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Journal articles on the topic 'A9 neurons'

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 та 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, № 12 (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-c

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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 (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 anatomic

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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 (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 (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

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5

Yang, S., L. C. Edman, J. A. Sanchez-Alcaniz, et al. "Cxcl12/Cxcr4 signaling controls the migration and process orientation of A9-A10 dopaminergic neurons." Journal of Cell Science 126, no. 22 (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 (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, et al. "Cxcl12/Cxcr4 signaling controls the migration and process orientation of A9-A10 dopaminergic neurons." Development 140, no. 22 (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 (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 (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 (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 (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 st

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12

Courtois, Elise T., Claudia G. Castillo, Emma G. Seiz, et al. "In Vitroandin VivoEnhanced Generation of Human A9 Dopamine Neurons from Neural Stem Cells by Bcl-XL." Journal of Biological Chemistry 285, no. 13 (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 (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 (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, et al. "Sigma receptors modulate both A9 and A10 dopaminergic neurons in the rat brain: functional interaction with NMDA receptors." Brain Research 524, no. 2 (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 (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 (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 (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 b

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21

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 (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. Inde

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22

Trudler, Dorit, Kristopher L. Nazor, Yvonne S. Eisele та ін. "Soluble α-synuclein–antibody complexes activate the NLRP3 inflammasome in hiPSC-derived microglia". Proceedings of the National Academy of Sciences 118, № 15 (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 microgli

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23

O’Keeffe, Fiona E., Sarah A. Scott, Pam Tyers, et al. "Induction of A9 dopaminergic neurons from neural stem cells improves motor function in an animal model of Parkinson's disease." Brain 131, no. 3 (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 (1999): 2561–71. http://dx.doi.org/10.1016/s0024-3205(99)00525-1.

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25

Sánchez-Arroyos, Ricardo, та 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, № 1 (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 (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, et al. "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 (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 (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 (1986): 995–1001. http://dx.doi.org/10.1016/0028-3908(86)90193-0.

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31

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 (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 openin

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32

Penna, Vanessa, Niamh Moriarty, Yi Wang, et al. "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 (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, c

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33

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 (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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35

Kuter, Katarzyna, Klemencja Berghauzen-Maciejewska, Anna Górska, et al. "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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36

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 (1986): 651–58. http://dx.doi.org/10.1016/0024-3205(86)90047-0.

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37

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 (1992): 131–40. http://dx.doi.org/10.1002/syn.890100208.

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38

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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39

Sánchez-Danés, A., A. Consiglio, Y. Richaud, 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 (2012): 56–69. http://dx.doi.org/10.1089/hum.2011.054.

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40

Bymaster, Franklin, Kenneth W. Perry, David L. Nelson, et al. "Olanzapine: a basic science update." British Journal of Psychiatry 174, S37 (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

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41

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 (1988): 175–80. http://dx.doi.org/10.1016/0014-2999(88)90419-0.

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42

Czaniecki, Christopher, Tammy Ryan, Morgan G. Stykel, 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 (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 i

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43

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 (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 (S

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44

Seiz, Emma G., Milagros Ramos-Gómez, Elise T. Courtois, et al. "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 (2012): 2446–59. http://dx.doi.org/10.1016/j.yexcr.2012.07.018.

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45

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 (2006): 786–92. http://dx.doi.org/10.1038/sj.npp.1301239.

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46

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 (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 in

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47

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 (2001): 13–20. http://dx.doi.org/10.1016/s0165-3806(00)00121-8.

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48

Kulas, Joshua A., Whitney F. Franklin, Nicholas A. Smith, et al. "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 (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 wi

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49

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 (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 unpredictab

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50

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 (2001): 363–76. http://dx.doi.org/10.1006/exnr.2001.7823.

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