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Relevant bibliographies by topics / Dopamine neurons, parkinson's disease, neuroscience

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Academic literature on the topic 'Dopamine neurons, parkinson's disease, neuroscience'

Author: Grafiati

Published: 10 March 2023

Last updated: 11 March 2023

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Journal articles on the topic "Dopamine neurons, parkinson's disease, neuroscience"

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Granado, Noelia, Sara Ares-Santos, and Rosario Moratalla. "Methamphetamine and Parkinson's Disease." Parkinson's Disease 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/308052.

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Parkinson's disease (PD) is a neurodegenerative disorder predominantly affecting the elderly. The aetiology of the disease is not known, but age and environmental factors play an important role. Although more than a dozen gene mutations associated with familial forms of Parkinson's disease have been described, fewer than 10% of all cases can be explained by genetic abnormalities. The molecular basis of Parkinson's disease is the loss of dopamine in the basal ganglia (caudate/putamen) due to the degeneration of dopaminergic neurons in the substantia nigra, which leads to the motor impairment characteristic of the disease. Methamphetamine is the second most widely used illicit drug in the world. In rodents, methamphetamine exposure damages dopaminergic neurons in the substantia nigra, resulting in a significant loss of dopamine in the striatum. Biochemical and neuroimaging studies in human methamphetamine users have shown decreased levels of dopamine and dopamine transporter as well as prominent microglial activation in the striatum and other areas of the brain, changes similar to those observed in PD patients. Consistent with these similarities, recent epidemiological studies have shown that methamphetamine users are almost twice as likely as non-users to develop PD, despite the fact that methamphetamine abuse and PD have distinct symptomatic profiles.

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Bishop, Matthew W., Subhojit Chakraborty, Gillian A. C. Matthews, Antonios Dougalis, Nicholas W. Wood, Richard Festenstein, and Mark A. Ungless. "Hyperexcitable Substantia Nigra Dopamine Neurons in PINK1- and HtrA2/Omi-Deficient Mice." Journal of Neurophysiology 104, no. 6 (December 2010): 3009–20. http://dx.doi.org/10.1152/jn.00466.2010.

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The electrophysiological properties of substantia nigra pars compacta (SNC) dopamine neurons can influence their susceptibility to degeneration in toxin-based models of Parkinson's disease (PD), suggesting that excitotoxic and/or hypoactive mechanisms may be engaged during the early stages of the disease. It is unclear, however, whether the electrophysiological properties of SNC dopamine neurons are affected by genetic susceptibility to PD. Here we show that deletion of PD-associated genes, PINK1 or HtrA2/Omi, leads to a functional reduction in the activity of small-conductance Ca2+-activated potassium channels. This reduction causes SNC dopamine neurons to fire action potentials in an irregular pattern and enhances burst firing in brain slices and in vivo. In contrast, PINK1 deletion does not affect firing regularity in ventral tegmental area dopamine neurons or substantia nigra pars reticulata GABAergic neurons. These findings suggest that changes in SNC dopamine neuron excitability may play a role in their selective vulnerability in PD.

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Kesslak, J. Patrick. "Transplantation of embryonic dopamine neurons for severe Parkinson's disease." Neuroreport 12, no. 7 (May 2001): A47. http://dx.doi.org/10.1097/00001756-200105250-00002.

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Taylor, Tonya N., W. Michael Caudle, and Gary W. Miller. "VMAT2-Deficient Mice Display Nigral and Extranigral Pathology and Motor and Nonmotor Symptoms of Parkinson's Disease." Parkinson's Disease 2011 (2011): 1–9. http://dx.doi.org/10.4061/2011/124165.

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Dopamine is transported into synaptic vesicles by the vesicular monoamine transporter (VMAT2; SLC18A2). Disruption of dopamine storage has been hypothesized to damage the dopamine neurons that are lost in Parkinson's disease. By disrupting vesicular storage of dopamine and other monoamines, we have created a progressive mouse model of PD that exhibits catecholamine neuron loss in the substantia nigra pars compacta and locus coeruleus and motor and nonmotor symptoms. With a 95% reduction in VMAT2 expression, VMAT2-deficient animals have decreased motor function, progressive deficits in olfactory discrimination, shorter latency to behavioral signs of sleep, delayed gastric emptying, anxiety-like behaviors at younger ages, and a progressive depressive-like phenotype. Pathologically, the VMAT2-deficient mice display progressive neurodegeneration in the substantia nigra (SNpc), locus coeruleus (LC), and dorsal raphe (DR) coupled withα-synuclein accumulation. Taken together, these studies demonstrate that reduced vesicular storage of monoamines and the resulting disruption of the cytosolic environment may play a role in the pathogenesis of parkinsonian symptoms and neurodegeneration. The multisystem nature of the VMAT2-deficient mice may be useful in developing therapeutic strategies that go beyond the dopamine system.

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Denyer, Rachel, and Michael R. Douglas. "Gene Therapy for Parkinson's Disease." Parkinson's Disease 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/757305.

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Current pharmacological and surgical treatments for Parkinson's disease offer symptomatic improvements to those suffering from this incurable degenerative neurological disorder, but none of these has convincingly shown effects on disease progression. Novel approaches based on gene therapy have several potential advantages over conventional treatment modalities. These could be used to provide more consistent dopamine supplementation, potentially providing superior symptomatic relief with fewer side effects. More radically, gene therapy could be used to correct the imbalances in basal ganglia circuitry associated with the symptoms of Parkinson's disease, or to preserve or restore dopaminergic neurons lost during the disease process itself. The latter neuroprotective approach is the most exciting, as it could theoretically be disease modifying rather than simply symptom alleviating. Gene therapy agents using these approaches are currently making the transition from the laboratory to the bedside. This paper summarises the theoretical approaches to gene therapy for Parkinson's disease and the findings of clinical trials in this rapidly changing field.

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Murase, S. "A Specific Survival Response in Dopamine Neurons at Most Risk in Parkinson's Disease." Journal of Neuroscience 26, no. 38 (September 20, 2006): 9750–60. http://dx.doi.org/10.1523/jneurosci.2745-06.2006.

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Bogetofte, Helle, Arezo Alamyar, Morten Blaabjerg, and Morten Meyer. "Levodopa Therapy for Parkinson's Disease: History, Current Status and Perspectives." CNS & Neurological Disorders - Drug Targets 19, no. 8 (December 24, 2020): 572–83. http://dx.doi.org/10.2174/1871527319666200722153156.

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Parkinson’s Disease (PD) is a neurodegenerative disorder characterized by a preferential degeneration of dopaminergic neurons in the substantia nigra pars compacta. This results in a profound decrease of striatal dopamine (DA) levels, which in turn leads to the cardinal motor symptoms of PD; muscle rigidity, hypo- and bradykinesia and resting tremor. Even 50 years after its initial use, the DA precursor levodopa (L-dopa), is still the most effective medical therapy for the symptomatic treatment of PD. Long-term L-dopa treatment is however, unfortunately associated with undesirable side effects such as motor fluctuations and dyskinesias. Furthermore, despite the disease alleviating effects of L-dopa, it is still discussed whether L-dopa has a neurotoxic or neuroprotective effect on dopaminergic neurons. Here we review the history of L-dopa, including its discovery, development and current use in the treatment of PD. We furthermore review current evidence of the L-dopa-induced side effects and perspectives of L-dopa treatment in PD compared to other established treatments such as DA-agonists and the inhibitors of catechol-o-methyltransferase and monoamine oxidase B.

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Barker, Roger A., Anders Björklund, Steven J. Frucht, and Clive N. Svendsen. "Stem Cell-Derived Dopamine Neurons: Will They Replace DBS as the Leading Neurosurgical Treatment for Parkinson’s Disease?" Journal of Parkinson's Disease 11, no. 3 (July 30, 2021): 909–17. http://dx.doi.org/10.3233/jpd-219008.

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The use of stem cell-derived dopamine neurons or deep brain stimulation (DBS) represents two alternative approaches to treat Parkinson’s Disease. DBS is a widely used FDA-approved treatment and stem cell-derived dopamine neuron replacement has now evolved to the first in-human clinical trials. In this debate, we discuss which of these approaches will evolve to be the treatment of choice for Parkinsonian patients in the future.

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FEDOROW, H., F. TRIBL, G. HALLIDAY, M. GERLACH, P. RIEDERER, and K. DOUBLE. "Neuromelanin in human dopamine neurons: Comparison with peripheral melanins and relevance to Parkinson's disease." Progress in Neurobiology 75, no. 2 (February 2005): 109–24. http://dx.doi.org/10.1016/j.pneurobio.2005.02.001.

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Parker, Krystal L., Kuan-Hua Chen, Johnathan R. Kingyon, James F. Cavanagh, and Nandakumar S. Narayanan. "Medial frontal ∼4-Hz activity in humans and rodents is attenuated in PD patients and in rodents with cortical dopamine depletion." Journal of Neurophysiology 114, no. 2 (August 2015): 1310–20. http://dx.doi.org/10.1152/jn.00412.2015.

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The temporal control of action is a highly conserved and critical mammalian behavior. Here, we investigate the neuronal basis of this process using an interval timing task. In rats and humans, instructional timing cues triggered spectral power across delta and theta bands (2–6 Hz) from the medial frontal cortex (MFC). Humans and rodents with dysfunctional dopamine have impaired interval timing, and we found that both humans with Parkinson's disease (PD) and rodents with local MFC dopamine depletion had attenuated delta and theta activity. In rodents, spectral activity in this range could functionally couple single MFC neurons involved in temporal processing. Without MFC dopamine, these neurons had less functional coupling with delta/theta activity and less temporal processing. Finally, in humans this 2- to 6-Hz activity was correlated with executive function in matched controls but not in PD patients. Collectively, these findings suggest that cue-evoked low-frequency rhythms could be a clinically important biomarker of PD that is translatable to rodent models, facilitating mechanistic inquiry and the development of neurophysiological biomarkers for human disease.

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Dissertations / Theses on the topic "Dopamine neurons, parkinson's disease, neuroscience"

1

Wiemerslage, Lyle N. "Neuroprotection of Dopaminergic Neurons and their Subcellular Structures from Parkinson's Disease-like Treatment." Ohio University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1395669814.

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Kaufmann, Anna-Kristin. "Functional properties of the intact and compromised midbrain dopamine system." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:8769a453-aa91-4509-b06e-48f25e88f15a.

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The midbrain dopamine system is involved in many aspects of purposeful behaviour and, when compromised, can have devastating effects on movement and cognition as seen in diseases like Parkinson's. In the healthy brain, dopamine neurons are thought to play particularly important roles in learning by signalling errors in reward prediction. The objective of this thesis was to investigate the diversity in the functional properties of the midbrain dopamine system, and how this is altered through genetic variation of relevance to Parkinson's and development of cell phenotype. This objective was addressed with a combination of behavioural experiments, in vivo single-cell recording and labelling (both in anaesthetised as well as awake rodents), immunofluorescence labelling, retrograde tracing and stereology. In a first set of experiments, it was demonstrated that chronic as well as acute genetic challenges can alter the firing patterns of midbrain dopamine neurons. Using a novel bacterial artificial chromosome-transgenic rat model, it was shown that the R1441C mutation in human leucine-rich repeat kinase 2, which is linked to Parkinson's, leads to motor deficits and an age-dependent reduction in the in vivo firing variability and burst firing of substantia nigra pars compacta (SNc) dopamine neurons. These findings help reveal processes of early, pre-degenerative dysfunction in dopamine neurons in Parkinson's. Similar effects on firing variability and burst firing of SNc dopamine neurons were found in a mouse model with conditional knock- out of the transcription factors Forkhead box A1 and A2 (FoxA1/2) in midbrain dopamine neurons. These findings indicate that FoxA1/2 are not only crucial for the early development of dopamine neurons, but also their function in the mature brain. In a second set of experiments in wildtype mice, it was demonstrated that midbrain dopamine neurons (located in SNc and ventral tegmental area) show diverse expression of the molecular markers Calbindin, Calretinin, Aldh1a1, Sox6, Girk2, SatB1 and Otx2. It was found that selective expression of these markers is of use for discriminating between midbrain dopamine neurons that project to dorsal striatum or nucleus accumbens. To elucidate whether the diverse molecular marker expression would map onto dopamine neurons whose firing correlates with distinct behavioural events, midbrain dopamine neurons were recorded and labelled in head-fixed awake mice either exposed to neutral sensory stimuli or performing a classical conditioning paradigm. The population activity of midbrain dopamine neurons was not modulated by neutral sensory stimuli. Interestingly, fewer than 50% of identified dopamine neurons showed phasic firing increases following reward- predicting cue and/or reward delivery, despite the common assumption that most (if not all) midbrain dopamine neurons signal reward prediction errors. Instead, firing was modulated by other explanatory factors, such as licking, or showed no modulation during the task. Response types of midbrain dopamine neurons were not correlated with their anatomical location nor the selective or combinatorial expression of the markers Aldh1a1, Calbindin and Sox6. In conclusion, the first set of experiments identified how different genetic burdens can alter the in vivo firing of midbrain dopamine neurons, and provide new insights into how circuits can change in pathological or compensatory ways at early disease stages in Parkinson's. The second set of experiments revealed striking heterogeneity of midbrain dopamine neurons in the intact system, and established further a functional diversity in the response types of identified midbrain dopamine neurons that is only partially consistent with canonical reward prediction error signalling.

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Bishop, Matthew William. "Electrophysiological properties of midbrain dopamine neurons in genetic mouse models of Parkinson's disease." Thesis, Imperial College London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.528309.

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Vinciati, Federica. "Electrophysiological properties of striatal neurons in the dopamine-intact and Parkinsonian brain." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:e4e84e31-bc00-43b2-a930-dc7fa4143b1a.

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The striatum is the major input structure of the basal ganglia, and is composed of two major populations of spiny projection neurons (MSNs), which give rise to the socalled direct and indirect pathways, and several types of interneuron. Dopaminergic inputs to striatum are critical for its proper function. Indeed, loss of dopaminergic neurons in Parkinsonism leads to motor disturbances, grossly disturbs striatal activity, and is associated with the emergence of excessively-synchronized network oscillations at beta frequencies (15-30 Hz) throughout the basal ganglia. How the distinct structural, neurochemical and other properties of striatal neurons are reflected in their firing rates and patterns in vivo is poorly defined, as are their possible cell-type-selective contributions to the aberrant oscillations arising in the Parkinsonian brain. To address these issues, I first used multi-electrode arrays to record the spontaneous firing of ensembles of neurons in dorsal striatum in both anaesthetised dopamine-intact and Parkinsonian (6-hydroxydopamine-lesioned) rats during two well-defined brain states, slow-wave activity (SWA) and spontaneous activation. The chronic loss of dopamine led to an overall increase in the average firing rates of striatal neurons, irrespective of brain state. However, many neurons in the Parkinsonian striatum still exhibited the low firing rates and irregular firing patterns typical of neurons in the dopamine-intact striatum. During SWA in Parkinsonian rats, the firing of striatal neurons was more strongly synchronized at low frequencies, in time with cortical slow (~1 Hz) oscillations. During spontaneous cortical activation in Parkinsonian rats, more striatal neurons engaged in synchronized firing in time with cortical beta oscillations. Under the same experimental conditions, I then recorded the spontaneous firing of individual striatal neurons and juxtacellularly labelled the same neurons to verify their cell types, and locations; indirect pathway and direct pathway MSNs were distinguished by the expression (and lack of expression respectively), of the neuropeptide precursor preproenkephalin (PPE). After chronic dopamine loss, and on average, only indirect pathway (PPE+) MSNs significantly increased their firing rates during both brain states, and engaged in widespread, synchronized firing in the beta-frequency range. This did not hold true for all PPE+ MSNs; the Parkinsonian striatum contained many MSNs that were virtually quiescent, which were just as likely to belong to the indirect pathway as the direct pathway. Direct pathway (PPE-) MSNs increased their firing only during SWA after chronic dopamine loss and rarely engaged in aberrant beta oscillations. Taken together, these data suggest that (1) the firing patterns, as well as the firing rates of many striatal neurons are grossly disturbed by chronic loss of dopamine and (2) that the pathological synchronization of the rhythmic firing of a subpopulation of indirect pathway MSNs could contribute to the propagation of aberrant beta-frequency oscillations to downstream basal ganglia nuclei in Parkinsonism.

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Heshka, Timothy William. "Effects of hypoxanthine upon dopamine neurons : an animal model for Lesch-Nyhan disease." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=59392.

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In Lesch-Nyhan disease, concentrations of hypoxanthine are elevated especially in the brain and cerebrospinal fluid; dopamine and its metabolites are reduced in the caudate and putamen. Hence we investigated the possibility that hypoxanthine has direct effects on dopamine neurons.
Hypoxanthine, adenine or allopurinol was delivered unilaterally into the rat brain. Behavioural effects were monitored by apomorphine-induced rotation; ipsilateral turning was time and dose-dependent. Turning was competitively blocked by a non-specific DA antagonist, suggesting that dopamine neurons were altered. In hypoxanthine treated animals, a D1 antagonist specifically blocked rotation; catalepsy occurred after caffeine administration.
After two or three weeks treatment all groups had elevated purine levels in the caudate nuclei, while catecholamine levels were variably altered.

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Mecconi, Alessandro. "Dopamine replacement therapy reduces beta band burst duration in Parkinson’s disease." Thesis, KTH, Skolan för teknik och hälsa (STH), 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-215055.

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One of the main characteristics of Parkinson's disease (PD) is an exaggerated oscillatory activity in the beta band (12-30 Hz). This activity has been linked to the rise of symptoms such as bradykinesia and akinesia. Even if dopamine replacement therapy (oral intake of dopamine pro-drug levodopa) reverses these symptoms, the effect of the treatment on the beta band activity has still not been completely understood. Therefore, here the temporal dynamics of beta band activity in human patients affected by PD were characterized with and without levodopa treatment. Local-field-potential (LFP) recordings from five patients undergoing dopamine replacement therapy were used. From the LFPs, the extracted beta epochs with significantly higher power than expected from a comparable noisy signal were analyzed. This analysis showed that beta band activity occurred in bursts meaning that high amplitude oscillation alternated with silenced periods. The pathological state also distinguished itself for longer epochs and with power that increased with the length of the epoch. The administration of levodopa reduced the duration of bursts and decreased the overall mean power of the beta band activity. Finally, epochs with the same number of cycles were compared. The Coefficient of Variation prior such epochs suggested that the ongoing activity might lock into a synchronization process prior the burst. These results provide important information to better understand how levodopa alleviates some of the symptoms of PD and pave the way to develop better computational models for the emergence of beta oscillations.

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Nikkhah, Guido. "Microtransplantation of nigral dopamine neurons in a rat model of Parkinson's disease studies on functional recovery and structural repair in adult and neonatal rats with lesions of the mesotelencephalic dopamine system /." Lund : Dept. of Medical Cell Research, Lund University, 1994. http://catalog.hathitrust.org/api/volumes/oclc/39693821.html.

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Eckert, Laurie Leigh. "Parkinson's disease and a dopamine-derived neurotoxin, 3,4-Dihydroxyphenylacetaldehyde : implications for proteins, microglia, and neurons." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/1592.

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Parkinson's disease (PD) is a prevalent neurodegenerative disorder for which the greatest risk factor is age. Four to five percent of 85-year-olds suffer from this debilitating disease, which is characterized by the selective loss of dopaminergic neurons within the substantia nigra and the presence of protein aggregates known as Lewy bodies. While the etiology of this disease is still unknown, recent research implicates oxidative stress, activated microglia, and reactive dopamine (DA) metabolites to play a role in the initiation or progression of the disease. Activated microglia cause injury to dopaminergic neurons via a host of mechanisms, including reactive oxygen species production, release of cytokines, and phagocytic activity. Microglial activation has been detected in the brains of PD patients, but the source of this activation has not been elucidated. Previous research has shown electrophiles and endogenous neurotoxins to play a role in this microglial activation. The interaction between the neurotoxic metabolite of DA, 3,4-dihydroxyphenylacetaldehyde (DOPAL), and microglia has not been explored. DOPAL is a highly reactive, bifunctional electrophile produced by oxidative deamination of DA by monoamine oxidase (MAO). DOPAL is oxidized in the major metabolism pathway to 3,4-dihydroxyphenylacetic acid (DOPAC) by aldehyde dehydrogenase (ALDH). DOPAL has previously been shown to be 100-fold more toxic than DA in vitro and in vivo. Potent inhibition of the rate-limiting enzyme in DA biosynthesis, tyrosine hydroxylase, by DOPAL has been well-established. DOPAL-mediated aggregation of Α-synuclein, the primary component of PD-hallmark Lewy bodies, has been suggested but was further explored in this work. Results presented in this body of work include further determination of the aggregation of Α-synuclein by DOPAL, including evidence of covalent modification. The interaction of DOPAL with BV-2 microglia, an immortalized cell line, was addressed in depth through exploration of DOPAL catabolism, toxicity, and generation of an activational response. Metabolism of DOPAL to DOPAC was altered in activated microglia, with the production of DOPAC reduced by ~40%. Metabolism of DOPAL to DOPAC was also inhibited by both 4-hydroxynonenal and malondialdehyde, gold standards of lipid peroxidation. Both of these compounds were found to be significantly toxic to BV-2 cells at concentrations well below those considered toxic to dopaminergic cells. Alternatively, DOPAL and DA were found to be non-toxic to this cell line, while DOPAL was shown to be significantly toxic to dopaminergic cells at concentrations as low as 10 ΜM. Significant activation of BV-2 microglia by DOPAL was observed at 10 ΜM and above by release of TNF-Α. Morphological changes, release of IL-6, and changes in expression of COX-2 also indicated activation by DOPAL but not DA or DOPAC. BV-2-conditioned media, generated by incubation with DA, DOPAL, or DOPAC, was added to MN9D cells, and toxicity was measured by the MTT assay. BV-2 conditioned media generated by DOPAL incubation produced the greatest toxicity for MN9D cells. These results implicate DOPAL in dopaminergic cell death through microglial activation.

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Ahmadi, Ferogh Ali. "The mechanism of pesticide rotenone-induced cell death in models of Parkinson's disease /." Connect to full text via ProQuest. IP filtered, 2005.

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Thesis (Ph.D. in Neuroscience) -- University of Colorado at Denver and Health Sciences Center, 2005.
Typescript. Includes bibliographical references (leaves 110-128). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;

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Kosillo, Polina. "Investigating circuits underlying acetylcholine-evoked striatal dopamine release in health and disease." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:1675813e-0b07-4ede-9094-cdc442679394.

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Dopamine (DA) is a key striatal neuromodulator central to normal functioning of the basal ganglia. Identifying and characterizing circuits governing striatal DA transmission is necessary for understanding DA involvement in adaptive behaviour and pathology. Properties of evoked striatal DA release can be examined using fast-scan cyclic voltammetry at carbon fibre microelectrodes, a technique enabling live monitoring of transmitter release events with sub-millisecond resolution. Experimental work presented in this thesis employed this approach to study regulation of striatal DA by acetylcholine (ACh) in health and disease in acute brain slices. Synchronous activity in a small population of striatal cholinergic interneurons (ChIs) was previously shown to directly drive striatal DA release. Here using optogenetic approach I explore physiological relevance of ChI-evoked drive of striatal DA by examining whether corticostriatal and thalamostriatal afferents to ChIs can trigger ACh-evoked DA events. Following floxed vector injections in motor cortex or caudal intralaminar thalamus of CaMK2a-Cre mice I examine the properties of evoked DA upon light activation of channelrhodopsin-2-transduced inputs to striatal ChIs. These experiments revealed that both cortical and thalamic afferents are capable of driving ACh-evoked DA release, but operate using a different complement of post-synaptic ionotropic glutamate receptors and display distinct release recovery profiles. I further explore if rebound excitation in a population of striatal ChIs could drive DA events by examining whether ACh-evoked DA release follows optical inhibition of striatal ChIs selectively expressing hyperpolarizing halorhodopsin 3.0 or archaerhodopsin 3.0 in ChAT-Cre mice. This work showed that hyperpolarizing ion pumps were not successful in triggering ChI-evoked DA release. I also investigate whether cholinergic brainstem innervation of striatum could contribute to or drive ACh-evoked striatal DA events in ChAT-Cre rat, concurrently showing that ChI-evoked DA release is not a species artefact, and is present in mouse and rat alike. Current results also suggest that cholinergic brainstem afferents do not drive or contribute to striatal ACh-evoked DA events. Close interaction between DA and ACh systems further indicates that ACh could impact dopaminergic dysfunction. To explore this I examined the state of ACh transmission in a mouse model of Parkinson’s disease overexpressing human wild type alpha–synuclein protein. These animals present with impaired striatal DA release from young age, but DA deficits could be mediated by changes in ACh tone. Here I show that impaired striatal DA release is the results of primary DA axon dysfunction, although in ventral striatum DA release deficits could be partially compensated by increased ACh tone at nicotinic receptors. I further show that the functional state of muscarinic ACh receptors in not altered following decreased DA transmission, although the data from aged animals suggest that alpha–synuclein-dependent changes in vesicle handling could contribute to impaired DA releasability. Finally, I show that vesicle handling may indeed be altered in this mouse model as impaired DA release is evident with short stimulation protocols, while with prolonged depolarization of DA axon terminals alpha–synuclein-overexpressor mice are better able to sustain evoked DA release. Overall, the main body of work presented in this thesis examined the processes regulating striatal DA transmission via ACh system. In particular, I show that ChI-evoked drive of striatal DA release can be recruited physiologically and further establish that changes in ACh transmission are not the primary drivers of impaired DA releasability in a mouse model of Parkinson’s disease overexpressing human alpha–synuclein protein.

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Books on the topic "Dopamine neurons, parkinson's disease, neuroscience"

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Giovanni, Giuseppe. Birth, Life and Death of Dopaminergic Neurons in the Substantia Nigra. Vienna: Springer-Verlag Vienna, 2009.

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CorticoSubcortical Dynamics in Parkinsons Disease Contemporary Neuroscience. Humana Press, 2009.

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Towards a Transplantation Therapy for Parkinson's Disease (An Experimental study on intracerebral grafts of fetal dopamine neurons). University of Lund, 1988.

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(Editor), Howard J. Federoff, Robert E. Burke (Editor), Stanley Fahn (Editor), and Gary Fiskum (Editor), eds. Parkinson's Disease: The Life Cycle of the Dopamine Neuron (Annals of the New York Academy of Sciences, V. 991). New York Academy of Sciences, 2003.

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Gage, Greg, and Tim Marzullo. How Your Brain Works. The MIT Press, 2022. http://dx.doi.org/10.7551/mitpress/12429.001.0001.

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Discover the hidden electrical world inside your nervous system using DIY, hands-on experiments, for all ages. No MD or PhD required! The workings of the brain are mysterious: What are neural signals? What do they mean? How do our senses really sense? How does our brain control our movements? What happens when we meditate? Techniques to record signals from living brains were once thought to be the realm of advanced university labs... but not anymore! This book allows anyone to participate in the discovery of neuroscience through hands-on experiments that record the hidden electrical world beneath our skin and skulls. In How Your Brain Works, neuroscientists Greg Gage and Tim Marzullo offer a practical guide—accessible and useful to readers from middle schoolers to college undergraduates to curious adults—for learning about the brain through hands-on experiments. Armed with some DIY electrodes, readers will get to see what brain activity really looks like through simple neuroscience experiments. Written by two neuroscience researchers who invented open-source techniques to record signals from neurons, muscles, hearts, eyes, and brains, How Your Brain Works includes more than forty-five experiments to gain a deeper understanding of your brain. Using a homemade scientific instrument called a SpikerBox, readers can see how fast neural signals travel by recording electrical signals from an earthworm. Or, turning themselves into subjects, readers can strap on some electrode stickers to detect the nervous system in their own bodies. Each chapter begins by describing some phenomenology of a particular area of neuroscience, then guides readers step-by-step through an experiment, and concludes with a series of open-ended questions to inspire further investigation. Some experiments use invertebrates (such as insects), and the book provides a thoughtful framework for the ethical use of these animals in education. How Your Brain Works offers fascinating reading for students at any level, curious readers, and scientists interested in using electrophysiology in their research or teaching. Example Experiments How fast do signals travel down a neuron? The brain uses electricity. . . but do neurons communicate as fast as lightning inside our bodies? In this experiment you will make a speed trap for spikes! Can we really enhance our memories during sleep? Strap on a brainwave-reading sweatband and test the power of cueing up and strengthening memories while you dream away! Wait, that's my number! Ever feel that moment of excitement when you see your number displayed while waiting for an opening at the counter? In this experiment, you will peer into your brainwaves to see what happens when the unexpected occurs and how the brain gets your attention. Using hip hop to talk to the brain. Tired of simply “reading” the electricity from the brain? Would you like to “write” to the nervous system as well? In this experiment you will use a smartphone and hack a headphone cable to see how brain stimulators (used in treating Parkinson's disease) really work. How long does it take the brain to decide? Using simple classroom rulers and a clever technique, readers can determine how long it takes the brain to make decisions.

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Book chapters on the topic "Dopamine neurons, parkinson's disease, neuroscience"

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Zampese, E., D. J. Galtieri, P. T. Schumacker, and D. J. Surmeier. "Determinants of Selective Vulnerability of Dopamine Neurons in Parkinson's Disease." In Handbook of Behavioral Neuroscience, 821–37. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-802206-1.00041-6.

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Leak, Rehana K., and Michael J. Zigmond. "Endogenous Defenses that Protect Dopamine Neurons." In Parkinson's Disease, 173–94. Elsevier, 2008. http://dx.doi.org/10.1016/b978-0-12-374028-1.00013-0.

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Kittappa, Raja, Wendy Chang, and Ronald McKay. "The role of the foxa2 gene in the birth and death of dopamine neurons." In Parkinson's Disease, 449–60. Elsevier, 2008. http://dx.doi.org/10.1016/b978-0-12-374028-1.00034-8.

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Pascual, Alberto, Javier Villadiego, María Hidalgo-Figueroa, Simón Méndez-Ferrer, Raquel Gómez-Díaz, Juan José Toledo-Aral, and José Lopez-Barneo. "Neuroprotection in Parkinson's Disease." In Animal Models for Neurodegenerative Disease, 162–76. The Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/bk9781849731843-00162.

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Neurotrophic factors (NTFs) are small natural proteins that promote survival of nerve cells as well as the maintenance of their morphological and functional phenotype. NTFs, particularly the glial cell line-derived neurotrophic factor (GDNF), have aroused clinical interest as potential neuroprotective agents that could prevent or retard the progression of Parkinson's disease (PD). Numerous studies have shown that intrastriatal administration of exogenous GDNF has protective effects of mesencephalic dopaminergic neurons in vitro and in vivo. Similarly, intrastriatal grafting of dopamine- and GDNF-producing carotid body glomus cells has clinical benefit in parkinsonian animal models, and possibly in PD patients. However, the clinical effect of continuous intraputaminal recombinant GDNF infusion through a canula in advanced PD patients is practically negligible. These studies have, however, raised numerous concerns regarding the compatibility of recombinant GDNF and the route of administration of the protein. We have recently developed the conditional GDNF knock out mice in which GDNF production can be drastically reduced during adulthood. These animals develop a parkinsonian motor syndrome with selective destruction of dopaminergic substantia nigra neurons as well as noradrenergic neurons in the locus coeruleus. These data suggest that GDNF is absolutely required for the survival of adult catecholaminergic neurons. They also strongly support the view that, if adequately designed, intrastriatal GDNF delivery should have a neuroprotective therapeutic action in PD.

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Dunnett, Stephen B., and Anders Björklund. "Transplantation of Dopamine Neurons: Extent and Mechanisms of Functional Recovery in Rodent Models of Parkinson's Disease." In Dopamine Handbook, 454–77. Oxford University Press, 2009. http://dx.doi.org/10.1093/acprof:oso/9780195373035.003.0032.

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Brundin, Patrik, Mia Emgrd, and Ulrika Mundt-Petersen. "Grafts of Embryonic Dopamine Neurons in Rodent Models of Parkinson's Disease." In CNS Regeneration, 299–320. Elsevier, 1999. http://dx.doi.org/10.1016/b978-012705070-6/50012-3.

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Rideout, Hardy J., and Leonidas Stefanis. "Animal Models of Parkinson's Disease." In Animal Models for Neurodegenerative Disease, 86–112. The Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/bk9781849731843-00086.

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Parkinson's Disease (PD) is the second most common neurodegenerative disorder, characterized by the progressive loss of neurons beginning in the ventral midbrain, eventually spreading to higher cortical areas. Animal models of PD must recapitulate a complex set of motor and non-motor alterations that are the result of degeneration of widespread neuronal circuits and neurotransmitter systems. As expected, no one model has been devised that exhibits all clinical features of PD. Nevertheless, there are multiple model systems that have been developed that accurately reflect specific pathological, neurochemical, or neurophysiological disruptions that have allowed investigators to better understand aspects of the pathogenesis of PD, and begin to develop both symptom-targeted as well as neuroprotective therapeutic strategies. Multiples genetic approaches exist to model the rare familial autosomal dominant (e.g. transgenic and targeted over-expression of the mutant gene of interest; á-synuclein or LRRK2); and recessive cases of PD (targeted deletion of the relevant gene; e.g. parkin, DJ-1, etc.). Alternatively, toxins causing broad or dopamine neuron-specific mitochondrial dysfunction have been employed to model the complex I deficiency reported in sporadic cases of PD; or those that impair proteasomal-based protein degradation effectively model the formation of neuronal Lewy bodies. In this chapter we will present each class of PD animal model, their strengths and weaknesses, as well as insights gained from these approaches into the pathogenesis and treatment of PD.

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Asahara, Yuki, Taiji Mukai, Machiko Suda, and Masahiko Suzuki. "Etiology and Treatment Approach for Visual Hallucinations in PD Dementia." In Dementia in Parkinson's Disease [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98821.

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Visual hallucinations are a common symptom of Parkinson’s disease dementia. These can cause delusions and violent behaviors that can be significant burdens on patients and caregivers. The cause of visual hallucinations is considered to be the dysregulation of the default mode network due to the presence of Lewy bodies in the cortex and the degeneration of dopaminergic and cholinergic neurons. Dopaminergic agents, especially non-ergoline dopamine agonists, can exacerbate visual hallucinations. Reducing the dosage can ameliorate symptoms in many cases; however, this frequently worsens parkinsonism. In contrast, the administration of cholinesterase inhibitors is effective and rarely worsens motor symptoms. In advanced cases, antipsychotic drugs are required; clinical studies have shown that some drugs are beneficial while the adverse events are acceptable. An optimal treatment protocol should be selected depending on the patient’s condition.

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Horne, Mal, Kate Lord, and Tim Aum. "Activity-Dependent Regulation of the Dopamine Phenotype in the Adult Substantia Nigra: Prospects for Treating Parkinson's Disease." In Neuroscience - Dealing With Frontiers. InTech, 2012. http://dx.doi.org/10.5772/35221.

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Castilho, Roger F., Oskar Hansson, and Patrik Brundin. "Chapter 10 Improving the survival of grafted embryonic dopamine neurons in rodent models of Parkinson's disease." In Functional Neural Transplantation II. Novel Cell Therapies For CNS Disorders, 203–31. Elsevier, 2000. http://dx.doi.org/10.1016/s0079-6123(00)27011-8.

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Conference papers on the topic "Dopamine neurons, parkinson's disease, neuroscience"

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Rajendran, Arathi, Anuja Thankamani, Nishamol Nirmala, Bipin Nair, and Shyam Diwakar. "Computational neuroscience of substantia nigra circuit and dopamine modulation during parkinson's disease." In 2017 International Conference on Advances in Computing, Communications and Informatics (ICACCI). IEEE, 2017. http://dx.doi.org/10.1109/icacci.2017.8125892.

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Reports on the topic "Dopamine neurons, parkinson's disease, neuroscience"

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Mytilineou, Catherine. Inflammatory Response and Oxidative Stress in the Degeneration of Dopamine Neurons in Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada397697.

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Olanow, C. W. Inflammatory Response and Oxidative Stress in the Degeneration of Dopamine Neurons in Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada407775.

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Zigmond, Michael J., Amanda Smith, and Anthony Liou. The Impact of Exercise on the Vulnerability of Dopamine Neurons to Cell Death in Animal Models of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, July 2008. http://dx.doi.org/10.21236/ada501105.

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Singh, Ruchi, Akhiya Nail, and Nirendra Kumar Rai. Effectiveness of Vitamin B12 Supplementation on cognitive, motor & mood instability of Parkinson’s disease patients on levodopa treatment :A Systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0066.

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Review question / Objective: The treatment of choice for patients of Parkinson's disease is levodopa. However, levodopa has been suggested to decrease Vit B12 level in these patients. Thus, the research question for this systematic review is whether vit B 12 supplementation in Parkinson's disease(PD) patients on treatment with levodopa improves vit B12 level effecting the Cognition, Motor functions and Mood instability among them in comparison to PD patients on levodopa treatment who are not supplemented with Vit B12. Condition being studied: Parkinson disease is the progressive degeneration of dopaminergic neurons present within the substantia nigra that can lead to altered movements along with the prevalence of cognitive and mood instability as a result of dopamine(neurotransmitter) deficiency. The most effective treatment for the Parkinson's disease is the administration of levodopa, a dopamine precursor . Long term treatment with levodopa causes an increase in homocysteine levels and tissue deficiency of vitamin B12 and folate may occur. Vitamin B12 supplementation is administered as after management regime, in Parkinson patient on levodopa treatment . This study aims to conduct a systematic review, of studies , randomized control trials investigating the ability of vitamin B12 supplementation to enhances the recovery/reduce the decline, if any, of the symptoms of cognitive, motor, mood impairments associated with Parkinson's disease patient on levodopa treatment.

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