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Journal articles on the topic 'A9 neurons'

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Author: Grafiati

Published: 14 March 2023

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1

Haynes, John M., Shanti M. Sibuea, Alita A. Aguiar, Fangwei Li, Joan K. Ho, and Colin W. Pouton. "Inhibition of β-catenin dependent WNT signalling upregulates the transcriptional repressor NR0B1 and downregulates markers of an A9 phenotype in human embryonic stem cell-derived dopaminergic neurons: Implications for Parkinson’s disease." PLOS ONE 16, no. 12 (December 23, 2021): e0261730. http://dx.doi.org/10.1371/journal.pone.0261730.

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In this study we investigate how β-catenin-dependent WNT signalling impacts midbrain dopaminergic neuron (mDA) specification. mDA cultures at day 65 of differentiation responded to 25 days of the tankyrase inhibitor XAV969 (XAV, 100nM) with reduced expression of markers of an A9 mDA phenotype (KCNJ6, ALDH1A1 and TH) but increased expression of the transcriptional repressors NR0B1 and NR0B2. Overexpression of NR0B1 and or NR0B2 promoted a loss of A9 dopaminergic neuron phenotype markers (KCNJ6, ALDH1A1 and TH). Overexpression of NR0B1, but not NR0B2 promoted a reduction in expression of the β-catenin-dependent WNT signalling pathway activator RSPO2. Analysis of Parkinson’s disease (PD) transcriptomic databases shows a profound PD-associated elevation of NR0B1 as well as reduced transcript for RSPO2. We conclude that reduced β-catenin-dependent WNT signalling impacts dopaminergic neuron identity, in vitro, through increased expression of the transcriptional repressor, NR0B1. We also speculate that dopaminergic neuron regulatory mechanisms may be perturbed in PD and that this may have an impact upon both existing nigral neurons and also neural progenitors transplanted as PD therapy.

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2

Fiorenzano, Alessandro, Edoardo Sozzi, Malin Parmar, and Petter Storm. "Dopamine Neuron Diversity: Recent Advances and Current Challenges in Human Stem Cell Models and Single Cell Sequencing." Cells 10, no. 6 (June 1, 2021): 1366. http://dx.doi.org/10.3390/cells10061366.

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Human midbrain dopamine (DA) neurons are a heterogeneous group of cells that share a common neurotransmitter phenotype and are in close anatomical proximity but display different functions, sensitivity to degeneration, and axonal innervation targets. The A9 DA neuron subtype controls motor function and is primarily degenerated in Parkinson’s disease (PD), whereas A10 neurons are largely unaffected by the condition, and their dysfunction is associated with neuropsychiatric disorders. Currently, DA neurons can only be reliably classified on the basis of topographical features, including anatomical location in the midbrain and projection targets in the forebrain. No systematic molecular classification at the genome-wide level has been proposed to date. Although many years of scientific efforts in embryonic and adult mouse brain have positioned us to better understand the complexity of DA neuron biology, many biological phenomena specific to humans are not amenable to being reproduced in animal models. The establishment of human cell-based systems combined with advanced computational single-cell transcriptomics holds great promise for decoding the mechanisms underlying maturation and diversification of human DA neurons, and linking their molecular heterogeneity to functions in the midbrain. Human pluripotent stem cells have emerged as a useful tool to recapitulate key molecular features of mature DA neuron subtypes. Here, we review some of the most recent advances and discuss the current challenges in using stem cells, to model human DA biology. We also describe how single cell RNA sequencing may provide key insights into the molecular programs driving DA progenitor specification into mature DA neuron subtypes. Exploiting the state-of-the-art approaches will lead to a better understanding of stem cell-derived DA neurons and their use in disease modeling and regenerative medicine.

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3

GRENHOFF, J., L. UGEDO, and T. H. SVENSSON. "Firing patterns of midbrain dopamine neurons: differences between A9 and A10 cells." Acta Physiologica Scandinavica 134, no. 1 (September 1988): 127–32. http://dx.doi.org/10.1111/j.1748-1716.1988.tb08468.x.

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4

Pujo, J., G. De Palma, J. Lu, S. M. Collins, and P. Bercik. "A9 DORSAL ROOT GANGLIA NEURONAL RESPONSES AND SUBSTANCE P PRODUCTION ARE HIGHER IN MALE MICE." Journal of the Canadian Association of Gastroenterology 4, Supplement_1 (March 1, 2021): 10–11. http://dx.doi.org/10.1093/jcag/gwab002.008.

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Abstract Background Abdominal pain is a common complaint in patients with chronic gastrointestinal disorders. Accumulating evidence suggests that gut microbiota is an important determinant of gut function, including visceral sensitivity. Germ-free (GF) mice have been shown to display visceral hypersensitivity, which normalizes after colonization. Sex also appears to play a key role in visceral sensitivity, as women report more abdominal pain than men. Thus, both gut bacteria and sex are important in the regulation of gut nociception, but the underlying mechanisms remain poorly understood. Aims To investigate the role of gut microbiota and sex in abdominal pain. Methods We used primary cultures of sensory neurons from dorsal root ganglia (DRG) of female and male conventionally raised (SPF) or germ-free (GF) mice (7–18 weeks old). To study the visceral afferent activity in vitro, calcium mobilization in DRG sensory neurons was measured by inverted fluorescence microscope using a fluorescent calcium probe Fluo-4 (1mM). Two parameters were considered i) the percentage of responding neurons ii) the intensity of the neuronal response. First, DRG sensory neurons were stimulated by a TRPV1 agonist capsaicin (12.5nM, 125nM and 1.25µM) or by a mixture of G-protein coupled receptors agonist (GPCR: bradykinin, histamine and serotonin; 1µM, 10µM and 100µM). We next measured the neuronal production of substance P and calcitonin gene-related peptide (CGRP), two neuropeptides associated with nociception, in response to capsaicin (1.25µM) or GPCR agonists (100µM) by ELISA and EIA, respectively. Results The percentage of neurons responding to capsaicin and GPCR agonists was similar in male and female SPF and GF mice. However, the intensity of the neuronal response was higher in SPF male compared to SPF female in response to capsaicin (125nM: p=0.0336; 1.25µM: p=0.033) but not to GPCR agonists. Neuronal activation was similar in GF and SPF mice of both sexes after administration of capsaicin or GPCR agonists. Furthermore, substance P and CGRP production by sensory neurons induced by capsaicin or GPCR agonists was similar in SPF and GF mice, regardless of sex. However, while the response to capsaicin was similar, the GPCR agonists-induced production of substance P was higher in SPF male mice compared to SPF females (p=0.003). The GPCR agonists-induced production of CGRP was similar in SPF male and female mice. Conclusions Our data suggest that at the level of DRG neurons, the absence of gut microbiota does not predispose to visceral hypersensitivity. The intensity of DRG neuronal responses to capsaicin and the GPCR agonists-induced production of substance P are higher in male compared to female mice, in contrast to previously published studies in various models of acute and chronic pain. Further studies are thus needed to investigate the role of sex in visceral sensitivity. Funding Agencies CIHR

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5

Yang, S., L. C. Edman, J. A. Sanchez-Alcaniz, N. Fritz, S. Bonilla, J. Hecht, P. Uhlen, et al. "Cxcl12/Cxcr4 signaling controls the migration and process orientation of A9-A10 dopaminergic neurons." Journal of Cell Science 126, no. 22 (November 15, 2013): e1-e1. http://dx.doi.org/10.1242/jcs.145136.

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6

Stockton, Marsha E., and Kurt Rasmussen. "Electrophysiological Effects of Olanzapine, a Novel Atypical Antipsychotic, on A9 and A10 Dopamine Neurons." Neuropsychopharmacology 14, no. 2 (February 1996): 97–104. http://dx.doi.org/10.1016/0893-133x(94)00130-r.

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7

Yang, S., L. C. Edman, J. A. Sanchez-Alcaniz, N. Fritz, S. Bonilla, J. Hecht, P. Uhlen, et al. "Cxcl12/Cxcr4 signaling controls the migration and process orientation of A9-A10 dopaminergic neurons." Development 140, no. 22 (October 23, 2013): 4554–64. http://dx.doi.org/10.1242/dev.098145.

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8

German, Dwight C., and Kebreten F. Manaye. "Midbrain dopaminergic neurons (nuclei A8, A9, and A10): Three-dimensional reconstruction in the rat." Journal of Comparative Neurology 331, no. 3 (May 15, 1993): 297–309. http://dx.doi.org/10.1002/cne.903310302.

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9

Bye, Christopher R., Lachlan H. Thompson, and Clare L. Parish. "Birth dating of midbrain dopamine neurons identifies A9 enriched tissue for transplantation into Parkinsonian mice." Experimental Neurology 236, no. 1 (July 2012): 58–68. http://dx.doi.org/10.1016/j.expneurol.2012.04.002.

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10

Goldstein, Jeffrey M., Linda C. Litwin, E. B. Sutton, and Jeffrey B. Malick. "D-2 dopamine antagonist-like effects of SCH 23390 on A9 and A10 dopamine neurons." Life Sciences 40, no. 11 (March 1987): 1039–44. http://dx.doi.org/10.1016/0024-3205(87)90565-0.

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11

Aldhshan, Muhammad S., Gursagar Jhanji, Nicole J. Poritsanos, and Tooru M. Mizuno. "Glucose Stimulates Glial Cell Line-Derived Neurotrophic Factor Gene Expression in Microglia through a GLUT5-Independent Mechanism." International Journal of Molecular Sciences 23, no. 13 (June 25, 2022): 7073. http://dx.doi.org/10.3390/ijms23137073.

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Feeding-regulating neurotrophic factors are expressed in both neurons and glial cells. However, nutritional regulation of anorexigenic glial cell line-derived neurotrophic factor (GDNF) and orexigenic mesencephalic astrocyte-derived neurotrophic factor (MANF) expression in specific cell types remains poorly understood. Hypothalamic glucose sensing plays a critical role in the regulation of food intake. It has been theorized that local glucose concentration modulates microglial activity partially via glucose transporter 5 (GLUT5). We hypothesized that an increased local glucose concentration stimulates GDNF expression while inhibiting MANF expression in the hypothalamus and microglia via GLUT5. The present study investigated the effect of glucose on Gdnf and Manf mRNA expression in the mouse hypothalamus and murine microglial cell line SIM-A9. Intracerebroventricular glucose treatment significantly increased Gdnf mRNA levels in the hypothalamus without altering Manf mRNA levels. Exposure to high glucose caused a significant increase in Gdnf mRNA expression and a time-dependent change in Manf mRNA expression in SIM-A9 cells. GLUT5 inhibitor treatment did not block glucose-induced Gdnf mRNA expression in these cells. These findings suggest that microglia are responsive to changes in the local glucose concentration and increased local glucose availability stimulates the expression of microglial GNDF through a GLUT5-independent mechanism, contributing to glucose-induced feeding suppression.

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Courtois, Elise T., Claudia G. Castillo, Emma G. Seiz, Milagros Ramos, Carlos Bueno, Isabel Liste, and Alberto Martínez-Serrano. "In Vitroandin VivoEnhanced Generation of Human A9 Dopamine Neurons from Neural Stem Cells by Bcl-XL." Journal of Biological Chemistry 285, no. 13 (January 27, 2010): 9881–97. http://dx.doi.org/10.1074/jbc.m109.054312.

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13

Lokwan, S. J. A., P. G. Overton, M. S. Berry, and D. Clark. "Stimulation of the pedunculopontine tegmental nucleus in the rat produces burst firing in A9 dopaminergic neurons." Neuroscience 92, no. 1 (August 1999): 245–54. http://dx.doi.org/10.1016/s0306-4522(98)00748-9.

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14

Kawashima, Naoya, Shigeru Okuyama, Tomohiro Omura, Shigeyuki Chaki, and Kazuyuki Tomisawa. "Effect of NRA0160, a selective dopamine D4 receptor antagonist, on A9 and A10 dopmaine neurons in rats." Japanese Journal of Pharmacology 79 (1999): 231. http://dx.doi.org/10.1016/s0021-5198(19)34937-6.

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15

German, Dwight C., Eric L. Nelson, Chang-Lin Liang, Samuel G. Speciale, Christopher M. Sinton, and Patricia K. Sonsalla. "The Neurotoxin MPTP Causes Degeneration of Specific Nucleus A8, A9 and A10 Dopaminergic Neurons in the Mouse." Neurodegeneration 5, no. 4 (December 1996): 299–312. http://dx.doi.org/10.1006/neur.1996.0041.

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16

Morrow, Bret A., D. Eugene Redmond, Robert H. Roth, and John D. Elsworth. "Development of A9/A10 dopamine neurons during the second and third trimesters in the African green monkey." Journal of Comparative Neurology 488, no. 2 (2005): 215–23. http://dx.doi.org/10.1002/cne.20599.

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17

Iyengar, Smriti, Vicki M. Dilworth, Steven J. Mick, Patricia C. Contreras, Joseph B. Monahan, Tadimeti S. Rao, and Paul L. Wood. "Sigma receptors modulate both A9 and A10 dopaminergic neurons in the rat brain: functional interaction with NMDA receptors." Brain Research 524, no. 2 (August 1990): 322–26. http://dx.doi.org/10.1016/0006-8993(90)90709-k.

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18

Sorensen, Stephen M., Teresa M. Humphreys, and Michael G. Palfreyman. "Effect of acute and chronic MDL 73,147EF, a 5-HT3 receptor antagonist, on A9 and A10 dopamine neurons." European Journal of Pharmacology 163, no. 1 (April 1989): 115–18. http://dx.doi.org/10.1016/0014-2999(89)90402-0.

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19

Freeman, Arthur S., and Benjamin S. Bunney. "Activity of A9 and A10 dopaminergic neurons in unrestrained rats: further characterization and effects of apomorphine and cholecystokinin." Brain Research 405, no. 1 (March 1987): 46–55. http://dx.doi.org/10.1016/0006-8993(87)90988-7.

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20

Ljungberg, T., P. Apicella, and W. Schultz. "Responses of monkey dopamine neurons during learning of behavioral reactions." Journal of Neurophysiology 67, no. 1 (January 1, 1992): 145–63. http://dx.doi.org/10.1152/jn.1992.67.1.145.

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1. Previous studies have shown that dopamine (DA) neurons respond to stimuli of behavioral significance, such as primary reward and conditioned stimuli predicting reward and eliciting behavioral reactions. The present study investigated how these responses develop and vary when the behavioral significance of stimuli changes during different stages of learning. Impulses from DA neurons were recorded with movable microelectrodes from areas A8, A9, and A10 in two awake monkeys during the successive acquisition of two behavioral tasks. Impulses of DA neurons were distinguished from other neurons by their long duration (1.8-5.0 ms) and low spontaneous frequency (0.5-7.0 imp/s). 2. In the first task, animals learned to reach in a small box in front of them when it opened visibly and audibly. Before conditioning, DA neurons were activated the first few times that the empty box opened and animals reacted with saccadic eye movements. Neuronal and behavioral responses disappeared on repeated stimulus presentation. Thus neuronal responses were related to the novelty of an unexpected stimulus eliciting orienting behavior. 3. Subsequently, the box contained a small morsel of apple in one out of six trials. Animals reacted with ocular saccades to nearly every box opening and reached out when the morsel was present. One-third of 49 neurons were phasically activated by every door opening. The response was stronger when food was present. Thus DA neurons responded simultaneously to the sight of primary food reward and to the conditioned stimulus associated with reward. 4. When the box contained a morsel of apple on every trial, animals regularly reacted with target-directed eye and arm movements, and the majority of 76 DA neurons responded to door opening. The same neurons lacked responses to a light not associated with task performance that was illuminated at the position of the food box in alternate sessions, thus demonstrating specificity for the behavioral significance of stimuli. 5. The second task employed the operant conditioning of a reaction time situation in which animals reached from a resting key toward a lever when a small light was illuminated. DA neurons lacked responses to the unconditioned light. During task acquisition lasting 2-3 days, one-half of 25 DA neurons were phasically activated when a drop of liquid reward was delivered for reinforcing the reaching movement. In contrast, neurons were not activated when reward was delivered at regular intervals (2.5-3.5 s) but a task was not performed.(ABSTRACT TRUNCATED AT 400 WORDS)

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Yeap, Yee Jie, Tng J. W. Teddy, Mok Jung Lee, Micaela Goh, and Kah Leong Lim. "From 2D to 3D: Development of Monolayer Dopaminergic Neuronal and Midbrain Organoid Cultures for Parkinson’s Disease Modeling and Regenerative Therapy." International Journal of Molecular Sciences 24, no. 3 (January 28, 2023): 2523. http://dx.doi.org/10.3390/ijms24032523.

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Parkinson’s Disease (PD) is a prevalent neurodegenerative disorder that is characterized pathologically by the loss of A9-specific dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) of the midbrain. Despite intensive research, the etiology of PD is currently unresolved, and the disease remains incurable. This, in part, is due to the lack of an experimental disease model that could faithfully recapitulate the features of human PD. However, the recent advent of induced pluripotent stem cell (iPSC) technology has allowed PD models to be created from patient-derived cells. Indeed, DA neurons from PD patients are now routinely established in many laboratories as monolayers as well as 3D organoid cultures that serve as useful toolboxes for understanding the mechanism underlying PD and also for drug discovery. At the same time, the iPSC technology also provides unprecedented opportunity for autologous cell-based therapy for the PD patient to be performed using the patient’s own cells as starting materials. In this review, we provide an update on the molecular processes underpinning the development and differentiation of human pluripotent stem cells (PSCs) into midbrain DA neurons in both 2D and 3D cultures, as well as the latest advancements in using these cells for drug discovery and regenerative medicine. For the novice entering the field, the cornucopia of differentiation protocols reported for the generation of midbrain DA neurons may seem daunting. Here, we have distilled the essence of the different approaches and summarized the main factors driving DA neuronal differentiation, with the view to provide a useful guide to newcomers who are interested in developing iPSC-based models of PD.

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22

Trudler, Dorit, Kristopher L. Nazor, Yvonne S. Eisele, Titas Grabauskas, Nima Dolatabadi, James Parker, Abdullah Sultan, et al. "Soluble α-synuclein–antibody complexes activate the NLRP3 inflammasome in hiPSC-derived microglia." Proceedings of the National Academy of Sciences 118, no. 15 (April 8, 2021): e2025847118. http://dx.doi.org/10.1073/pnas.2025847118.

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Parkinson’s disease is characterized by accumulation of α-synuclein (αSyn). Release of oligomeric/fibrillar αSyn from damaged neurons may potentiate neuronal death in part via microglial activation. Heretofore, it remained unknown if oligomeric/fibrillar αSyn could activate the nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) inflammasome in human microglia and whether anti-αSyn antibodies could prevent this effect. Here, we show that αSyn activates the NLRP3 inflammasome in human induced pluripotent stem cell (hiPSC)-derived microglia (hiMG) via dual stimulation involving Toll-like receptor 2 (TLR2) engagement and mitochondrial damage. In vitro, hiMG can be activated by mutant (A53T) αSyn secreted from hiPSC-derived A9-dopaminergic neurons. Surprisingly, αSyn–antibody complexes enhanced rather than suppressed inflammasome-mediated interleukin-1β (IL-1β) secretion, indicating these complexes are neuroinflammatory in a human context. A further increase in inflammation was observed with addition of oligomerized amyloid-β peptide (Aβ) and its cognate antibody. In vivo, engraftment of hiMG with αSyn in humanized mouse brain resulted in caspase-1 activation and neurotoxicity, which was exacerbated by αSyn antibody. These findings may have important implications for antibody therapies aimed at depleting misfolded/aggregated proteins from the human brain, as they may paradoxically trigger inflammation in human microglia.

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23

O’Keeffe, Fiona E., Sarah A. Scott, Pam Tyers, Gerard W. O’Keeffe, Jeffrey W. Dalley, Romain Zufferey, and Maeve A. Caldwell. "Induction of A9 dopaminergic neurons from neural stem cells improves motor function in an animal model of Parkinson's disease." Brain 131, no. 3 (January 17, 2008): 630–41. http://dx.doi.org/10.1093/brain/awm340.

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24

Kawashima, Naoya, Shigeru Okuyama, Tomohiro Omura, Shigeyuki Chaki, and Kazuyuki Tomisawa. "Effects of selective dopamine D4 receptor blockers, NRA0160 and L-745,870, on A9 and A10 dopamine neurons in rats." Life Sciences 65, no. 24 (November 1999): 2561–71. http://dx.doi.org/10.1016/s0024-3205(99)00525-1.

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25

Sánchez-Arroyos, Ricardo, and Xavier Guitart. "Electrophysiological effects of E-5842, a σ1 receptor ligand and potential atypical antipsychotic, on A9 and A10 dopamine neurons." European Journal of Pharmacology 378, no. 1 (July 1999): 31–37. http://dx.doi.org/10.1016/s0014-2999(99)00440-9.

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26

Hand, Timothy H., Xiu-Ti Hu, and Rex Y. Wang. "Differential effects of acute clozapine and haloperidol on the activity of ventral tegmental (A10) and nigrostriatal (A9) dopamine neurons." Brain Research 415, no. 2 (July 1987): 257–69. http://dx.doi.org/10.1016/0006-8993(87)90207-1.

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27

Busti, Daniela, Thomas Bienvenu, Ben Micklem, Peter J. Magill, Ryuichi Shigemoto, Marco Capogna, and Francesco Ferraguti. "Morphological characterization of large intercalated neurons provides novel insight on intrinsic networks of the amygdala." BMC Pharmacology 11, Suppl 2 (2011): A9. http://dx.doi.org/10.1186/1471-2210-11-s2-a9.

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28

Kuan, Wei-Li, Rachel Lin, Pam Tyers, and Roger A. Barker. "The importance of A9 dopaminergic neurons in mediating the functional benefits of fetal ventral mesencephalon transplants and levodopa-induced dyskinesias." Neurobiology of Disease 25, no. 3 (March 2007): 594–608. http://dx.doi.org/10.1016/j.nbd.2006.11.001.

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29

Mereu, Giampaolo, Francesco Muntoni, Paolo Calabresi, Franco Romani, Virgilio Boi, and Gian Luigi Gessa. "Responsiveness to ‘autoreceptor’ doses of apomorphine is inversely correlated with the firing rate of dopaminergic A9 neurons: Action of baclofen." Neuroscience Letters 65, no. 2 (April 1986): 161–66. http://dx.doi.org/10.1016/0304-3940(86)90297-1.

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30

White, F. J., and R. Y. Wang. "Effects of tiaspirone (BMY-13859) and a chemical congener (BMY-13980) on A9 and A10 dopamine neurons in the rat." Neuropharmacology 25, no. 9 (September 1986): 995–1001. http://dx.doi.org/10.1016/0028-3908(86)90193-0.

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Romo, R., and W. Schultz. "Dopamine neurons of the monkey midbrain: contingencies of responses to active touch during self-initiated arm movements." Journal of Neurophysiology 63, no. 3 (March 1, 1990): 592–606. http://dx.doi.org/10.1152/jn.1990.63.3.592.

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1. Previous studies have shown that midbrain dopamine (DA) neurons in monkeys respond to external stimuli that are used to initiate behavioral reactions. In the present study, we investigated to what extent changes in neuronal activity would occur when behavioral acts are generated internally or whether they would depend solely on external stimuli. 2. Monkeys performed self-initiated arm movements from a resting key into a covered, food-containing box at a self-chosen moment and without external preparatory or triggering signals. In a second task, the arm movement was triggered by rapid opening of the door of the food box. This stimulus was either audible and visible or only audible to the animal. Impulses of DA neurons were recorded with movable microelectrodes from the pars compacta of substantia nigra (area A9) and areas A8 and A10 and were discriminated from those of other neurons by their long duration (1.5-5.0 ms) and low spontaneous frequency (0.5-8.5 imp/s). 3. The activity of 12% of 104 DA neurons increased slowly and moderately up to 1,500 ms before the onset of individual self-initiated arm movements. Median increases amounted to 91% over background discharge rate. A further 16% of DA neurons were activated together with the onset of muscle activity and during the movement. 4. During self-initiated movements, a nonhabituating, phasic burst of impulses occurred when the monkey's hand touched a morsel of food inside the box. This response was seen in 84% of 154 neurons on the contralateral side, with median onset latency of 65 ms and duration of 160 ms. A comparable percentage of neurons responded to ipsilateral touch with similar latency and duration. 5. The touch response during self-initiated movements was absent, both on the contra- and ipsilateral sides, when the animal's hand touched the bare wire normally holding the food, when touching nonfood objects, or during tactile exploration of the empty interior of the food box. Thus responses appeared to be related to the appetitive properties of the object being touched rather than the object itself. 6. In the task employing stimulus-triggered movements, 77% of 86 DA neurons discharged a burst of impulses in response to door opening but entirely failed to respond to the touch of food in the box. The response to door opening in this task was similar to the touch response during self-initiated movements in the same neurons in terms of latency, duration, and magnitude.(ABSTRACT TRUNCATED AT 400 WORDS)

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Penna, Vanessa, Niamh Moriarty, Yi Wang, Kevin C. L. Law, Carlos W. Gantner, Richard J. Williams, David R. Nisbet, and Clare L. Parish. "Extracellular Matrix Biomimetic Hydrogels, Encapsulated with Stromal Cell-Derived Factor 1, Improve the Composition of Foetal Tissue Grafts in a Rodent Model of Parkinson’s Disease." International Journal of Molecular Sciences 23, no. 9 (April 22, 2022): 4646. http://dx.doi.org/10.3390/ijms23094646.

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Clinical studies have provided evidence for dopamine (DA) cell replacement therapy in Parkinson’s Disease. However, grafts derived from foetal tissue or pluripotent stem cells (PSCs) remain heterogeneous, with a high proportion of non-dopaminergic cells, and display subthreshold reinnervation of target tissues, thereby highlighting the need to identify new strategies to improve graft outcomes. In recent work, Stromal Cell-Derived Factor-1 (SDF1), secreted from meninges, has been shown to exert many roles during ventral midbrain DA development and DA-directed differentiation of PSCs. Related, co-implantation of meningeal cells has been shown to improve neural graft outcomes, however, no direct evidence for the role of SDF1 in neural grafting has been shown. Due to the rapid degradation of SDF1 protein, here, we utilised a hydrogel to entrap the protein and sustain its delivery at the transplant site to assess the impact on DA progenitor differentiation, survival and plasticity. Hydrogels were fabricated from self-assembling peptides (SAP), presenting an epitope for laminin, the brain’s main extracellular matrix protein, thereby providing cell adhesive support for the grafts and additional laminin–integrin signalling to influence cell fate. We show that SDF1 functionalised SAP hydrogels resulted in larger grafts, containing more DA neurons, increased A9 DA specification (the subpopulation of DA neurons responsible for motor function) and enhanced innervation. These findings demonstrate the capacity for functionalised, tissue-specific hydrogels to improve the composition of grafts targeted for neural repair.

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Redmond, Andy J., Bret A. Morrow, John D. Elsworth, and Robert H. Roth. "Selective activation of the A10, but not A9, dopamine neurons in the rat by the predator odor, 2,5-dihydro-2,4,5-trimethylthiazoline." Neuroscience Letters 328, no. 3 (August 2002): 209–12. http://dx.doi.org/10.1016/s0304-3940(02)00566-9.

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34

Seiz, E. G., M. Ramos-Gómez, E. T. Courtois, I. Liste, and A. Martínez-Serrano. "3.340 HUMAN MIDBRAIN PRECURSORS DIFFERENTIATE TO MATURE FUNCTIONAL A9 DOPAMINE NEURONS IN VITRO. SHORT AND LONG-TERM ENHANCEMENT BY BCL-XL." Parkinsonism & Related Disorders 18 (January 2012): S229. http://dx.doi.org/10.1016/s1353-8020(11)70973-7.

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Kuter, Katarzyna, Klemencja Berghauzen-Maciejewska, Anna Górska, Katarzyna Kamińska, Jadwiga Wardas, Krystyna Gołembiowska, and Krystyna Ossowska. "The 6-hydroxydopamine-induced lesion of A8 and A9 mesencephalic dopaminergic neurons decreases the harmaline-induced glutamate release in the cerebellum." Pharmacological Reports 65 (May 2013): 61–62. http://dx.doi.org/10.1016/s1734-1140(13)71349-5.

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Piontek, Julie A., and Rex Y. Wang. "Acute and subchronic effects of Rimcazole (BW 234U), a potential antipsychotic drug, on A9 and A10 dopamine neurons in the rat." Life Sciences 39, no. 7 (August 1986): 651–58. http://dx.doi.org/10.1016/0024-3205(86)90047-0.

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Overton, Paul, and David Clark. "Iontophoretically administered drugs acting at the N-methyl-D-aspartate receptor modulate burst firing in A9 dopamine neurons in the rat." Synapse 10, no. 2 (February 1992): 131–40. http://dx.doi.org/10.1002/syn.890100208.

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Kolasiewicz, Wacław, Katarzyna Kuter, Klemencja Berghauzen, Przemysław Nowak, Gert Schulze, and Krystyna Ossowska. "6-OHDA injections into A8–A9 dopaminergic neurons modelling early stages of Parkinson's disease increase the harmaline-induced tremor in rats." Brain Research 1477 (October 2012): 59–73. http://dx.doi.org/10.1016/j.brainres.2012.08.015.

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Sánchez-Danés, A., A. Consiglio, Y. Richaud, I. Rodríguez-Pizà, B. Dehay, M. Edel, J. Bové, et al. "Efficient Generation of A9 Midbrain Dopaminergic Neurons by Lentiviral Delivery of LMX1A in Human Embryonic Stem Cells and Induced Pluripotent Stem Cells." Human Gene Therapy 23, no. 1 (January 2012): 56–69. http://dx.doi.org/10.1089/hum.2011.054.

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Bymaster, Franklin, Kenneth W. Perry, David L. Nelson, David T. Wong, Kurt Rasmussen, Nick A. Moore, and David O. Calligaro. "Olanzapine: a basic science update." British Journal of Psychiatry 174, S37 (February 1999): 36–40. http://dx.doi.org/10.1192/s0007125000293653.

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Olanzapine, an atypical antipsychotic, has a broad receptor binding profile, which may account for its pharmacological effects in schizophrenia. In vitro receptor binding studies showed a high affinity for dopamine D2, D3, and D4 receptors; all 5-HT2 receptor subtypes and the 5-HT6 receptor; muscarinic receptors, especially the M1 subtype; and α1-adrenergic receptors. In vivo studies showed that olanzapine had potent activity at D2 and 5 -HT2A receptors, but much less activity at D1 and muscarinic receptors, and that it inhibited dopaminergic neurons in the A10 but not the A9 tract, suggesting that this agent will not cause extrapyramidal side-effects (EPS). Microdialysis studies showed that olanzapine increased the extracellular levels of norepinephrine and dopamine, but not 5-HT, in the prefrontal cortex, and increased extracellular dopamine levels in the neostriatum and nucleus accumbens, areas ofthe brain associated with schizophrenia. Studies of gene expression showed that olanzapine 10 mg/kg also increased Fos expression in the prefrontal cortex, the dorsolateral striatum, and the nucleus accumbens. These findings are consistent with the effectiveness of olanzapine on both negative and positive symptoms and suggest that, with careful dosing, olanzapine should not cause EPS.

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Goldstein, Jeffrey M., and Linda C. Litwin. "Spontaneous activity of A9 and A10 dopamine neurons after acute and chronic administration of the selective dopamine D-1 receptor antagonist SCH 23390." European Journal of Pharmacology 155, no. 1-2 (October 1988): 175–80. http://dx.doi.org/10.1016/0014-2999(88)90419-0.

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Czaniecki, Christopher, Tammy Ryan, Morgan G. Stykel, Jennifer Drolet, Juliane Heide, Ryan Hallam, Shalandra Wood, et al. "Axonal pathology in hPSC-based models of Parkinson’s disease results from loss of Nrf2 transcriptional activity at the Map1b gene locus." Proceedings of the National Academy of Sciences 116, no. 28 (June 24, 2019): 14280–89. http://dx.doi.org/10.1073/pnas.1900576116.

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While mutations in theSNCAgene (α-synuclein [α-syn]) are causal in rare familial forms of Parkinson’s disease (PD), the prevalence of α-syn aggregates in the cortices of sporadic disease cases emphasizes the need to understand the link between α-syn accumulation and disease pathogenesis. By employing a combination of human pluripotent stem cells (hPSCs) that harbor theSNCA-A53T mutation contrasted against isogenic controls, we evaluated the consequences of α-syn accumulation in human A9-type dopaminergic (DA) neurons (hNs). We show that the early accumulation of α-syn inSNCA-A53T hNs results in changes in gene expression consistent with the expression profile of the substantia nigra (SN) from PD patients, analyzed post mortem. Differentially expressed genes from both PD patient SN andSNCA-A53T hNs were associated with regulatory motifs transcriptionally activated by the antioxidant response pathway, particularly Nrf2 gene targets. Differentially expressed gene targets were also enriched for gene ontologies related to microtubule binding processes. We thus assessed the relationship between Nrf2-mediated gene expression and neuritic pathology inSNCA-A53T hNs. We show thatSNCA-mutant hNs have deficits in neuritic length and complexity relative to isogenic controls as well as contorted axons with Tau-positive varicosities. Furthermore, we show that mutant α-syn fails to complex with protein kinase C (PKC), which, in turn, results in impaired activation of Nrf2. These neuritic defects result from impaired Nrf2 activity on antioxidant response elements (AREs) localized to a microtubule-associated protein (Map1b) gene enhancer and are rescued by forced expression of Map1b as well as by both Nrf2 overexpression and pharmaceutical activation in PD neurons.

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Ngwa, Conelius, Abdullah Al Mamun, Yan Xu, Romana Sharmeen, and Fudong Liu. "Phosphorylation of Microglial IRF5 and IRF4 by IRAK4 Regulates Inflammatory Responses to Ischemia." Cells 10, no. 2 (January 30, 2021): 276. http://dx.doi.org/10.3390/cells10020276.

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Background: Interferon Regulatory Factor (IRF) 5 and 4 play a determinant role in regulating microglial pro- and anti-inflammatory responses to cerebral ischemia. How microglial IRF5 and IRF4 signaling are activated has been elusive. We hypothesized that interleukin-1 receptor associated kinase 4 (IRAK4) phosphorylates and activates IRF5 and IRF4 in ischemic microglia. We aimed to explore the upstream signals of the two IRFs, and to determine how the IRAK4-IRF signaling regulates the expression of inflammatory mediators, and impacts neuropathology. Methods: Spontaneously Immortalized Murine (SIM)-A9 microglial cell line, primary microglia and neurons from C57BL/6 WT mice were cultured and exposed to oxygen-glucose deprivation (OGD), followed by stimulation with LPS or IL-4. An IRAK4 inhibitor (ND2158) was used to examine IRAK4′s effects on the phosphorylation of IRF5/IRF4 and the impacts on neuronal morphology by co-immunoprecipitation (Co-IP)/Western blot, ELISA, and immunofluorescence assays. Results: We confirmed that IRAK4 formed a Myddosome with MyD88/IRF5/IRF4, and phosphorylated both IRFs, which subsequently translocated into the nucleus. Inhibition of IRAK4 phosphorylation quenched microglial pro-inflammatory response primarily, and increased neuronal viability and neurite lengths after ischemia. Conclusions: IRAK4 signaling is critical for microglial inflammatory responses and a potential therapeutic target for neuroinflammatory diseases including cerebral ischemia.

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Seiz, Emma G., Milagros Ramos-Gómez, Elise T. Courtois, Jan Tønnesen, Merab Kokaia, Isabel Liste Noya, and Alberto Martínez-Serrano. "Human midbrain precursors activate the expected developmental genetic program and differentiate long-term to functional A9 dopamine neurons in vitro. Enhancement by Bcl-XL." Experimental Cell Research 318, no. 19 (November 2012): 2446–59. http://dx.doi.org/10.1016/j.yexcr.2012.07.018.

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Rasmussen, Kurt, Mei-Ann Hsu, and Yili Yang. "The Orexin-1 Receptor Antagonist SB-334867 Blocks the Effects of Antipsychotics on the Activity of A9 and A10 Dopamine Neurons: Implications for Antipsychotic Therapy." Neuropsychopharmacology 32, no. 4 (October 25, 2006): 786–92. http://dx.doi.org/10.1038/sj.npp.1301239.

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Taleb, Omar, Mohammed Maammar, Christian Klein, Michel Maitre, and Ayikoe Guy Mensah-Nyagan. "A Role for Xanthurenic Acid in the Control of Brain Dopaminergic Activity." International Journal of Molecular Sciences 22, no. 13 (June 28, 2021): 6974. http://dx.doi.org/10.3390/ijms22136974.

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Xanthurenic acid (XA) is a metabolite of the kynurenine pathway (KP) synthetized in the brain from dietary or microbial tryptophan that crosses the blood-brain barrier through carrier-mediated transport. XA and kynurenic acid (KYNA) are two structurally related compounds of KP occurring at micromolar concentrations in the CNS and suspected to modulate some pathophysiological mechanisms of neuropsychiatric and/or neurodegenerative diseases. Particularly, various data including XA cerebral distribution (from 1 µM in olfactory bulbs and cerebellum to 0.1–0.4 µM in A9 and A10), its release, and interactions with G protein-dependent XA-receptor, glutamate transporter and metabotropic receptors, strongly support a signaling and/or neuromodulatory role for XA. However, while the parent molecule KYNA is considered as potentially involved in neuropsychiatric disorders because of its inhibitory action on dopamine release in the striatum, the effect of XA on brain dopaminergic activity remains unknown. Here, we demonstrate that acute local/microdialysis-infusions of XA dose-dependently stimulate dopamine release in the rat prefrontal cortex (four-fold increase in the presence of 20 µM XA). This stimulatory effect is blocked by XA-receptor antagonist NCS-486. Interestingly, our results show that the peripheral/intraperitoneal administration of XA, which has been proven to enhance intra-cerebral XA concentrations (about 200% increase after 50 mg/kg XA i.p), also induces a dose-dependent increase of dopamine release in the cortex and striatum. Furthermore, our in vivo electrophysiological studies reveal that the repeated/daily administrations of XA reduce by 43% the number of spontaneously firing dopaminergic neurons in the ventral tegmental area. In the substantia nigra, XA treatment does not change the number of firing neurons. Altogether, our results suggest that XA may contribute together with KYNA to generate a KYNA/XA ratio that may crucially determine the brain normal dopaminergic activity. Imbalance of this ratio may result in dopaminergic dysfunctions related to several brain disorders, including psychotic diseases and drug dependence.

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Banrezes, Bernadette, Yves Maurin, and Catherine Verney. "Intrauterine growth retardation does not alter the distribution of tyrosine hydroxylase-immunoreactive neurons of A8, A9 and A10 groups in the rat: a three-dimensional reconstruction study." Developmental Brain Research 126, no. 1 (January 2001): 13–20. http://dx.doi.org/10.1016/s0165-3806(00)00121-8.

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Kulas, Joshua A., Whitney F. Franklin, Nicholas A. Smith, Gunjan D. Manocha, Kendra L. Puig, Kumi Nagamoto-Combs, Rachel D. Hendrix, Giulio Taglialatela, Steven W. Barger, and Colin K. Combs. "Ablation of amyloid precursor protein increases insulin-degrading enzyme levels and activity in brain and peripheral tissues." American Journal of Physiology-Endocrinology and Metabolism 316, no. 1 (January 1, 2019): E106—E120. http://dx.doi.org/10.1152/ajpendo.00279.2018.

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The amyloid precursor protein (APP) is a type I transmembrane glycoprotein widely studied for its role as the source of β-amyloid peptide, accumulation of which is causal in at least some cases of Alzheimer’s disease (AD). APP is expressed ubiquitously and is involved in diverse biological processes. Growing bodies of evidence indicate connections between AD and somatic metabolic disorders related to type 2 diabetes, and App−/− mice show alterations in glycemic regulation. We find that App−/− mice have higher levels of insulin-degrading enzyme (IDE) mRNA, protein, and activity compared with wild-type controls. This regulation of IDE by APP was widespread across numerous tissues, including liver, skeletal muscle, and brain as well as cell types within neural tissue, including neurons, astrocytes, and microglia. RNA interference-mediated knockdown of APP in the SIM-A9 microglia cell line elevated IDE levels. Fasting levels of blood insulin were lower in App−/− than App+/+ mice, but the former showed a larger increase in response to glucose. These low basal levels may enhance peripheral insulin sensitivity, as App−/− mice failed to develop impairment of glucose tolerance on a high-fat, high-sucrose (“Western”) diet. Insulin levels and insulin signaling were also lower in the App−/− brain; synaptosomes prepared from App−/− hippocampus showed diminished insulin receptor phosphorylation compared with App+/+ mice when stimulated ex vivo. These findings represent a new molecular link connecting APP to metabolic homeostasis and demonstrate a novel role for APP as an upstream regulator of IDE in vivo.

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Osacka, J., L. Horvathova, Z. Majercikova, and Alexander Kiss. "Eff ect of a single asenapine treatment on Fos expression in the brain catecholamine-synthesizing neurons: impact of a chronic mild stress preconditioning." Endocrine Regulations 51, no. 2 (April 25, 2017): 73–83. http://dx.doi.org/10.1515/enr-2017-0007.

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AbstractObjective. Fos protein expression in catecholamine-synthesizing neurons of the substantia nigra (SN) pars compacta (SNC, A8), pars reticulata (SNR, A9), and pars lateralis (SNL), the ventral tegmental area (VTA, A10), the locus coeruleus (LC, A6) and subcoeruleus (sLC), the ventrolateral pons (PON-A5), the nucleus of the solitary tract (NTS-A2), the area postrema (AP), and the ventrolateral medulla (VLM-A1) was quantitatively evaluated aft er a single administration of asenapine (ASE) (designated for schizophrenia treatment) in male Wistar rats preconditioned with a chronic unpredictable variable mild stress (CMS) for 21 days. Th e aim of the present study was to reveal whether a single ASE treatment may 1) activate Fos expression in the brain areas selected; 2) activate tyrosine hydroxylase (TH)-synthesizing cells displaying Fos presence; and 3) be modulated by CMS preconditioning.Methods. Control (CON), ASE, CMS, and CMS+ASE groups were used. CMS included restraint, social isolation, crowding, swimming, and cold. Th e ASE and CMS+ASE groups received a single dose of ASE (0.3 mg/kg, s.c.) and CON and CMS saline (300 μl/rat, s.c.). The animals were sacrificed 90 min aft er the treatments. Fos protein and TH-labeled immunoreactive perikarya were analyzed on double labeled histological sections and enumerated on captured pictures using combined light and fluorescence microscope illumination.Results. Saline or CMS alone did not promote Fos expression in any of the structures investigated. ASE alone or in combination with CMS elicited Fos expression in two parts of the SN (SNC, SNR) and the VTA. Aside from some cells in the central gray tegmental nuclei adjacent to LC, where a small number of Fos profiles occurred, none or negligible Fos occurrence was detected in the other structures investigated including the LC and sLC, PON-A5, NTS-A2, AP, and VLM-A1. CMS preconditioning did not infl uence the level of Fos induction in the SN and VTA elicited by ASE administration. Similarly, the ratio between the amount of free Fos and Fos colocalized with TH was not aff ected by stress preconditioning in the SNC, SNR, and the VTA.Conclusions. Th e present study provides an anatomical/functional knowledge about the nature of the acute ASE treatment on the catecholamine-synthesizing neurons activity in certain brain structures and their missing interplay with the CMS preconditioning.

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Moore, A. E., F. Cicchetti, J. Hennen, and O. Isacson. "Parkinsonian Motor Deficits Are Reflected by Proportional A9/A10 Dopamine Neuron Degeneration in the Rat." Experimental Neurology 172, no. 2 (December 2001): 363–76. http://dx.doi.org/10.1006/exnr.2001.7823.

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