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Initial elevations in glutamate and dopamine neurotransmission decline with age, as does exploratory behavior, in LRRK2 G2019S knock-in mice

Volta, Mattia, Beccano-Kelly, Dayne A, Paschall, Sarah A, Cataldi, Stefano, MacIsaac, Sarah E, Kuhlmann, Naila, Kadgien, Chelsie A, Tatarnikov, Igor, Fox, Jesse, Khinda, Jaskaran, Mitchell, Emma, Bergeron, Sabrina, Melrose, Heather, Farrer, Matthew J, Milnerwood, Austen J·2017·eLife
DOI 10.7554/elife.28377PMC PMC5633343
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Abstract

LRRK2 mutations produce end-stage Parkinson’s disease (PD) with reduced nigrostriatal dopamine, whereas, asymptomatic carriers have increased dopamine turnover and altered brain connectivity. LRRK2 pathophysiology remains unclear, but reduced dopamine and mitochondrial abnormalities occur in aged G2019S mutant knock-in (GKI) mice. Conversely, cultured GKI neurons exhibit increased synaptic transmission. We assessed behavior and synaptic glutamate and dopamine function across a range of ages. Young GKI mice exhibit more vertical exploration, elevated glutamate and dopamine transmission, and aberrant D2-receptor responses. These phenomena decline with age, but are stable in littermates. In young GKI mice, dopamine transients are slower, independent of dopamine transporter (DAT), increasing the lifetime of extracellular dopamine. Slowing of dopamine transients is observed with age in littermates, suggesting premature ageing of dopamine synapses in GKI mice. Thus, GKI mice exhibit early, but declining, synaptic and behavioral phenotypes, making them amenable to investigation of early pathophysiological, and later parkinsonian-like, alterations. This model will prove valuable in efforts to develop neuroprotection for PD.

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Research works printed but not linked: 54

  1. Adams, 2005, PET in LRRK2 mutations: comparison to sporadic Parkinson's disease and evidence for presymptomatic compensation, Brain, 128, 2777, 10.1093/brain/awh607 · DOI
  2. Ade, 2011, An Improved BAC transgenic fluorescent reporter line for sensitive and specific identification of striatonigral medium spiny neurons, Frontiers in Systems Neuroscience, 5, 32, 10.3389/fnsys.2011.00032 · DOI
  3. Akopian, 2007, Reliable long-lasting depression interacts with variable short-term facilitation to determine corticostriatal paired-pulse plasticity in young rats, The Journal of Physiology, 580, 225, 10.1113/jphysiol.2006.115790 · DOI
  4. Bamford, 2004, Heterosynaptic dopamine neurotransmission selects sets of corticostriatal terminals, Neuron, 42, 653, 10.1016/S0896-6273(04)00265-X · DOI
  5. Beccano-Kelly, 2014, Synaptic function is modulated by LRRK2 and glutamate release is increased in cortical neurons of G2019S LRRK2 knock-in mice, Frontiers in Cellular Neuroscience, 8, 10.3389/fncel.2014.00301 · DOI · Paper page
  6. Beccano-Kelly, 2015, LRRK2 overexpression alters glutamatergic presynaptic plasticity, striatal dopamine tone, postsynaptic signal transduction, motor activity and memory, Human Molecular Genetics, 24, 1336, 10.1093/hmg/ddu543 · DOI · Paper page
  7. Broeders, 2013, Cognitive change in newly-diagnosed patients with Parkinson's disease: a 5-year follow-up study, Journal of the International Neuropsychological Society, 19, 695, 10.1017/S1355617713000295 · DOI
  8. Calabresi, 2014, Direct and indirect pathways of basal ganglia: a critical reappraisal, Nature Neuroscience, 17, 1022, 10.1038/nn.3743 · DOI
  9. Cepeda, 2008, Differential electrophysiological properties of dopamine D1 and D2 receptor-containing striatal medium-sized spiny neurons, European Journal of Neuroscience, 27, 671, 10.1111/j.1460-9568.2008.06038.x · DOI
  10. Chaudhuri, 2009, Non-motor symptoms of Parkinson's disease: dopaminergic pathophysiology and treatment, The Lancet Neurology, 8, 464, 10.1016/S1474-4422(09)70068-7 · DOI
  11. Crawford, 2015, Molecular underpinnings of synaptic vesicle pool heterogeneity, Traffic, 16, 338, 10.1111/tra.12262 · DOI
  12. Ding, 2008, Corticostriatal and thalamostriatal synapses have distinctive properties, Journal of Neuroscience, 28, 6483, 10.1523/JNEUROSCI.0435-08.2008 · DOI
  13. Gaig, 2014, Nonmotor symptoms in LRRK2 G2019S associated Parkinson's disease, PLoS One, 9, e108982, 10.1371/journal.pone.0108982 · DOI
  14. Gainetdinov, 2008, Dopamine transporter mutant mice in experimental neuropharmacology, Naunyn-Schmiedeberg's Archives of Pharmacology, 377, 301, 10.1007/s00210-007-0216-0 · DOI
  15. Gerfen, 2011, Modulation of striatal projection systems by dopamine, Annual Review of Neuroscience, 34, 441, 10.1146/annurev-neuro-061010-113641 · DOI
  16. Goldman, 2014, Premotor and nonmotor features of Parkinson's disease, Current Opinion in Neurology, 27, 434, 10.1097/WCO.0000000000000112 · DOI
  17. Goldman, 2015, Mild cognitive impairment: an update in Parkinson's disease and lessons learned from Alzheimer's disease, Neurodegenerative Disease Management, 5, 425, 10.2217/nmt.15.34 · DOI
  18. Haugland, 2002, Handbook of Fluorescent Probes and Research Products, 554
  19. Helmich, 2015, Reorganization of corticostriatal circuits in healthy G2019S LRRK2 carriers, Neurology, 84, 399, 10.1212/WNL.0000000000001189 · DOI
  20. Hulihan, 2008, LRRK2 Gly2019Ser penetrance in Arab-Berber patients from Tunisia: a case-control genetic study, The Lancet Neurology, 7, 591, 10.1016/S1474-4422(08)70116-9 · DOI
  21. Jenner, 2013, Parkinson's disease--the debate on the clinical phenomenology, aetiology, pathology and pathogenesis, Journal of Parkinson's disease, 3, 1, 10.3233/JPD-130175 · DOI
  22. Jones, 1998, Profound neuronal plasticity in response to inactivation of the dopamine transporter, PNAS, 95, 4029, 10.1073/pnas.95.7.4029 · DOI
  23. Kachergus, 2005, Identification of a novel LRRK2 mutation linked to autosomal dominant parkinsonism: evidence of a common founder across European populations, The American Journal of Human Genetics, 76, 672, 10.1086/429256 · DOI
  24. Kalia, 2015, Parkinson's disease, The Lancet, 386, 896, 10.1016/S0140-6736(14)61393-3 · DOI · Paper page
  25. Kordower, 2013, Disease duration and the integrity of the nigrostriatal system in Parkinson's disease, Brain, 136, 2419, 10.1093/brain/awt192 · DOI
  26. Litvan, 2011, MDS Task Force on mild cognitive impairment in Parkinson's disease: critical review of PD-MCI, Movement Disorders, 26, 1814, 10.1002/mds.23823 · DOI
  27. Longo, 2014, Genetic and pharmacological evidence that G2019S LRRK2 confers a hyperkinetic phenotype, resistant to motor decline associated with aging, Neurobiology of Disease, 71, 62, 10.1016/j.nbd.2014.07.013 · DOI
  28. Longo, 2017, Age-dependent dopamine transporter dysfunction and Serine129 phospho-α-synuclein overload in G2019S LRRK2 mice, Acta Neuropathologica Communications, 5, 22, 10.1186/s40478-017-0426-8 · DOI
  29. Matikainen-Ankney, 2016, Altered development of synapse structure and function in striatum caused by parkinson's disease-linked lrrk2-g2019s mutation, Journal of Neuroscience, 36, 7128, 10.1523/JNEUROSCI.3314-15.2016 · DOI · Paper page
  30. Mei, 2016, Adult restoration of Shank3 expression rescues selective autistic-like phenotypes, Nature, 530, 481, 10.1038/nature16971 · DOI · Paper page
  31. Milnerwood, 2010, Early increase in extrasynaptic nmda receptor signaling and expression contributes to phenotype onset in huntington's disease mice, Neuron, 65, 178, 10.1016/j.neuron.2010.01.008 · DOI
  32. Milnerwood, 2013, Memory and synaptic deficits in Hip14/DHHC17 knockout mice, PNAS, 110, 20296, 10.1073/pnas.1222384110 · DOI
  33. Nandhagopal, 2008, Progression of dopaminergic dysfunction in a LRRK2 kindred: a multitracer PET study, Neurology, 71, 1790, 10.1212/01.wnl.0000335973.66333.58 · DOI
  34. Ozelius, 2006, LRRK2 G2019S as a cause of Parkinson's disease in Ashkenazi Jews, New England Journal of Medicine, 354, 424, 10.1056/NEJMc055509 · DOI
  35. Parisiadou, 2014, LRRK2 regulates synaptogenesis and dopamine receptor activation through modulation of PKA activity, Nature Neuroscience, 17, 367, 10.1038/nn.3636 · DOI
  36. Pedersen, 2013, Prognosis of mild cognitive impairment in early Parkinson disease: the Norwegian ParkWest study, JAMA neurology, 70, 580, 10.1001/jamaneurol.2013.2110 · DOI · Paper page
  37. Petkau, 2012, Synaptic dysfunction in progranulin-deficient mice, Neurobiology of Disease, 45, 711, 10.1016/j.nbd.2011.10.016 · DOI
  38. Phillips, 2002, Time window of autoreceptor-mediated inhibition of limbic and striatal dopamine release, Synapse, 44, 15, 10.1002/syn.10049 · DOI
  39. Ramirez, 2012, Vti1a identifies a vesicle pool that preferentially recycles at rest and maintains spontaneous neurotransmission, Neuron, 73, 121, 10.1016/j.neuron.2011.10.034 · DOI
  40. Rice, 2011, Dopamine release in the basal ganglia, Neuroscience, 198, 112, 10.1016/j.neuroscience.2011.08.066 · DOI
  41. Sara, 2005, An isolated pool of vesicles recycles at rest and drives spontaneous neurotransmission, Neuron, 45, 563, 10.1016/j.neuron.2004.12.056 · DOI
  42. Sciamanna, 2015, Optogenetic stimulation reveals distinct modulatory properties of thalamostriatal vs corticostriatal glutamatergic inputs to fast-spiking interneurons, Scientific Reports, 5, 16742, 10.1038/srep16742 · DOI
  43. Sossi, 2010, Dopamine turnover increases in asymptomatic LRRK2 mutations carriers, Movement Disorders, 25, 2717, 10.1002/mds.23356 · DOI
  44. Thaler, 2013, Neural correlates of executive functions in healthy G2019S LRRK2 mutation carriers, Cortex, 49, 2501, 10.1016/j.cortex.2012.12.017 · DOI
  45. Tolosa, 2007, The premotor phase of Parkinson's disease, Parkinsonism & Related Disorders, 13, S2, 10.1016/j.parkreldis.2007.06.007 · DOI
  46. Trinh, 2014, Comparative study of Parkinson's disease and leucine-rich repeat kinase 2 p.G2019S parkinsonism, Neurobiology of Aging, 35, 1125, 10.1016/j.neurobiolaging.2013.11.015 · DOI
  47. Vilas, 2015, Clinical and imaging markers in premotor LRRK2 G2019S mutation carriers, Parkinsonism & Related Disorders, 21, 1170, 10.1016/j.parkreldis.2015.08.007 · DOI
  48. Volta, 2015, Insights from late-onset familial parkinsonism on the pathogenesis of idiopathic Parkinson's disease, The Lancet Neurology, 14, 1054, 10.1016/S1474-4422(15)00186-6 · DOI
  49. Volta, 2015, Chronic and acute LRRK2 silencing has no long-term behavioral effects, whereas wild-type and mutant LRRK2 overexpression induce motor and cognitive deficits and altered regulation of dopamine release, Parkinsonism & Related Disorders, 21, 1156, 10.1016/j.parkreldis.2015.07.025 · DOI
  50. Weintraub, 2008, Parkinson's disease--Part 2: Treatment of motor symptoms, The American Journal of Managed Care, 14, S49
  51. Weintraub, 2008, Parkinson's disease--Part 3: neuropsychiatric symptoms, The American Journal of Managed Care, 14, S59
  52. Weintraub, 2008, Parkinson's disease--Part 1: Pathophysiology, symptoms, burden, diagnosis, and assessment, The American Journal of Managed Care, 14, S40
  53. Wile, 2017, Serotonin and dopamine transporter PET changes in the premotor phase of LRRK2 parkinsonism: cross-sectional studies, The Lancet Neurology, 16, 351, 10.1016/S1474-4422(17)30056-X · DOI
  54. Yue, 2015, Progressive dopaminergic alterations and mitochondrial abnormalities in LRRK2 G2019S knock-in mice, Neurobiology of Disease, 78, 172, 10.1016/j.nbd.2015.02.031 · DOI · Paper page

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Metadata

Authors
Volta, M., Beccano-Kelly, D. A., Paschall, S. A., Cataldi, S., MacIsaac, S. E., Kuhlmann, N., Kadgien, C. A., Tatarnikov, I., Fox, J., Khinda, J., Mitchell, E., Bergeron, S., Melrose, H., Farrer, M. J., & Milnerwood, A. J.
Venue
eLife
Publisher
eLife Sciences Publications, Ltd
Published
2017-09-20
Volume
6
ISSN
2050-084X
DOI
10.7554/elife.28377
PMC
PMC5633343
Cited by
108
References
2
Language
en
Licence
Funders
  • Michael J. Fox Foundation for Parkinson's Research
  • Parkinson Canada
  • Canadian Institutes of Health Research
  • Canada Excellence Research Chairs, Government of Canada

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