Analysis of Acute and Chronic Methamphetamine Treatment in Mice on Gdnf System Expression Reveals a Potential Mechanism of Schizophrenia Susceptibility
Abstract
:1. Introduction
2. Materials and Methods
2.1. Animals
2.2. Methamphetamine Injections
2.3. Reverse Transcription and Quantitative PCR
2.4. Statistical Analysis
3. Results
3.1. Acute Methamphetamine Application Induces a 2-Fold Increase in Striatal Gdnf Expression
3.2. Acute Methamphetamine Treatment Enhances Expression of Genes Related to Dopaminergic and Serotonergic System Function
3.3. Chronic Methamphetamine Treatment Upregulates Ret Expression in the Substantia Nigra but Downregulates Gfra1 and Ret mRNA Levels in the Striatum
3.4. Chronic Methamphetamine Maintain Elevated D2R Expression in the Prefrontal Cortex and Induces DAT Expression in the Substantia Nigra
3.5. The Effect of Acute E11–E12.5 Methamphetamine Application on GDNF and Monoamine Systems-Related Gene Expression in the Brain
4. Discussion
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Acknowledgments
Conflicts of Interest
Abbreviations
A2A | Adenosine receptor 2A |
CSF | Cerebrospinal fluid |
DA | Dopamine |
DAT | Dopamine reuptake transporter |
D1Ra | Dopamine 1 receptor |
D2R | Dopamine 2 receptor |
FEP | First-episode psychosis |
GAPDH | Glyceraldehyde 3-phosphate dehydrogenase |
GDNF | Glial cell line-derived neurotrophic factor |
GFRa1 | GDNF family receptor alpha 1 |
HTR2a | 5-hydroxytryptamine receptor 2a |
HTR2b | 5-hydroxytryptamine receptor 2b |
aMETH | acute methamphetamine |
cMETH | chronic methamphetamine |
PFC | Prefrontal cortex |
Pvalb | Parvalbumin |
RET | Rearranged during transfection receptor tyrosine kinase |
RPS6 | Ribosomal protein subunit 61 |
SCZ | Schizophrenia |
SERT | 5-hydroxytryptamine reuptake transporter |
SPECT | Single-photon emission computed tomography |
SN | Substantia Nigra |
TH | Tyrosine hydroxylase |
Vmat2 | Vesicular monoamine transporter 2 |
WT | Wild-type |
References
- Stępnicki, P.; Kondej, M.; Kaczor, A.A. Current Concepts and Treatments of Schizophrenia. Molecules 2018, 23, 2087. [Google Scholar] [CrossRef] [PubMed]
- Mätlik, K.; Garton, D.R.; Montaño-Rodríguez, A.R.; Olfat, S.; Eren, F.; Casserly, L.; Damdimopoulos, A.; Panhelainen, A.; Porokuokka, L.L.; Kopra, J.J.; et al. Elevated endogenous GDNF induces altered dopamine signalling in mice and correlates with clinical severity in schizophrenia. Mol. Psychiatry 2022, 27, 3247–3261. [Google Scholar] [CrossRef] [PubMed]
- Chen, C.K.; Lin, S.K.; Sham, P.C.; Ball, D.; Loh, E.W.; Hsiao, C.C.; Chiang, Y.L.; Ree, S.C.; Lee, C.H.; Murray, R.M. Pre-morbid characteristics and co-morbidity of methamphetamine users with and without psychosis. Psychol. Med. 2003, 33, 1407–1414. [Google Scholar] [CrossRef] [PubMed]
- McKetin, R.; McLaren, J.; Lubman, D.I.; Hides, L. The prevalence of psychotic symptoms among methamphetamine users. Addiction 2006, 101, 1473–1478. [Google Scholar] [CrossRef] [PubMed]
- McKetin, R.; Lubman, D.I.; Baker, A.L.; Dawe, S.; Ali, R.L. Dose-Related Psychotic Symptoms in Chronic Methamphetamine Users: Evidence From a Prospective Longitudinal Study. JAMA Psychiatry 2013, 70, 319–324. [Google Scholar] [CrossRef] [PubMed]
- Kesby, J.P.; Eyles, D.W.; McGrath, J.J.; Scott, J.G. Dopamine, psychosis and schizophrenia: The widening gap between basic and clinical neuroscience. Transl. Psychiatry 2018, 8, 30. [Google Scholar] [CrossRef] [PubMed]
- Howes, O.D.; Kambeitz, J.; Kim, E.; Stahl, D.; Slifstein, M.; Abi-Dargham, A.; Kapur, S. The nature of dopamine dysfunction in schizophrenia and what this means for treatment. Arch. Gen. Psychiatry 2012, 69, 776–786. [Google Scholar] [CrossRef]
- Howes, O.D.; Kapur, S. The dopamine hypothesis of schizophrenia: Version III--the final common pathway. Schizophr. Bull. 2009, 35, 549–562. [Google Scholar] [CrossRef]
- Jauhar, S.; Veronese, M.; Nour, M.M.; Rogdaki, M.; Hathway, P.; Turkheimer, F.E.; Stone, J.; Egerton, A.; McGuire, P.; Kapur, S.; et al. Determinants of treatment response in first-episode psychosis: An 18F-DOPA PET study. Mol. Psychiatry 2019, 24, 1502–1512. [Google Scholar] [CrossRef]
- Masri, B.; Salahpour, A.; Didriksen, M.; Ghisi, V.; Beaulieu, J.M.; Gainetdinov, R.R.; Caron, M.G. Antagonism of dopamine D2 receptor/beta-arrestin 2 interaction is a common property of clinically effective antipsychotics. Proc. Natl. Acad. Sci. USA 2008, 105, 13656–13661. [Google Scholar] [CrossRef]
- Hidalgo-Figueroa, M.; Bonilla, S.; Gutiérrez, F.; Pascual, A.; López-Barneo, J. GDNF Is Predominantly Expressed in the PV+ Neostriatal Interneuronal Ensemble in Normal Mouse and after Injury of the Nigrostriatal Pathway. J. Neurosci. 2012, 32, 864–872. [Google Scholar] [CrossRef] [PubMed]
- D’Anglemont de Tassigny, X.; Pascual, A.; López-Barneo, J. GDNF-based therapies, GDNF-producing interneurons, and trophic support of the dopaminergic nigrostriatal pathway. Implications for Parkinson’s disease. Front. Neuroanat. 2015, 9, 10. [Google Scholar] [PubMed]
- Kopra, J.J.; Panhelainen, A.; Af Bjerkén, S.; Porokuokka, L.L.; Varendi, K.; Olfat, S.; Montonen, H.; Piepponen, T.P.; Saarma, M.; Andressoo, J.-O. Dampened Amphetamine-Stimulated Behavior and Altered Dopamine Transporter Function in the Absence of Brain GDNF. J. Neurosci. Off. J. Soc. Neurosci. 2017, 37, 1581–1590. [Google Scholar] [CrossRef]
- Kumar, A.; Kopra, J.; Varendi, K.; Porokuokka, L.L.; Panhelainen, A.; Kuure, S.; Marshall, P.; Karalija, N.; Härma, M.-A.; Vilenius, C.; et al. GDNF Overexpression from the Native Locus Reveals its Role in the Nigrostriatal Dopaminergic System Function. PLoS Genet. 2015, 11, e1005710. [Google Scholar] [CrossRef] [PubMed]
- Ibáñez, C.F.; Andressoo, J.-O. Biology of GDNF and its receptors—Relevance for disorders of the central nervous system. Neurobiol. Dis. 2017, 97, 80–89. [Google Scholar] [CrossRef] [PubMed]
- Tomac, A.; Lindqvist, E.; Lin, L.F.H.; Ögren, S.O.; Young, D.; Hoffer, B.J.; Olson, L. Protection and repair of the nigrostriatal dopaminergic system by GDNF in vivo. Nature 1995, 373, 335–339. [Google Scholar] [CrossRef]
- Gash, D.M.; Zhang, Z.; Ovadia, A.; Cass, W.A.; Yi, A.; Simmerman, L.; Russell, D.; Martin, D.; Lapchak, P.A.; Collins, F.; et al. Functional recovery in parkinsonian monkeys treated with GDNF. Nature 1996, 380, 252–255. [Google Scholar] [CrossRef]
- Love, S.; Plaha, P.; Patel, N.K.; Hotton, G.R.; Brooks, D.J.; Gill, S.S. Glial cell line–derived neurotrophic factor induces neuronal sprouting in human brain. Nat. Med. 2005, 11, 703–704. [Google Scholar] [CrossRef]
- Kirik, D.; Rosenblad, C.; Björklund, A.; Mandel, R.J. Long-Term rAAV-Mediated Gene Transfer of GDNF in the Rat Parkinson’s Model: Intrastriatal But Not Intranigral Transduction Promotes Functional Regeneration in the Lesioned Nigrostriatal System. J. Neurosci. 2000, 20, 4686–4700. [Google Scholar] [CrossRef]
- Moriarty, N.; Gantner, C.W.; Hunt, C.P.J.; Ermine, C.M.; Frausin, S.; Viventi, S.; Ovchinnikov, D.A.; Kirik, D.; Parish, C.L.; Thompson, L.H. A combined cell and gene therapy approach for homotopic reconstruction of midbrain dopamine pathways using human pluripotent stem cells. Cell Stem Cell 2022, 29, 434–448.e5. [Google Scholar] [CrossRef]
- Kordower, J.H.; Emborg, M.E.; Bloch, J.; Ma, S.Y.; Chu, Y.; Leventhal, L.; McBride, J.; Chen, E.Y.; Palfi, S.; Roitberg, B.Z.; et al. Neurodegeneration prevented by lentiviral vector delivery of GDNF in primate models of Parkinson’s disease. Science 2000, 290, 767–773. [Google Scholar] [CrossRef]
- Glasner-Edwards, S.; Mooney, L.J. Methamphetamine Psychosis: Epidemiology and Management. CNS Drugs 2014, 28, 1115–1126. [Google Scholar] [CrossRef]
- Wearne, T.A.; Cornish, J.L. A Comparison of Methamphetamine-Induced Psychosis and Schizophrenia: A Review of Positive, Negative, and Cognitive Symptomatology. Front. Psychiatry 2018, 9, 491. [Google Scholar] [CrossRef]
- O’Dell, S.J.; Weihmuller, F.B.; Marshall, J.F. Multiple methamphetamine injections induce marked increases in extracellular striatal dopamine which correlate with subsequent neurotoxicity. Brain Res. 1991, 564, 256–260. [Google Scholar] [CrossRef]
- Stephans, S.E.; Yamamoto, B.K. Methamphetamine-induced neurotoxicity: Roles for glutamate and dopamine efflux. Synapse 1994, 17, 203–209. [Google Scholar] [CrossRef] [PubMed]
- Akiyama, K.; Kanzaki, A.; Tsuchida, K.; Ujike, H. Methamphetamine-induced behavioral sensitization and its implications for relapse of schizophrenia. Schizophr. Res. 1994, 12, 251–257. [Google Scholar] [CrossRef] [PubMed]
- Archer, T.; Kostrzewa, R.M. Neuroteratology and Animal Modeling of Brain Disorders. In Neurotoxin Modeling of Brain Disorders—Life-Long Outcomes in Behavioral Teratology; Kostrzewa, R.M., Archer, T., Eds.; Springer International Publishing: Cham, Switzerland, 2016; pp. 1–40. [Google Scholar]
- Jones, C.A.; Watson, D.J.G.; Fone, K.C.F. Animal models of schizophrenia. Br. J. Pharmacol. 2011, 164, 1162–1194. [Google Scholar] [CrossRef]
- Machiyama, Y. Chronic methamphetamine intoxication model of schizophrenia in animals. Schizophr. Bull. 1992, 18, 107–113. [Google Scholar] [CrossRef]
- Oka, M.; Ito, K.; Koga, M.; Kusumi, I. Changes in subunit composition of NMDA receptors in animal models of schizophrenia by repeated administration of methamphetamine. Prog. Neuro Psychopharmacol. Biol. Psychiatry 2020, 103, 109984. [Google Scholar] [CrossRef]
- Shin, E.-J.; Dang, D.-K.; Tran, T.-V.; Tran, H.-Q.; Jeong, J.H.; Nah, S.-Y.; Jang, C.-G.; Yamada, K.; Nabeshima, T.; Kim, H.-C. Current understanding of methamphetamine-associated dopaminergic neurodegeneration and psychotoxic behaviors. Arch. Pharmacal Res. 2017, 40, 403–428. [Google Scholar]
- Greening, D.W.; Notaras, M.; Chen, M.; Xu, R.; Smith, J.D.; Cheng, L.; Simpson, R.J.; Hill, A.F.; van den Buuse, M. Chronic methamphetamine interacts with BDNF Val66Met to remodel psychosis pathways in the mesocorticolimbic proteome. Mol. Psychiatry 2021, 26, 4431–4447. [Google Scholar] [CrossRef] [PubMed]
- Kramer, J.C.; Fischman, V.S.; Littlefield, D.C. Amphetamine Abuse: Pattern and Effects of High Doses Taken Intravenously. JAMA 1967, 201, 305–309. [Google Scholar] [CrossRef] [PubMed]
- Manning, E.E.; van den Buuse, M. BDNF deficiency and young-adult methamphetamine induce sex-specific effects on prepulse inhibition regulation. Front. Cell. Neurosci. 2013, 7, 92. [Google Scholar] [CrossRef]
- Paulson, P.E.; Camp, D.M.; Robinson, T.E. Time course of transient behavioral depression and persistent behavioral sensitization in relation to regional brain monoamine concentrations during amphetamine withdrawal in rats. Psychopharmacology 1991, 103, 480–492. [Google Scholar] [CrossRef] [PubMed]
- Pogorelov, V.; Nomura, J.; Kim, J.; Kannan, G.; Yang, C.; Taniguchi, Y.; Abazyan, B.; Valentine, H.; Krasnova, I.N.; Kamiya, A.; et al. Mutant DISC1 affects methamphetamine-induced sensitization and conditioned place preference: A comorbidity model. Neuropharmacology 2012, 62, 1242–1251. [Google Scholar] [CrossRef] [PubMed]
- Manning, E.E.; Halberstadt, A.L.; van den Buuse, M. BDNF-Deficient Mice Show Reduced Psychosis-Related Behaviors Following Chronic Methamphetamine. Int. J. Neuropsychopharmacol. 2016, 19, pyv116. [Google Scholar] [CrossRef]
- Varendi, K.; Kumar, A.; Härma, M.-A.; Andressoo, J.-O. miR-1, miR-10b, miR-155, and miR-191 are novel regulators of BDNF. Cell. Mol. Life Sci. 2014, 71, 4443–4456. [Google Scholar] [CrossRef]
- Ashburner, M.; Ball, C.A.; Blake, J.A.; Botstein, D.; Butler, H.; Cherry, J.M.; Davis, A.P.; Dolinski, K.; Dwight, S.S.; Eppig, J.T.; et al. Gene Ontology: Tool for the unification of biology. Nat. Genet. 2000, 25, 25–29. [Google Scholar] [CrossRef]
- The Gene Ontology, C.; Carbon, S.; Douglass, E.; Good, B.M.; Unni, D.R.; Harris, N.L.; Mungall, C.J.; Basu, S.; Chisholm, R.L.; Dodson, R.J.; et al. The Gene Ontology resource: Enriching a GOld mine. Nucleic Acids Res. 2021, 49, D325–D334. [Google Scholar] [CrossRef]
- Lee, T.; Seeman, P. Brain dopamine receptors in schizophrenia. In Biological Markers in Psychiatry and Neurology; Usdin, E., Hanin, I., Eds.; Pergamon: Oxford, UK, 1982; pp. 219–226. [Google Scholar]
- Hirvonen, J.; van Erp, T.G.M.; Huttunen, J.; Aalto, S.; Någren, K.; Huttunen, M.; Lönnqvist, J.; Kaprio, J.; Hietala, J.; Cannon, T.D. Increased Caudate Dopamine D2 Receptor Availability as a Genetic Marker for Schizophrenia. Arch. Gen. Psychiatry 2005, 62, 371–378. [Google Scholar] [CrossRef]
- Seeman, P.; Kapur, S. Schizophrenia: More dopamine, more D2 receptors. Proc. Natl. Acad. Sci. USA 2000, 97, 7673–7675. [Google Scholar] [CrossRef]
- Brisch, R.; Saniotis, A.; Wolf, R.; Bielau, H.; Bernstein, H.-G.; Steiner, J.; Bogerts, B.; Braun, K.; Jankowski, Z.; Kumaratilake, J.; et al. The Role of Dopamine in Schizophrenia from a Neurobiological and Evolutionary Perspective: Old Fashioned, but Still in Vogue. Front. Psychiatry 2014, 5, 47. [Google Scholar]
- Brunelin, J.; Fecteau, S.; Suaud-Chagny, M.-F. Abnormal Striatal Dopamine Transmission in Schizophrenia. Curr. Med. Chem. 2013, 20, 397–404. [Google Scholar] [PubMed]
- Toda, M.; Abi-Dargham, A. Dopamine hypothesis of schizophrenia: Making sense of it all. Curr. Psychiatry Rep. 2007, 9, 329–336. [Google Scholar] [PubMed]
- Okubo, Y.; Suhara, T.; Suzuki, K.; Kobayashi, K.; Inoue, O.; Terasaki, O.; Someya, Y.; Sassa, T.; Sudo, Y.; Matsushima, E.; et al. Decreased prefrontal dopamine D1 receptors in schizophrenia revealed by PET. Nature 1997, 385, 634–636. [Google Scholar] [CrossRef] [PubMed]
- Daubner, S.C.; Le, T.; Wang, S. Tyrosine Hydroxylase and Regulation of Dopamine Synthesis. Arch. Biochem. Biophys. 2011, 508, 1–12. [Google Scholar] [CrossRef] [PubMed]
- Mueller, H.T.; Haroutunian, V.; Davis, K.L.; Meador-Woodruff, J.H. Expression of the ionotropic glutamate receptor subunits and NMDA receptor-associated intracellular proteins in the substantia nigra in schizophrenia. Brain Res. Mol. Brain Res. 2004, 121, 60–69. [Google Scholar] [CrossRef] [PubMed]
- Ichinose, H.; Ohye, T.; Fujita, K.; Pantucek, F.; Lange, K.; Riederer, P.; Nagatsu, T. Quantification of mRNA of tyrosine hydroxylase and aromatic L-amino acid decarboxylase in the substantia nigra in Parkinson’s disease and schizophrenia. Journal of Neural Transmission. Park. Dis. Dement. Sect. 1994, 8, 149–158. [Google Scholar] [CrossRef]
- Purves-Tyson, T.D.; Owens, S.J.; Rothmond, D.A.; Halliday, G.M.; Double, K.L.; Stevens, J.; McCrossin, T.; Shannon Weickert, C. Putative presynaptic dopamine dysregulation in schizophrenia is supported by molecular evidence from post-mortem human midbrain. Transl. Psychiatry 2017, 7, e1003. [Google Scholar] [CrossRef]
- Bilic, P.; Jukic, V.; Vilibic, M.; Savic, A.; Bozina, N. Treatment-resistant schizophrenia and DAT and SERT polymorphisms. Gene 2014, 543, 125–132. [Google Scholar] [CrossRef]
- Dean, B.; Hayes, W.; Opeskin, K.; Naylor, L.; Pavey, G.; Hill, C.; Keks, N.; Copolov, D.L. Serotonin2 receptors and the serotonin transporter in the schizophrenic brain. Behav. Brain Res. 1996, 73, 169–175. [Google Scholar] [CrossRef] [PubMed]
- Cannon, M.; Murray, R.M. Neonatal origins of schizophrenia. Arch. Dis. Child. 1998, 78, 1–3. [Google Scholar] [CrossRef] [PubMed]
- Jenkins, T. Perinatal complications and schizophrenia: Involvement of the immune system. Front. Neurosci. 2013, 7, 110. [Google Scholar] [CrossRef]
- Aguilar-Valles, A.; Rodrigue, B.; Matta-Camacho, E. Maternal Immune Activation and the Development of Dopaminergic Neurotransmission of the Offspring: Relevance for Schizophrenia and Other Psychoses. Front. Psychiatry 2020, 11, 852. [Google Scholar] [CrossRef]
- Choudhury, Z.; Lennox, B. Maternal Immune Activation and Schizophrenia—Evidence for an Immune Priming Disorder. Front. Psychiatry 2021, 12, 585742. [Google Scholar] [CrossRef] [PubMed]
- Lee, K.; Holley, S.M.; Shobe, J.L.; Chong, N.C.; Cepeda, C.; Levine, M.S.; Masmanidis, S.C. Parvalbumin Interneurons Modulate Striatal Output and Enhance Performance during Associative Learning. Neuron 2017, 93, 1451–1463.e4. [Google Scholar] [CrossRef]
- Ola, R.; Jakobson, M.; Kvist, J.; Perälä, N.; Kuure, S.; Braunewell, K.-H.; Bridgewater, D.; Rosenblum, N.D.; Chilov, D.; Immonen, T.; et al. The GDNF target Vsnl1 marks the ureteric tip. J. Am. Soc. Nephrol. 2011, 22, 274–284. [Google Scholar] [CrossRef]
- Lu, B.C.; Cebrian, C.; Chi, X.; Kuure, S.; Kuo, R.; Bates, C.M.; Arber, S.; Hassell, J.; MacNeil, L.; Hoshi, M.; et al. Etv4 and Etv5 are required downstream of GDNF and Ret for kidney branching morphogenesis. Nat. Genet. 2009, 41, 1295–1302. [Google Scholar] [CrossRef]
- Bowenkamp, K.E.; Hoffman, A.F.; Gerhardt, G.A.; Henry, M.A.; Biddle, P.T.; Hoffer, B.J.; Granholm, A.-C.E. Glial cell line-derived neurotrophic factor supports survival of injured midbrain dopaminergic neurons. J. Comp. Neurol. 1995, 355, 479–489. [Google Scholar] [CrossRef]
- Lin, L.-F.H.; Doherty, D.H.; Lile, J.D.; Bektesh, S.; Collins, F. GDNF: A Glial Cell Line-Derived Neurotrophic Factor for Midbrain Dopaminergic Neurons. Science 1993, 260, 1130–1132. [Google Scholar] [CrossRef]
- Hoffer, B.J.; Hoffman, A.; Bowenkamp, K.; Huettl, P.; Hudson, J.; Martin, D.; Lin, L.-F.H.; Gerhardt, G.A. Glial cell line-derived neurotrophic factor reverses toxin-induced injury to midbrain dopaminergic neurons in vivo. Neurosci. Lett. 1994, 182, 107–111. [Google Scholar] [CrossRef]
- Taraviras, S.; Marcos-Gutierrez, C.V.; Durbec, P.; Jani, H.; Grigoriou, M.; Sukumaran, M.; Wang, L.C.; Hynes, M.; Raisman, G.; Pachnis, V. Signalling by the RET receptor tyrosine kinase and its role in the development of the mammalian enteric nervous system. Development 1999, 126, 2785–2797. [Google Scholar] [CrossRef] [PubMed]
- Drinkut, A.; Tillack, K.; Meka, D.P.; Schulz, J.B.; Kügler, S.; Kramer, E.R. Ret is essential to mediate GDNF’s neuroprotective and neuroregenerative effect in a Parkinson disease mouse model. Cell Death Dis. 2016, 7, e2359. [Google Scholar] [CrossRef] [PubMed]
- Lee, K.; Kunugi, H.; Nanko, S. Glial cell line-derived neurotrophic factor (GDNF) gene and schizophrenia: Polymorphism screening and association analysis. Psychiatry Res. 2001, 104, 11–17. [Google Scholar] [CrossRef]
- Skibinska, M.; Kapelski, P.; Pawlak, J.; Rajewska-Rager, A.; Dmitrzak-Weglarz, M.; Szczepankiewicz, A.; Czerski, P.; Twarowska-Hauser, J. Glial Cell Line-Derived Neurotrophic Factor (GDNF) serum level in women with schizophrenia and depression, correlation with clinical and metabolic parameters. Psychiatry Res. 2017, 256, 396–402. [Google Scholar] [CrossRef] [PubMed]
- Niitsu, T.; Shirayama, Y.; Matsuzawa, D.; Shimizu, E.; Hashimoto, K.; Iyo, M. Association between serum levels of glial cell-line derived neurotrophic factor and attention deficits in schizophrenia. Neurosci. Lett. 2014, 575, 37–41. [Google Scholar] [CrossRef] [PubMed]
- Chu, C.-S.; Chu, C.-L.; Wu, C.-C.; Lu, T. Serum nerve growth factor beta, brain- and glial-derived neurotrophic factor levels and psychopathology in unmedicated patients with schizophrenia. J. Chin. Med. Assoc. 2018, 81, 577–581. [Google Scholar] [CrossRef] [PubMed]
- Tunca, Z.; Akdede, B.K.; Özerdem, A.; Alkın, T.; Polat, S.; Ceylan, D.; Bayın, M.; Kocuk, N.C.; Şimşek, S.; Resmi, H.; et al. Diverse Glial Cell Line-Derived Neurotrophic Factor (GDNF) Support Between Mania and Schizophrenia: A Comparative Study in Four Major Psychiatric Disorders. Eur. Psychiatry 2015, 30, 198–204. [Google Scholar] [CrossRef]
- Grant, K.M.; LeVan, T.D.; Wells, S.M.; Li, M.; Stoltenberg, S.F.; Gendelman, H.E.; Carlo, G.; Bevins, R.A. Methamphetamine-associated psychosis. J. Neuroimmune Pharmacol. 2012, 7, 113–139. [Google Scholar] [CrossRef]
- Van den Buuse, M. Modeling the positive symptoms of schizophrenia in genetically modified mice: Pharmacology and methodology aspects. Schizophr. Bull. 2010, 36, 246–270. [Google Scholar] [CrossRef]
- Kopra, J.; Vilenius, C.; Grealish, S.; Härma, M.-A.; Varendi, K.; Lindholm, J.; Castrén, E.; Võikar, V.; Björklund, A.; Piepponen, T.P.; et al. GDNF is not required for catecholaminergic neuron survival in vivo. Nat. Neurosci. 2015, 18, 319–322. [Google Scholar] [CrossRef] [PubMed]
- Olfat, S.; Mätlik, K.; Kopra, J.J.; Garton, D.R.; Iivanainen, V.H.; Bhattacharya, D.; Jakobsson, J.; Piepponen, T.P.; Andressoo, J.-O. Increased Physiological GDNF Levels Have No Effect on Dopamine Neuron Protection and Restoration in a Proteasome Inhibition Mouse Model of Parkinson’s Disease. eNeuro 2023, 10. [Google Scholar] [CrossRef] [PubMed]
- Bonafina, A.; Trinchero, M.F.; Ríos, A.S.; Bekinschtein, P.; Schinder, A.F.; Paratcha, G.; Ledda, F. GDNF and GFRα1 Are Required for Proper Integration of Adult-Born Hippocampal Neurons. Cell Rep. 2019, 29, 4308–4319.e4. [Google Scholar] [CrossRef] [PubMed]
- He, Z.; Jiang, J.; Hofmann, M.C.; Dym, M. Gfra1 silencing in mouse spermatogonial stem cells results in their differentiation via the inactivation of RET tyrosine kinase. Biol. Reprod. 2007, 77, 723–733. [Google Scholar] [CrossRef]
- Pozas, E.; Ibáñez, C.F. GDNF and GFRalpha1 promote differentiation and tangential migration of cortical GABAergic neurons. Neuron 2005, 45, 701–713. [Google Scholar] [CrossRef]
- Kimura, T.; Yoshimoto, K.; Tanaka, C.; Ohkura, T.; Iwahana, H.; Miyauchi, A.; Sano, T.; Itakura, M. Obvious mRNA and protein expression but absence of mutations of the RET proto-oncogene in parathyroid tumors. Eur. J. Endocrinol. 1996, 134, 314–319. [Google Scholar] [CrossRef]
- Drilon, A.; Oxnard, G.R.; Tan, D.S.W.; Loong, H.H.F.; Johnson, M.; Gainor, J.; McCoach, C.E.; Gautschi, O.; Besse, B.; Cho, B.C.; et al. Efficacy of Selpercatinib in RET Fusion–Positive Non–Small-Cell Lung Cancer. N. Engl. J. Med. 2020, 383, 813–824. [Google Scholar] [CrossRef]
- Nguyen, L.; Monestime, S. Pralsetinib: Treatment of metastatic RET fusion–positive non–small cell lung cancer. Am. J. Health-Syst. Pharm. 2022, 79, 527–533. [Google Scholar] [CrossRef]
- Syed, Y.Y. Pralsetinib: A Review in Advanced RET Fusion-Positive NSCLC. Drugs 2022, 82, 811–816. [Google Scholar] [CrossRef]
- Burke, R.E. GDNF as a candidate striatal target-derived neurotrophic factor for the development of substantia nigra dopamine neurons. J. Neural Transm. 2006, 70, 41–45. [Google Scholar]
- Trupp, M.; Arenas, E.; Fainzilber, M.; Nilsson, A.-S.; Sieber, B.-A.; Grigoriou, M.; Kilkenny, C.; Salazar-Grueso, E.; Pachnis, V.; Arumäe, U.; et al. Functional receptor for GDNF encoded by the c-ret proto-oncogene. Nature 1996, 381, 785–789. [Google Scholar] [CrossRef]
- Meka, D.P.; Müller-Rischart, A.K.; Nidadavolu, P.; Mohammadi, B.; Motori, E.; Ponna, S.K.; Aboutalebi, H.; Bassal, M.; Annamneedi, A.; Finckh, B.; et al. Parkin cooperates with GDNF/RET signaling to prevent dopaminergic neuron degeneration. J. Clin. Investig. 2015, 125, 1873–1885. [Google Scholar] [CrossRef] [PubMed]
- Etemadi-Aleagha, A.; Akhgari, M. Psychotropic drug abuse in pregnancy and its impact on child neurodevelopment: A review. World J. Clin. Pediatr. 2022, 11, 1–13. [Google Scholar] [CrossRef] [PubMed]
- Airaksinen, M.S.; Saarma, M. The GDNF family: Signalling, biological functions and therapeutic value. Nat. Rev. Neurosci. 2002, 3, 383–394. [Google Scholar] [CrossRef] [PubMed]
- Grace, A.A.; Gomes, F.V. The Circuitry of Dopamine System Regulation and its Disruption in Schizophrenia: Insights Into Treatment and Prevention. Schizophr. Bull. 2019, 45, 148–157. [Google Scholar] [CrossRef]
Primer | Forward Sequence | Reverse Sequence |
---|---|---|
adora2a | TGG GAG CCA GAG CAA GA | GCA GCC CTT TCC TCA CAA GA |
actin | CTA AGG CCA ACC CTG AAA AG | ACC AGA GGC ATA CAG GGA CA |
b2m | CTC GTT GAC CCT GGT CTT TC | TTG AGG GGT TTT CTG GAT AG CA |
dat | AACCTGTACTGGCGGCTATG | GCTGACCACGACCACTACA |
drd1a | GCG TGG TCT CCC AGA TCG | GCA TTT CTC CTT CAA GCC CCT |
drd2 | ACA CAC CGT ACA GCT CCA AG | GGA GTA GAC GAC CAC GAA GGC AG |
gapdh | GCC TCG TCC CGT AGA CAA AA | ATG AAG GGG TCG TTG ATG GC |
gdnf | CGC TGA CCA GTG ACT CCA ATA TGC | TGC CGC TTG TTT ATC TGG TGA CC |
gfra1 | TTC CCA CAC ACG TTT TAC CA | GCC CGA TAC ATT GGA TTT CA |
htr2a | AAC CCC ATT CAC CAT AGC CG | CCG AAG ACT GGG ATT GGC AT |
htr2b | TGC CCT CTT GAC AAT CAT GT | AGG GAA ATG GCA CAG AGA TG |
pvalb | TGG AGA CAA GGA TGG GGA CG | CCA CTT ACG TTT CAG CCA CC |
ret | TCC CTT CCA CAT GGA TTG A | ATC GGC TCT CGT GAG TGG TA |
rps6 | GGT TGG GAC CTA AAA GGG CT | GGT CCT GGG CTT CTT ACC TT |
slc6a4 | CCC AGA CTC TTG TGG GTT CC | CTA GCT GAT GAC TGG GTG GC |
th | CCCAAGGGCTTCAGAAGAG | GGGCATCCTCGATGAGACT |
vmat2 | ATGCTGCTCACCGTCGTAGT | TTTTTCTCGTGCTTAATGCTGT |
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Casserly, L.; Garton, D.R.; Montaño-Rodriguez, A.; Andressoo, J.-O. Analysis of Acute and Chronic Methamphetamine Treatment in Mice on Gdnf System Expression Reveals a Potential Mechanism of Schizophrenia Susceptibility. Biomolecules 2023, 13, 1428. https://doi.org/10.3390/biom13091428
Casserly L, Garton DR, Montaño-Rodriguez A, Andressoo J-O. Analysis of Acute and Chronic Methamphetamine Treatment in Mice on Gdnf System Expression Reveals a Potential Mechanism of Schizophrenia Susceptibility. Biomolecules. 2023; 13(9):1428. https://doi.org/10.3390/biom13091428
Chicago/Turabian StyleCasserly, Laoise, Daniel R. Garton, Ana Montaño-Rodriguez, and Jaan-Olle Andressoo. 2023. "Analysis of Acute and Chronic Methamphetamine Treatment in Mice on Gdnf System Expression Reveals a Potential Mechanism of Schizophrenia Susceptibility" Biomolecules 13, no. 9: 1428. https://doi.org/10.3390/biom13091428
APA StyleCasserly, L., Garton, D. R., Montaño-Rodriguez, A., & Andressoo, J. -O. (2023). Analysis of Acute and Chronic Methamphetamine Treatment in Mice on Gdnf System Expression Reveals a Potential Mechanism of Schizophrenia Susceptibility. Biomolecules, 13(9), 1428. https://doi.org/10.3390/biom13091428