Glia and Addiction: A Review
Advances in Psychology and Neuroscience
Volume 2, Issue 2-1, March 2017, Pages: 38-41
Received: Nov. 14, 2016; Accepted: Nov. 19, 2016; Published: Feb. 14, 2017
Views 117      Downloads 10
Authors
Alhassan Abdulwahab, Department of Human Physiology, Faculty of Medicine, Ahmadu Bello University, Zaria, Nigeria
Sale Ibrahim Alhaji, Department of Human Physiology, Faculty of Medicine, Ahmadu Bello University, Zaria, Nigeria
Lawan Ibrahim, Department of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Ahmadu Bello University, Zaria, Nigeria
Uthman Garba Sadiq, Department of Pharmacology and Toxicology, Faculty of Pharmacy, University of Maiduguri, Maiduguri Nigeria
Article Tools
Follow on us
Abstract
Glia (including astrocytes, microglia and oligodendrocytes), which constitute the majority of cells in the brain were thought to function as passive supportive cells, bringing nutrients to and removing wastes from the neurons. Glia cells have almost the same receptors as neurons, secrete neurotransmitters, neurotrophic and neuroinflammatory factors and are intimately involved in synaptic plasticity. Glia has been found to have multiple functions in eventually all systems of the body (CNS, CVS, GIT etc) Considering the multiple functions of glia, and because glia are the most numerous cells in the brain, it is not surprising that psychostimulants affect their activity. Thus, this review is focused on works done to reveal the important roles played by glia in addiction and the possibility of manipulating the activity of glia as a target in the development of pharmacotherapeutic agents for treating disorders related to psychostimulants.
Keywords
Glia, Astroglia, Microglia, Oligodendrocytes, Addiction
To cite this article
Alhassan Abdulwahab, Sale Ibrahim Alhaji, Lawan Ibrahim, Uthman Garba Sadiq, Glia and Addiction: A Review, Advances in Psychology and Neuroscience. Special Issue:Substance Abuse: Perspectives, Trends, Issues and the Way Forward. Vol. 2, No. 2-1, 2017, pp. 38-41. doi: 10.11648/j.apn.s.2017020201.17
Copyright
Copyright © 2017 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
References
[1]
Volkow, N. D., Wang, G.-J., Fowler, J. S., and Tomasi, D. (2012). Addiction circuitry in the human brain. Annu. Rev. Pharmacol. Toxicol. 52, 321–336.
[2]
Sherwood CC, Stimpson CD, Raghanti MA, Wildman DE, Uddin M, Grossman LI, Goodman M, Redmond JC, Bonar CJ, Erwin JM, Hof PR (2006). Evolution of increased glia-neuron ratios in the human frontal cortex. Proc Natl Acad Sci U S A. 103(37):13606–13611.
[3]
Kettenmann H, Kirchhoff F, and Verkhratsky A. (2013). Microglia: new roles for the synaptic strippe. Neuron, 77(1):10-8.
[4]
Araque, A., Carmignoto, G., Haydon, P. G., Oliet, S. H., Robitaille, R., and Volterra, A. (2014). Gliotransmitters travel in time and space. Neuron 81, 728–739.
[5]
Benz B, Grima G, Do KQ.(2004). Glutamate-induced homocysteic acid release from astrocytes: possible implication in glia-neuron signaling. Neuroscience. 124(2):377–386.
[6]
Watkins LR, Hutchinson MR, Ledeboer A, Wieseler-Frank J, Milligan ED, Maier SF. Norman.
[7]
Camacho A, Massieu L. Role of glutamate transporters in the clearance and release of glutamate during ischemia and its relation to neuronal death. Arch Med Res. 2006; 37(1):11–18.
[8]
Ullian EM, Christopherson KS, Barres BA. Role for glia in synaptogenesis (2004). Glia; 47 (3):209–216.
[9]
Clark KH, Wiley CA, Bradberry CW (2013). Psychostimulant abuse and neuroinflammation: emerging evidence of their interconnection. Neurotox. Res. 23(2):174–188.
[10]
Jones RS, Minogue AM, Connor TJ, Lynch MA. ((2013). Amyloid-beta-induced astrocytic phagocytosis is mediated by CD36, CD47 and RAGE. J Neuroimmune. Pharmacol. 8(1):301–311
[11]
Haydon PG, Carmignoto G.(2006). Astrocyte control of synaptic transmission and neurovascular coupling. Physiol Rev 86(3): 1009-31.
[12]
Turner, J. R., Ecke, L. E., Briand, L. A., Haydon, P. G., and Blendy, J. A. (2013). Cocaine-related behaviors in mice with deficient gliotransmission. Psychopharmacology (Berl) 226, 167–176.
[13]
Tsunneko Mishima and Hajime Hirase (2010). In Vivo Intracellular Recording Suggests That Gray Matter Astrocytes in Mature Cerebral Cortex and Hippocampus Are Electrophysiologically Homogeneous. The Journal of Neuroscience 30 (8): 3093-3100.
[14]
Cadet, J. L., Bisagno, V., and Milroy, C. M. (2014). Neuropathology of substance use disorders. Acta Neuropathol. 127, 91–107.
[15]
Sekine Y, Ouchi Y, Sugihara G, Takei N, Yoshikawa E, Nakamura K (2008). Methamphetamine causes microglial activation in the brains of human abusers. J Neurosci. 28(22):5756-5761.
[16]
Schafer, D. P., Lehrman, E. K., and Stevens, B. (2013). The “quad-partite” synapse: microgliasynapse interactions in the developing and mature CNS. Glia 61, 24–36.
[17]
Noda M, Nakanishi H, Nabekura J, Akaike N (2000) AMPA-kainate subtypes of glutamate receptor in rat cerebral microglia. J Neurosci 20(1): 251-8.
[18]
Burnstock G. Historical review: (2006). ATP as a neurotransmitter. Trends Pharmacol Sci 2006; 27(3): 166-76.
[19]
Eljaschewitsch, E., Witting, A., Mawrin, C., Lee, T., Schmidt, P. M., Wolf, S., Hoertnagl, H., Raine, C. S., SchneiderStock, R., Nitsch, R., and Ullrich, O. (2006). The endocannabinoid anandamide protects neurons during CNS inflammation by induction of MKP-1 in microglial cells. Neuron 49, 67–79.
[20]
Witting, A., Chen, L., Cudaback, E., Straiker, A., Walter, L., Rickman, B., Moller, T., Brosnan, C., and Stella, N. (2006) Experimental autoimmune encephalomyelitis disrupts endocannabinoid-mediated neuroprotection. Proc. Natl. Acad. Sci. U. S. A. 103, 6362–6367.
[21]
Thomas DM, Dowgiert J, Geddes TJ, Francescutti-Verbeem D, Liu X, Kuhn DM (2004). Microglial activation is a pharmacologically specific marker for the neurotoxic amphetamines. Neurosci Lett; 367(3): 349-54.
[22]
Thomas DM, Walker PD, Benjamins JA, Geddes TJ, Kuhn DM (2004). Methamphetamine neurotoxicity in dopamine nerve endings of the striatum is associated with microglial activation. J Pharmacol Exp Ther 311(1): 1-7.
[23]
Kuhn, D. M., Francescutti-Verbeem, D. M., and Thomas, D. M. (2006) Dopamine quinones activate microglia and induce a neurotoxic gene expression profile: relationship to methamphetamine-induced nerve ending damage. Ann. N. Y. Acad. Sci. 1074, 31–41.
[24]
Kalehua A, Streit WJ, Walker DW, Hunter BE(1992). Chronic ethanol treatment promotes aberrant microglial morphology in area CA1 of the rat hippocampus. Alcohol Clin Exp Res. 16(2): 401
[25]
Hayashi T, Su TP. (2007). Sigma-1 receptor chaperones at the ER-mitochondrion interface regulate Ca(2+) signaling and cell survival. Cell. 131(3):596–610.
[26]
Kaushal N, Matsumoto RR. (2011) Role of sigma receptors in methamphetamine-induced neurotoxicity. Curr. Neuropharmacol. 9(1):54–57.
[27]
Katz JL, Su TP, Hiranita T, Hayashi T, Tanda G, Kopajtic T (2011). A Role for Sigma Receptors in Stimulant Self Administration and Addiction. Pharmaceuticals; 4(6):880–914.
[28]
Kourrich S, Hayashi T, Chuang JY, Tsai SY, Su TP, Bonci A (2013). Dynamic interaction between sigma-1 receptor and Kv1.2 shapes neuronal and behavioral responses to cocaine. Cell. 152(1–2): 236–247.
[29]
Jeong, H. K., Ji, K., Min, K., and Joe, E. H. (2013). Brain inflammation and microglia: facts and misconceptions. Exp. Neurobiol. 22, 59–67.
[30]
Pope A. Neuroglia: Quantitative aspects. In: Schoffeniels E, Franck G, Hertz L, Tower DB (1978). Dynamic Properties of Glia Cells. London: Pergamon, p. 13-20.
[31]
Hertz L, Zielke HR (2004). Astrocytic control of glutamatergic activity: astrocytes as stars of the show. Trends Neurosci: 27(12): 735-43.
[32]
Boileau I, Rusjan P, Houle S, Wilkins D, Tong J, Selby P (2008). Increased vesicular monoamine transporter binding during early abstinence in human methamphetamine users: Is VMAT2 a stable dopamine neuron biomarker? J Neurosci. 2008; 28(39):9850–9856.
[33]
Hyman SE.(2005). Addiction: a disease of learning and memory. Am J Psychiatry; 162(8): 1414-22.
[34]
Kalivas PW.(2003). Glutamate systems in cocaine addiction. Curr Opin Pharmacol 4(1): 23-29.
[35]
Itzhak Y, Achat-Mendes C. (2004). Methamphetamine and MDMA (ecstasy) neurotoxicity: 'of mice and men'. IUBMB Life 56(5): 249-55.
[36]
Hebert MA, O'Callaghan JP. (2000). Protein phosphorylation cascades associated with methamphetamine-induced glial activation. Ann N Y Acad Sci: 914: 238-62.
[37]
Snyder, A (1996) Responses of Glia to Alcohol. In: Aschner N, Kimelberg H, Eds. The Role of Glia in Neurotoxicity. Boca Raton: CRC Press; pp. 111-135.
[38]
Marie-Claire C, Courtin C, Roques BP, Noble F (2004). Cytoskeletal genes regulation by chronic morphine treatment in rat striatum. Neuropsychopharmacology 29(12): 2208 -2215.
[39]
Alonso E, Garrido E, Diez-Fernandez C (2007). Yohimbine prevents morphine-induced changes of glial fibrillary acidic protein in brainstem and alpha2-adrenoceptor gene expression in hippocampus. Neurosci Lett: 412(2): 163-7.
[40]
Mao J, Sung B, Ji RR, Lim G (2002). Chronic morphine induces downregulation of spinal glutamate transporters: implications in morphine tolerance and abnormal pain sensitivity. J Neurosci 22(18): 8312-8323.
[41]
Melendez RI, Hicks MP, Cagle SS, Kalivas PW (2005). Ethanol exposure decreases glutamate uptake in the nucleus accumbens. Alcohol Clin Exp Res: 29(3): 326-33.
[42]
Kalivas PW, Volkow ND.(2011) New medications for drug addiction hiding in glutamatergic neuroplasticity. Mol. Psychiatry. 16(10):974–986.
[43]
Stuber GD, Britt JP, Bonci A (2012). Optogenetic modulation of neural circuits that underlie reward seeking. Biol. Psychiatry: 71(12):1061–1067.
[44]
Nave, K. A. (2010). Myelination and support of axonal integrity by glia. Nature 468, 244–252.
[45]
George, O., Mandyam, C. D., Wee, S., and Koob, G. F. (2008). Extended access to cocaine selfadministration produces long-lasting prefrontal cortex-dependent working memory impairments. Neuropsychopharmacology 33, 2474–2482.
[46]
Kovalevich, J., Corley, G., Yen, W., Rawls, S. M., and Langford, D. (2012). Cocaine-induced loss of white matter proteins in the adult mouse nucleus accumbens is attenuated by administration of a β-lactam antibiotic during cocaine withdrawal. Am. J. Pathol. 181, 1921–1927.
ADDRESS
Science Publishing Group
548 FASHION AVENUE
NEW YORK, NY 10018
U.S.A.
Tel: (001)347-688-8931