study of the primate substantia nigra. I. Quantitative morphology and typology of nigral neurons." Journal of Comparative Neurology 265, no. 4 (November 22, 1987): 455–72. http://dx.doi.org/10.1002/cne.902650402.

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32

Ding, Shengyuan, Wei Wei, and Fu-Ming Zhou. "Molecular and functional differences in voltage-activated sodium currents between GABA projection neurons and dopamine neurons in the substantia nigra." Journal of Neurophysiology 106, no. 6 (December 2011): 3019–34. http://dx.doi.org/10.1152/jn.00305.2011.

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GABA projection neurons (GABA neurons) in the substantia nigra pars reticulata (SNr) and dopamine projection neurons (DA neurons) in substantia nigra pars compacta (SNc) have strikingly different firing properties. SNc DA neurons fire low-frequency, long-duration spikes, whereas SNr GABA neurons fire high-frequency, short-duration spikes. Since voltage-activated sodium (NaV) channels are critical to spike generation, the different firing properties raise the possibility that, compared with DA neurons, NaV channels in SNr GABA neurons have higher density, faster kinetics, and less cumulative inactivation. Our quantitative RT-PCR analysis on immunohistochemically identified nigral neurons indicated that mRNAs for pore-forming NaV1.1 and NaV1.6 subunits and regulatory NaVβ1 and Navβ4 subunits are more abundant in SNr GABA neurons than SNc DA neurons. These α-subunits and β-subunits are key subunits for forming NaV channels conducting the transient NaV current ( INaT), persistent Na current ( INaP), and resurgent Na current ( INaR). Nucleated patch-clamp recordings showed that INaT had a higher density, a steeper voltage-dependent activation, and a faster deactivation in SNr GABA neurons than in SNc DA neurons. INaT also recovered more quickly from inactivation and had less cumulative inactivation in SNr GABA neurons than in SNc DA neurons. Furthermore, compared with nigral DA neurons, SNr GABA neurons had a larger INaR and INaP. Blockade of INaP induced a larger hyperpolarization in SNr GABA neurons than in SNc DA neurons. Taken together, these results indicate that NaV channels expressed in fast-spiking SNr GABA neurons and slow-spiking SNc DA neurons are tailored to support their different spiking capabilities.

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Martín-Bastida, Antonio, Nicholas P. Lao-Kaim, Andreas Antonios Roussakis, Graham E. Searle, Yue Xing, Roger N. Gunn, Stefan T. Schwarz, Roger A. Barker, Dorothee P. Auer, and Paola Piccini. "Relationship between neuromelanin and dopamine terminals within the Parkinson’s nigrostriatal system." Brain 142, no. 7 (May 5, 2019): 2023–36. http://dx.doi.org/10.1093/brain/awz120.

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Abstract Parkinson’s disease is characterized by the progressive loss of pigmented dopaminergic neurons in the substantia nigra and associated striatal deafferentation. Neuromelanin content is thought to reflect the loss of pigmented neurons, but available data characterizing its relationship with striatal dopaminergic integrity are not comprehensive or consistent, and predominantly involve heterogeneous samples. In this cross-sectional study, we used neuromelanin-sensitive MRI and the highly specific dopamine transporter PET radioligand, 11C-PE2I, to assess the association between neuromelanin-containing cell levels in the substantia nigra pars compacta and nigrostriatal terminal density in vivo, in 30 patients with bilateral Parkinson’s disease. Fifteen healthy control subjects also underwent neuromelanin-sensitive imaging. We used a novel approach taking into account the anatomical and functional subdivision of substantia nigra into dorsal and ventral tiers and striatal nuclei into pre- and post-commissural subregions, in accordance with previous animal and post-mortem studies, and consider the clinically asymmetric disease presentation. In vivo, Parkinson’s disease subjects displayed reduced neuromelanin levels in the ventral (−30 ± 28%) and dorsal tiers (−21 ± 24%) as compared to the control group [F(1,43) = 11.95, P = 0.001]. Within the Parkinson’s disease group, nigral pigmentation was lower in the ventral tier as compared to the dorsal tier [F(1,29) = 36.19, P < 0.001] and lower in the clinically-defined most affected side [F(1,29) = 4.85, P = 0.036]. Similarly, lower dopamine transporter density was observed in the ventral tier [F(1,29) = 76.39, P < 0.001] and clinically-defined most affected side [F(1,29) = 4.21, P = 0.049]. Despite similar patterns, regression analysis showed no significant association between nigral pigmentation and nigral dopamine transporter density. However, for the clinically-defined most affected side, significant relationships were observed between pigmentation of the ventral nigral tier with striatal dopamine transporter binding in pre-commissural and post-commissural striatal subregions known to receive nigrostriatal projections from this tier, while the dorsal tier correlated with striatal projection sites in the pre-commissural striatum (P < 0.05, Benjamini-Hochberg corrected). In contrast, there were no statistically significant relationships between these two measures in the clinically-defined least affected side. These findings provide important insights into the topography of nigrostriatal neurodegeneration in Parkinson’s disease, indicating that the characteristics of disease progression may fundamentally differ across hemispheres and support post-mortem data showing asynchrony in the loss of neuromelanin-containing versus tyrosine hydroxylase positive nigral cells.

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Galpern, Wendy R., David M. Frim, Stephen B. Tatter, C. Anthony Altar, M. Flint Beal, and Ole Isacson. "Cell-Mediated Delivery of Brain-Derived Neurotrophic Factor Enhances Dopamine Levels in an Mpp+ Rat Model of Substantia Nigra Degeneration." Cell Transplantation 5, no. 2 (March 1996): 225–32. http://dx.doi.org/10.1177/096368979600500211.

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Brain-derived neurotrophic factor (BDNF) promotes the survival of fetal mesencephalic dopaminergic cells and protects dopaminergic neurons against the toxicity of MPP+ in vitro. Supranigral implantation of fibroblasts genetically engineered to secrete BDNF attenuates the loss of substantia nigra pars compacta (SNc) dopaminergic neurons associated with striatal infusion of MPP+ in the adult rat. Using this MPP+ rat model of nigral degeneration, we evaluated the neurochemical effects of supranigral, cell-mediated delivery of BDNF on substantia nigra (SN) dopamine (DA) content and turnover. Genetically engineered BDNF-secreting fibroblasts (~12 ng BDNF/24 h) were implanted dorsal to the SN 7 days prior to striatal MPP+ administration. The present results demonstrate that BDNF-secreting fibroblasts, as compared to control fibroblasts, enhance SN DA levels ipsilateral as well as contralateral to the graft without altering DA turnover. This augmentation of DA levels suggests that local neurotrophic factor delivery by genetically engineered cells may provide a therapeutic strategy for preventing neuronal death or enhancing neuronal function in neurodegenerative diseases characterized by dopaminergic neuronal dysfunction, such as Parkinson's disease.

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35

McRitchie, D. A., G. M. Halliday, and R. Pamphlett. "Diagnostic evaluation of the substantia nigra." Neuropathology and Applied Neurobiology 22, no. 3 (June 1996): 228–32. http://dx.doi.org/10.1046/j.1365-2990.1996.4698046.x.

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36

McRitchiet, D. A., G. M. Halliday, and R. Pamphlett. "Diagnostic evaluation of the substantia nigra." Neuropathology and Applied Neurobiology 22, no. 3 (June 1996): 228–32. http://dx.doi.org/10.1111/j.1365-2990.1996.tb00898.x.

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37

Kapsa, Robert M. I., M. J. Bernadette Jean-Francois, Patcharee Lertrit, Shan Weng, Nurjati Siregar, Joseline Ojaimi, Geoffrey Donnan, Colin Masters, and Edward Byrne. "Mitochondrial DNA polymorphism in substantia nigra." Journal of the Neurological Sciences 144, no. 1-2 (December 1996): 204–11. http://dx.doi.org/10.1016/s0022-510x(96)00247-x.

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38

Walker, Courtney K., Joy K. Roche, Vidushi Sinha, and Rosalinda C. Roberts. "Substantia nigra ultrastructural pathology in schizophrenia." Schizophrenia Research 197 (July 2018): 209–18. http://dx.doi.org/10.1016/j.schres.2017.12.004.

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39

Christensson-Nylander, Ingrid, and Lars Terenius. "Dynorphin peptides in human substantia nigra." Neuropeptides 6, no. 5 (September 1985): 391–96. http://dx.doi.org/10.1016/0143-4179(85)90137-4.

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40

Iova, Alexander, Andrew Garmashov, Natalia Androuchtchenko, Martin Kehrer, Daniela Berg, Georg Becker†, and Yurii Garmashov. "Postnatal decrease in substantia nigra echogenicity." Journal of Neurology 251, no. 12 (December 2004): 1451–54. http://dx.doi.org/10.1007/s00415-004-0556-3.

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41

Pinnock, R. D. "Neurotensin depolarizes substantia nigra dopamine neurones." Brain Research 338, no. 1 (July 1985): 151–54. http://dx.doi.org/10.1016/0006-8993(85)90258-6.

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42

Bor-Seng-Shu, Edson, Erich Talamoni Fonoff, Egberto Reis Barbosa, and Manoel Jacobsen Teixeira. "Substantia nigra hyperechogenicity in Parkinson’s disease." Acta Neurochirurgica 152, no. 12 (July 11, 2010): 2085–87. http://dx.doi.org/10.1007/s00701-010-0736-0.

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43

Stockner, Heike, Martin Sojer, Sascha Hering, Wolfgang Nachbauer, Klaus Seppi, Christoph Schmidauer, Werner Poewe, and Sylvia M. Boesch. "Substantia nigra hypoechogenicity in Friedreich ataxia." Movement Disorders 27, no. 2 (December 9, 2011): 332–33. http://dx.doi.org/10.1002/mds.23989.

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44

Savant, Charulata Sankhla, B. S. Singhal, Joseph Jankovic, Mak Khan, and Amin Virani. "Substantia nigra lesions in viral encephalitis." Movement Disorders 18, no. 2 (January 21, 2003): 213–16. http://dx.doi.org/10.1002/mds.10339.

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45

Bove, Cecilia, and R. Alberto Travagli. "Neurophysiology of the brain stem in Parkinson’s disease." Journal of Neurophysiology 121, no. 5 (May 1, 2019): 1856–64. http://dx.doi.org/10.1152/jn.00056.2019.

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Parkinson’s disease (PD) is predominantly idiopathic in origin, and a large body of evidence indicates that gastrointestinal (GI) dysfunctions are a significant comorbid clinical feature; these dysfunctions include dysphagia, nausea, delayed gastric emptying, and severe constipation, all of which occur commonly before the onset of the well-known motor symptoms of PD. Based on a distinct distribution pattern of Lewy bodies (LB) in the enteric nervous system (ENS) and in the preganglionic neurons of the dorsal motor nucleus of the vagus (DMV), and together with the early onset of GI symptoms, it was suggested that idiopathic PD begins in the ENS and spreads to the central nervous system (CNS), reaching the DMV and the substantia nigra pars compacta (SNpc). These two areas are connected by a recently discovered monosynaptic nigro-vagal pathway, which is dysfunctional in rodent models of PD. An alternative hypothesis downplays the role of LB transport through the vagus nerve and proposes that PD pathology is governed by regional or cell-restricted factors as the leading cause of nigral neuronal degeneration. The purpose of this brief review is to summarize the neuronal electrophysiological findings in the SNpc and DMV in PD.

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Korzhevskii, D. E., D. A. Sufieva, and M. A. Brovko. "MICROGLIA AND ASTROCYTES OF THE HUMAN BRAIN SUBSTANTIA NIGRA." Medical academic journal 19, no. 1S (December 15, 2019): 135. http://dx.doi.org/10.17816/maj191s1135.

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In recent years, attention of researches has focused on glial cells of different brain formations - astrocytes and microglial cells. This is due to active role of these cells in ensuring synaptic plasticity and regulation of neurogenesis. The study aimed at analyzing the structural organization of microglia and astrocytes of the human brain substantia nigra, which is the main dopaminergic nerve center. For the study, material from the archive of the Morphology Department (Institute of Experimental Medicine, Saint Petersburg, Russia) was used. Cells were detected using immunocytochemical markers (GFAP for astrocytes and Iba-1 for microglia). It has been established that microglial cells bodies in substantia nigra are located in neuropile singly. In pars compacta of substantia nigra these cells distributed relatively evenly, rarely being in close proximity to neurons. An unexpected fact was that the processes of microglia cells of the human brain substantia nigra have a sufficiently large thickness - 1.5-3 microns, which is not typical for a ramified microglia. Astrocytes of substantis nigra were characterized by the presence of very long processes (more than 100 microns) and the formation of the pericellular sheath around the nerve cells. These sheaths consisted of a dense interweaving of thin sparingly branched astrocyte processes. The processes of microglia were rarely present within such sheaths. The results obtained indicate moderate activation of microglia in substantia nigra and the special role of astrocytes in ensuring the compartmentalization of the pericellular zones in this nerve center.

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47

Raziya Banu, Mohammad, Muhammed Ibrahim, K. Prabhu, and Srinivasagam Rajasankar. "Ameliorative Effect of Withaferin A on Ageing-Mediated Impairment in the Dopamine System and Its Associated Behavior of Wistar Albino Rat." Pharmacology 103, no. 3-4 (December 13, 2018): 114–19. http://dx.doi.org/10.1159/000495510.

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Withaferin A (WA) was evaluated for its neuro-protective efficacy on ageing induced striatal dopamine (DA) and behavioural changes in aged rats. Wistar albino rats were divided into group I – young (3 months), Group II – aged (24 months), Group III – aged rats supplemented with WA (50 mg/kg b.w once in a day for 30 days) and Group IV – young rats supplemented with WA (50 mg/kg b.w). The HPLC assay revealed significant decline in the levels of DA and homovanillic acid (HVA) in substantia nigra (SN) and striatum (ST) of aged rat. A marked decline in motor activity of aged rat was observed through open field, beam walking and grid walking motor experiments. These results indicate that ageing reduces nigro-striatal activity as well as nigro-striatal DA levels. Interestingly, the administration of WA (50 mg\kg b.w) resulted in a substantial resurge of DA and HVA in SN and ST and a significant reversal of motor impairment in aged rats. This study is the first report that evidently determines the neuro-protective efficacy of WA on dopaminergic system of SN and ST in aged rats.

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Celada, P., C. A. Paladini, and J. M. Tepper. "Gabaergic control of rat substantia nigra dopaminergic neurons: role of globus pallidus and substantia nigra pars reticulata." Neuroscience 89, no. 3 (March 1999): 813–25. http://dx.doi.org/10.1016/s0306-4522(98)00356-x.

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49

Chen, Yun-Hsiang, Kuo-Jen Wu, Wei Hsieh, Brandon K. Harvey, Barry J. Hoffer, Yun Wang, and Seong-Jin Yu. "Administration of AAV-Alpha Synuclein NAC Antibody Improves Locomotor Behavior in Rats Overexpressing Alpha Synuclein." Genes 12, no. 6 (June 21, 2021): 948. http://dx.doi.org/10.3390/genes12060948.

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Accumulation of α-Synuclein (αSyn) in nigral dopaminergic neurons is commonly seen in patients with Parkinson′s disease (PD). We recently reported that transduction of intracellular single-chain intrabody targeting the 53–87 amino acid residues of human αSyn by recombinant adeno associated viral vector (AAV-NAC32) downregulated αSyn protein in SH-SY5Y cells and rat brain. This study characterizes the behavioral phenotype and dopaminergic protection in animals receiving AAV-NAC32. Our results show that adult DAT-Cre rats selectively overexpress αSyn in nigra dopaminergic neurons after local administration of AAV-DIO-αSyn. These animals develop PD-like phenotype, including bradykinesia and loss of tyrosine hydroxylase (TH) immunoreactivity in substantia nigra pars compacta dorsal tier (SNcd). An injection of AAV-NAC32 to nigra produces a selective antibody against αSyn and normalizes the behavior. AAV-NAC32 significantly increases TH, while reduces αSyn immunoreactivity in SNcd. Altogether, our data suggest that an AAV-mediated gene transfer of NAC32 antibody effectively antagonizes αSyn-mediated dopaminergic degeneration in nigra, which may be a promising therapeutic candidate for synucleinopathy or PD.

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Simmons, D. V., M. H. Higgs, S. Lebby, and C. J. Wilson. "Predicting responses to inhibitory synaptic input in substantia nigra pars reticulata neurons." Journal of Neurophysiology 120, no. 5 (November 1, 2018): 2679–93. http://dx.doi.org/10.1152/jn.00535.2018.

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The changes in firing probability produced by a synaptic input are usually visualized using the poststimulus time histogram (PSTH). It would be useful if postsynaptic firing patterns could be predicted from patterns of afferent synaptic activation, but attempts to predict the PSTH from synaptic potential waveforms using reasoning based on voltage trajectory and spike threshold have not been successful, especially for inhibitory inputs. We measured PSTHs for substantia nigra pars reticulata (SNr) neurons inhibited by optogenetic stimulation of striato-nigral inputs or by matching artificial inhibitory conductances applied by dynamic clamp. The PSTH was predicted by a model based on each SNr cell’s phase-resetting curve (PRC). Optogenetic activation of striato-nigral input or artificial synaptic inhibition produced a PSTH consisting of an initial depression of firing followed by oscillatory increases and decreases repeating at the SNr cell’s baseline firing rate. The phase resetting model produced PSTHs closely resembling the cell data, including the primary pause in firing and the oscillation. Key features of the PSTH, including the onset rate and duration of the initial inhibitory phase, and the subsequent increase in firing probability could be explained from the characteristic shape of the SNr cell’s PRC. The rate of damping of the late oscillation was explained by the influence of asynchronous phase perturbations producing firing rate jitter and wander. Our results demonstrate the utility of phase-resetting models as a general method for predicting firing in spontaneously active neurons and their value in interpretation of the striato-nigral PSTH. NEW & NOTEWORTHY The coupling of patterned presynaptic input to sequences of postsynaptic firing is a Gordian knot, complicated by the multidimensionality of neuronal state and the diversity of potential initial states. Even so, it is fundamental for even the simplest understanding of network dynamics. We show that a simple phase-resetting model constructed from experimental measurements can explain and predict the sequence of spike rate changes following synaptic inhibition of an oscillating basal ganglia output neuron.

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