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 PP  Vol.4 No.5 , August 2013
D1 and TrkB Receptors Take Charge of the Molecular Antidepressant Action in Cultured Astroglial Cells
Abstract: In psychopharmacology of depression, we observe two ways of research. One group is focused on catecholamines action. Second one fixes attention on neuronal morphogenesis and synaptic plasticity. The intimate connection of astrocytes, neurons and synaptic endings determines glial participation in neural homeostasis. Consequently this situation enlarges the role of astrocytes in the CNS synaptic plasticity. Brain Derived Neurotrophic factor and its receptor TrkB suppose to coordinate both of the above mentioning signaling pathways in depression disturbances. In our experiment, we have exploited striatal tissue because in our opinion this structure is misjudged in pathophysiology of depression alas; Several hypothesis proposed striatum as important in future intention activity structure. RT-PCR analysis was used to determine D1, BDNF and TrkB mRNA expression in cultured striatal astroglial cells. Administration of three representative antidepressants (ADs) like amitriptyline, moclobemide and sertraline to astroglial culture medium increase the D1, BDNF/TrkB mRNA expression. Our previous study showed that the stimulation of cAMP to CREB pathway after D1 receptors excitation constituted a common response to ADs. The present results signify that D1, BDNF/TrkB link which is next neural track (after cAMP/PKA) involved in the CNS adaptation to external conditions altered by chronic ADs treatment. Moreover, the striatum tissue appears to be important formation which takes an active part in antidepressant action thus essential in depression disorder etiology.
Cite this paper: M. Huzarska, M. Zielinski and Z. Herman, "D1 and TrkB Receptors Take Charge of the Molecular Antidepressant Action in Cultured Astroglial Cells," Pharmacology & Pharmacy, Vol. 4 No. 5, 2013, pp. 443-446. doi: 10.4236/pp.2013.45063.
References

[1]   S. D. Skaper, ”The Biology of Neurotrophins, Signaling Pathways, and Functional Peptide Mimetics of Neurotrophins and Their Receptors,” CNS & Neurological Disorders-Drug Targets, Vol. 7, No. 7, 2008, pp. 46-62. doi:10.2174/187152708783885174

[2]   T. Numakawa, S. Suzuki and E. Kumamaru, “BDNF Function and Intracellular Signaling in Neurons,” Histology and Histopathology, Vol. 25, No. 2, 2010, pp. 237-258.

[3]   D. M. Juric, S. Miklic and M. Carman-Krzan, “Monoaminergic Neuronal Activity up Regulates BDNF Synthesis Cultured Neonatal Rat Astrocytes,” Brain Research, Vol. 1108, No. 1, 2006, pp. 54-62.

[4]   J. K. Todd, A. Serrano, J. C. Lacaille and R. Robitaille, “Glial Cells in Synaptic Plasticity,” Journal of Physiology-Paris, Vol. 99, No. 2-3, 2006, pp. 75-83. doi:10.1016/j.jphysparis.2005.12.002

[5]   S. Vesce, P. Bezzi and A. Volterra, “Synaptic Transmission with the Glia,” News in Physiological Science, Vol. 16, 2001, pp. 178-184.

[6]   M. Huzarska, M. Zielinski and Z. S. Herman, “Repeated Treatment with Antidepressants Enhances Dopamine D1 Receptor Gene Expression in the Rat Brain,” European Journal of Pharmacology, Vol. 532, No. 3, 2006, pp. 208-213.

[7]   B. Reuss, A. Lorenzen and K.Unsicker, “Dopamine and Epinephrine but Not Serotonin down Regulate Dopamine Sensitivity in Cultured Cortical and Striatal Astroglial Cells,” Receptors and Channels, Vol. 7, No. 6, 2001, pp. 441-451.

[8]   J. K. Seamans and C. R. Yang, “The Principal Features and Mechanisms of Dopamine Modulation in the Prefrontal Cortex,” Progress in Neurobiology, Vol. 74, No. 1, 2004, pp. 1-58. doi:10.1016/j.pneurobio.2004.05.006

[9]   A. Araque and G. Perea, “Glial Modulation of Synaptic Transmission in Culture,” Glia, Vol. 47, No. 3, 2004, pp. 241-248. doi:10.1002/glia.20026

[10]   J. A. Coles, “Glial Cells and the Supply of Substrates of Energy Metabolism to Neurons,” In: H. Kettenmann and B. R. Ransom, Eds., Neuroglia, Oxford University Press, Oxford, 1995.

[11]   L. Hertz, B. H. J. Juurling and S. Szuchet, “Cell Cultures,” In: A. Lajtha, Ed., Hand-Book of Neurochemistry, Plenum Press, New York and London, 1985.

[12]   P. Chomczynski and N. Sacchi,” Single-Step Method of RNA Isolation by Acid Guanidinum Thiocyanate-Phenol-Chloroform Extraction,” Analytical Biochemistry, Vol. 162, No. 1, 1987, pp. 156-159. doi:10.1016/0003-2697(87)90021-2

[13]   A. Bahi, F. Boyer, V. Chandrasekar and J. L. Dreyer, “Role of Accumbens BDNF and TrkB in Cocaine-Induced Psychomotor Sensitization, Conditioned-Place Preference, and Reinstatement in Rats,” Psychopharmacology, Vol. 199, No. 2, 2008, pp. 169-182. doi:10.1007/s00213-008-1164-1

[14]   A. L. Delaunois, “Biostatistics in Pharmacology,” In: H. Grimm, Analysis of Variance, Pergamon Press, Oxford, 1973, pp. 675-716.

[15]   Y. Dwivedi and N. G. Pandey, “Adenylyl Cyclase-Cyclic AMP Signaling in Mood Disorders: Role of the Crucial Phosphorylating Enzyme Protein Kinase A,” Neuropsychiatric Disease and Treatment, Vol. 4, No. 1, 2008, pp. 161-176. doi:10.2147/NDT.S2380

[16]   P. Zanassi, M. Paolilllo, A. Montecuco and E. V. Avvedimento, “Pharmacological and Molecular Evidence for Dopamine D1 Receptor Expression by Striatal Astrocytes in Culture,” Journal Neurosciences Research, Vol. 58, No. 4, 1999, pp. 544-552.

[17]   R. Spanagel and F. Weiss, “The Dopamine Hypothesis of Reward: Past and Current Status,” Trends in Neurosciences, Vol. 22, No. 11, 1999, pp. 521-527. doi:10.1016/S0166-2236(99)01447-2

 
 
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