Effects of Calcium on the GABAA-Coupled CI-/HCO3- -ATPase from Plasma Membrane of Rat Brain
Affiliation(s)
State Research Institute of General Pathology and Pathological Physiology RAS, Moscow, Russia.
State Research Institute of General Pathology and Pathological Physiology RAS, Moscow, Russia.
ABSTRACT
The work is a study of the influence of Ca2+ (0.01 - 1 mM) on neuronal CI-, HCO3-, -ATPase complex: an enzyme that is a CI--pump which is functionally and structurally coupled to GABAA-receptors. It is found that influence of Ca2+ on the multifunctional complex starts at concentration of 50·M and at concentration of 0.1 mM, it reduces the “basal” one and increases the CI-, HCO3-, -stimulated Mg2+-ATPase activities. GABA (0.1 - 100μM) activates the “basal” Mg2+-ATPase activity in the ab-sence of calcium. The effect of GABA on the enzyme in the presence of 0.01 ·M Ca2+ does not change. At the same time, 1 mM Ca2+eliminates the GABA effect on the “basal” Mg2+-ATPase activity. Competitive blocker of GABAA-receptors bicuculline (5 - 20 μM) in the absence of Ca2+ ions elimi-nates the stimulation of the “basal” Mg2+-ATPase by anions. When 0.25 mM Ca2+ is added to the in-cubation medium the inhibitory bicuculline effect on the enzyme does not appear. We found that 0.1 mM o-vanadate (protein tyrosine phosphatase blocker) reduces the GABA-activated ATPase activity. At the same time, 0.1 mM genistein (a protein tyrosine kinase blocker) has no effect on enzyme activity. In the presence of Ca2+ (0.25 mM), the effect of o-vanadate on the “basal” and CI-, HCO3-, -ATPase activities does not appear. It is shown for the first time that high concentrations of Ca2+prevent the action of GABAA-ergic ligands on the study ATPase. It is assumed that there is the involvement of protein kinases and protein phosphatases in the modulation of the enzyme activity by calcium. The observed effect of calcium on the ATPase may play an important role in the study of the mechanisms of epileptogenesis and seizure activity.
The work is a study of the influence of Ca2+ (0.01 - 1 mM) on neuronal CI-, HCO3-, -ATPase complex: an enzyme that is a CI--pump which is functionally and structurally coupled to GABAA-receptors. It is found that influence of Ca2+ on the multifunctional complex starts at concentration of 50·M and at concentration of 0.1 mM, it reduces the “basal” one and increases the CI-, HCO3-, -stimulated Mg2+-ATPase activities. GABA (0.1 - 100μM) activates the “basal” Mg2+-ATPase activity in the ab-sence of calcium. The effect of GABA on the enzyme in the presence of 0.01 ·M Ca2+ does not change. At the same time, 1 mM Ca2+eliminates the GABA effect on the “basal” Mg2+-ATPase activity. Competitive blocker of GABAA-receptors bicuculline (5 - 20 μM) in the absence of Ca2+ ions elimi-nates the stimulation of the “basal” Mg2+-ATPase by anions. When 0.25 mM Ca2+ is added to the in-cubation medium the inhibitory bicuculline effect on the enzyme does not appear. We found that 0.1 mM o-vanadate (protein tyrosine phosphatase blocker) reduces the GABA-activated ATPase activity. At the same time, 0.1 mM genistein (a protein tyrosine kinase blocker) has no effect on enzyme activity. In the presence of Ca2+ (0.25 mM), the effect of o-vanadate on the “basal” and CI-, HCO3-, -ATPase activities does not appear. It is shown for the first time that high concentrations of Ca2+prevent the action of GABAA-ergic ligands on the study ATPase. It is assumed that there is the involvement of protein kinases and protein phosphatases in the modulation of the enzyme activity by calcium. The observed effect of calcium on the ATPase may play an important role in the study of the mechanisms of epileptogenesis and seizure activity.
KEYWORDS
Mg2+-ATPase, Chloride, Bicarbonate, Calcium, Rat Brain Plasma Membranes, GABAA-Ergic Drugs, o-Vanadate, Genistein
Mg2+-ATPase, Chloride, Bicarbonate, Calcium, Rat Brain Plasma Membranes, GABAA-Ergic Drugs, o-Vanadate, Genistein
Cite this paper
Menzikov, S. and Kalinina, M. (2014) Effects of Calcium on the GABAA-Coupled CI-/HCO3- -ATPase from Plasma Membrane of Rat Brain. Advances in Enzyme Research, 2, 82-91. doi: 10.4236/aer.2014.22009.
Menzikov, S. and Kalinina, M. (2014) Effects of Calcium on the GABAA-Coupled CI-/HCO3- -ATPase from Plasma Membrane of Rat Brain. Advances in Enzyme Research, 2, 82-91. doi: 10.4236/aer.2014.22009.
References
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http://dx.doi.org/10.1017/S146479310200605X [2] Inagaki, C., Hara, M. and Zeng, X.T. (1996) A Cl--Pump in Rat-Brain Neurons. Journal of Experimental Zoology, 275, 262-268. [3] Menzikov, S.A. and Menzikova, O.V. (2007) Comparative Properties of Sensitive to GABAA-Ergic Ligands, Cl-, HCO3--Activated Mg2+-ATPase from Brain Plasma Membranes of Fish and Rats. Zhurnal Evoliutsionnoi Biokhimii Fiziologii, 43, 246-253. [4] Bormann, J., Hamill, O.P. and Sakmann, B. (1987) Mechanism of Anion Permeation through Channels Gated by Glycine and Gamma-Aminobutyric Acid in Mouse Cultured Spinal Neurones. Journal of Physiology (London), 385, 243- 286. [5] Menzikov, S.A., Ruzhinskaia, N.N. and Menzikova, O.V. (2000) Mg2+ -ATPase in the Fish Brain and Its Ultrastructural Localization. Zhurnal Evoliutsionnoi Biokhimii Fiziologii, 36, 263-267. [6] Menzikov, S.A., Karpova, M.N. and Kalinina, M.V. (2011) Effect of HCO3- Ions on the ATP-Dependent GABAA Receptor-Coupled Cl- Channel in Rat Brain Plasma Membranes. Bulletin of Experimental Biology and Medicine, 152, 38-42.
http://dx.doi.org/10.1007/s10517-011-1448-z [7] Menzikov, S.A. and Menzikova, O.V. (2006) Phosphorylation of Cl-, HCO3--Stimulated Mg2+ -ATPase of Plasma Membranes of Carp (Cyprinus carpio L.) Brain Sensitive to GABAA-Ergic Ligands. Ukrainskii Biokhimicheskii Zhurnal, 78, 63-69. [8] Menzikov, S.A., Karpova, M.N. and Kalinina, M.V. (2012) Effect of Pentylenetetrazole on the GABAA-Coupled Cl-, HCO3--Activated Mg2+ -ATPase Activity of the Plasma Membrane from Rat Brain Both in Vitro and in Vivo Experiences. Pathological Physiology and Experimental Therapy, 98-102. [9] Walton, N.Y., Nagy, A.K. and Treiman, D.M. (1998) Altered Residual ATP Content in Rat Brain Cortex Subcellular Fractions following Status Epilepticus Induced by Lithium and Pilocarpine. Journal of Molecular Neuroscience, 11, 233-242.
http://dx.doi.org/10.1385/JMN:11:3:233 [10] Palma, E., Ragozzino, D.A., Angelantonio, S., Spinelli, Di G., Trettel, F., Martinez-Torres, A., Torchia, G., Arcella, A., Gennaro, G. Di., Quarato, P.P., Esposito, V., Cantore, G., Miledi, R. and Eusebi, F. (2004) Phosphatase Inhibitors Remove the Run-Down of Gamma-Aminobutyric Acid Type A Receptors in the Human Epileptic Brain. Proceedings of the National Academy of Sciences of the USA, 101, 10183-10188.
http://dx.doi.org/10.1073/pnas.0403683101 [11] Kotova, S.M., Zasedateleva, I.Yu. and Koroleva, N.Yu. (2005) Peculiarities of Mineral Metabolism in Patients with Epilepsy. Journal of Neurology and Psychiatry (Russia), 3, 70-71. [12] Сupello, A., Hyden, H., Rapallino, M.V. and Robello, M. (1998) Regulation by Intracellular Calcium of the Activity of GABAA Receptors in Two Different Types of Neurons. Neural Circuits and Networks NATO ASI Series, 167, 53-69. [13] Chen, Q.X., Stelzer, A., Kay, A.R. and Wong, R.K. (1990) GABAA Receptor Function Is Regulated by Phosphorylation in Acutely Dissociated Guinea-Pig Hippocampal Neurons. The Journal of Physiology, 420, 207-221. [14] Corda, M.G. and Guidotti, A. (1983) Modulation of GABA Receptor Binding by Ca2+. Journal of Neurochemistry, 41, 277-280.
http://dx.doi.org/10.1111/j.1471-4159.1983.tb11840.x [15] Aguayo, L.G., Espinoza, F., Kunos, G. and Satin, L.S. (1998) Effects of Intracellular Calcium on GABAA Receptors in Mouse Cortical Neurons. Pflugers Archiv, 435, 382-387.
http://dx.doi.org/10.1007/s004240050527 [16] Chen, P.S., Toribara, T.Y. and Warner, H. (1990) Microdetermination of Phosphorus. Analytical Chemistry, 28, 1756- 1758.
http://dx.doi.org/10.1021/ac60119a033 [17] Bradford, M.M. (1976) A Rapid and Sensitive Method for the Quantitation of Microgram Quantities of Protein Utilizing the Principal of Protein-Dye Binding. Analytical Biochemistry, 72, 248-254.
http://dx.doi.org/10.1016/0003-2697(76)90527-3 [18] Menzikov, S.A. (2013) Neuronal Multifunctional ATPase. Biophysical Reviews and Letters, 8, 213-227.
http://dx.doi.org/10.1142/S1793048013300065 [19] Yingst, D.R. (1988) Modulation of the Na, K-ATPase by Ca and Intracellular Proteins. Annual Review of Physiology, 50, 291-303.
http://dx.doi.org/10.1146/annurev.ph.50.030188.001451 [20] Powis, D.A. and Wattus, G.D. (1981) The Stimulatory Effect of Calcium on Na, K-ATPase of Nervous Tissue. FEBS Letters, 126, 285-288.
http://dx.doi.org/10.1016/0014-5793(81)80262-1 [21] Tsakiris, S., Koromilas, C. and Schulpis, K.H. (2001) Reduced Mg2+-ATPase Activity in the Hypoglycemic Adult Rat Brain. Zeitschrift fur Naturforschung C-A. Journal of Biosciences, 56, 912-914. [22] Vasic, V., Jovanović, D., Krstić, D., Nikezić, G., Horvat, A., Vujisić, L., et al. (1999) Prevention and Recovery of CuSO4-Induced Inhibition of Na+/K+-ATPase and Mg2+-ATPase in Rat Brain Synaptosomes by EDTA. Toxicology Letters, 110, 95-103.
http://dx.doi.org/10.1016/S0378-4274(99)00144-7 [23] De Koninck, Y. and Mody, I. (1996) The Effects of Raising Intracellular Calcium on Synaptic GABAA Receptor-Channels. Neuropharmacology, 35, 1365-1374.
http://dx.doi.org/10.1016/S0028-3908(96)00063-9 [24] Li, L., Wang, Y., Ma, K.T., Cheng, H.J., Zhao, L. and Si, J.Q. (2013) The Effect of Niflumic Acid and Blocker of Calcium Channel on the Desensitization of Gamma Aminobutyric Acid-Activated Current. Zhongguo Ying Yong Sheng Li Xue Za Zhi, 29, 128-132. [25] Obrietan, K. and van den Pol, A.N. (1995) GABA Neurotransmission in the Hypothalamus: Developmental Reversal from Ca2+ Elevating to Depressing. The Journal of Neuroscience, 7, 5065-5077. [26] Akopian, A., Gabriel, R. and Witkovsky, P. (1998) Calcium Released from Intracellular Stores Inhibits GABAA-Me- diated Currents in Ganglion Cells of the Turtle Retina. Journal of Neurophysiology, 80, 1105-1115. [27] Stelzer, A., Kay, A.R. and Wong, R.K. (1988) GABAA-Receptor Function in Hippocampal Cells Is Maintained by Phosphorylation Factors. Science, 241, 339-341.
http://dx.doi.org/10.1126/science.2455347 [28] Jassar, B.S., Ostashewski, P.M. and Jhamandas, J.H. (1997) GABAA Receptor Modulation by Protein Tyrosine Kinase in the Rat Diagonal Band of Broca. Brain Research, 775, 127-133.
http://dx.doi.org/10.1016/S0006-8993(97)00892-5 [29] Hydén, H., Rapallino, M.V. and Cupello, A. (2000) Unraveling of Important Neurobiological Mechanisms by the Use of Pure, Fully Differentiated Neurons Obtained from Adult Animals. Progress in Neurobiology, 60, 471-499.
http://dx.doi.org/10.1016/S0301-0082(99)00035-0 [30] Simons, T.J. (1988) Calcium and Neuronal Function. Neurosurgical Review, 11, 119-129.
http://dx.doi.org/10.1007/BF01794675 [31] Taleb, O., Trouslard. J., Demeneix, B.A., Feltz, P., Bossu, J.L., Dupont, J.L. and Feltz, A. (1987) Spontaneous and GABA-Evoked Chloride Channels on Pituitary Intermediate Lobe Cells and Their Internal Ca Requirements. Pflügers Archiv, 409, 620-631.
http://dx.doi.org/10.1007/BF00584663 [32] Stelzer, A., and Wong, R.K. (1987) GABA Receptors of Isolated Guinea-Pig Hippocampal Neurons: Intra- and Extra-cellular Regulatory Factors. The Journal of Physiology (London), 394, 115-120. [33] Tapia, J.C., Espinoza, F. and Aguayo, L.G. (1997) Differential Intracellular Regulation of Cortical GABAA and Spinal Glycine Receptors in Cultured Neurons. Brain Research, 769, 203-210.
http://dx.doi.org/10.1016/S0006-8993(97)00672-0 [34] Abashidze, S., Jariashvili, T. and Kometiani, Z. (2001) The Effect of EGTA and Ca++ in Regulation of the Brain Na/K- ATP-ase by Noradrenaline. BMC Biochemistry, 2, 8.
http://dx.doi.org/10.1186/1471-2091-2-8 [35] Menzikov, S.A. and Menzikova, O.V. (2002) Effects of Orthovanadate and Genistein on the Plasma Membrane Cl-- ATPase Sensitive to GABAA-Ergic Ligands in the Bream (Abramis brama L.) Brain. Doklady Biological Sciences, 385, 334-336.
http://dx.doi.org/10.1023/A:1019952515746 [36] Farhat, G., Yamout, B., Mikati, M.A., Demirjian, S., Sawaya, R. and Fuleihan, G.E.H. (2002) Effect of Antiepileptic Drugs on Bone Density in Ambulatory Patients. Neurology, 58, 1348-1353.
http://dx.doi.org/10.1212/WNL.58.9.1348 [37] Cesur, Y., Yuca, S.A., Kaya, A., Yilmaz, C. and Bay, A. (2013) Vitamin D deficiency Rickets in Infants Presenting with Hypocalcaemic Convulsions. West Indian Medical Journal, 62, 201-204.
[1] Gerencser, G.A. and Zhang, J. L. (2003) Chloride ATPase Pumps in Nature: Do They Exist? Biological Reviews, 78, 197-218.
http://dx.doi.org/10.1017/S146479310200605X [2] Inagaki, C., Hara, M. and Zeng, X.T. (1996) A Cl--Pump in Rat-Brain Neurons. Journal of Experimental Zoology, 275, 262-268. [3] Menzikov, S.A. and Menzikova, O.V. (2007) Comparative Properties of Sensitive to GABAA-Ergic Ligands, Cl-, HCO3--Activated Mg2+-ATPase from Brain Plasma Membranes of Fish and Rats. Zhurnal Evoliutsionnoi Biokhimii Fiziologii, 43, 246-253. [4] Bormann, J., Hamill, O.P. and Sakmann, B. (1987) Mechanism of Anion Permeation through Channels Gated by Glycine and Gamma-Aminobutyric Acid in Mouse Cultured Spinal Neurones. Journal of Physiology (London), 385, 243- 286. [5] Menzikov, S.A., Ruzhinskaia, N.N. and Menzikova, O.V. (2000) Mg2+ -ATPase in the Fish Brain and Its Ultrastructural Localization. Zhurnal Evoliutsionnoi Biokhimii Fiziologii, 36, 263-267. [6] Menzikov, S.A., Karpova, M.N. and Kalinina, M.V. (2011) Effect of HCO3- Ions on the ATP-Dependent GABAA Receptor-Coupled Cl- Channel in Rat Brain Plasma Membranes. Bulletin of Experimental Biology and Medicine, 152, 38-42.
http://dx.doi.org/10.1007/s10517-011-1448-z [7] Menzikov, S.A. and Menzikova, O.V. (2006) Phosphorylation of Cl-, HCO3--Stimulated Mg2+ -ATPase of Plasma Membranes of Carp (Cyprinus carpio L.) Brain Sensitive to GABAA-Ergic Ligands. Ukrainskii Biokhimicheskii Zhurnal, 78, 63-69. [8] Menzikov, S.A., Karpova, M.N. and Kalinina, M.V. (2012) Effect of Pentylenetetrazole on the GABAA-Coupled Cl-, HCO3--Activated Mg2+ -ATPase Activity of the Plasma Membrane from Rat Brain Both in Vitro and in Vivo Experiences. Pathological Physiology and Experimental Therapy, 98-102. [9] Walton, N.Y., Nagy, A.K. and Treiman, D.M. (1998) Altered Residual ATP Content in Rat Brain Cortex Subcellular Fractions following Status Epilepticus Induced by Lithium and Pilocarpine. Journal of Molecular Neuroscience, 11, 233-242.
http://dx.doi.org/10.1385/JMN:11:3:233 [10] Palma, E., Ragozzino, D.A., Angelantonio, S., Spinelli, Di G., Trettel, F., Martinez-Torres, A., Torchia, G., Arcella, A., Gennaro, G. Di., Quarato, P.P., Esposito, V., Cantore, G., Miledi, R. and Eusebi, F. (2004) Phosphatase Inhibitors Remove the Run-Down of Gamma-Aminobutyric Acid Type A Receptors in the Human Epileptic Brain. Proceedings of the National Academy of Sciences of the USA, 101, 10183-10188.
http://dx.doi.org/10.1073/pnas.0403683101 [11] Kotova, S.M., Zasedateleva, I.Yu. and Koroleva, N.Yu. (2005) Peculiarities of Mineral Metabolism in Patients with Epilepsy. Journal of Neurology and Psychiatry (Russia), 3, 70-71. [12] Сupello, A., Hyden, H., Rapallino, M.V. and Robello, M. (1998) Regulation by Intracellular Calcium of the Activity of GABAA Receptors in Two Different Types of Neurons. Neural Circuits and Networks NATO ASI Series, 167, 53-69. [13] Chen, Q.X., Stelzer, A., Kay, A.R. and Wong, R.K. (1990) GABAA Receptor Function Is Regulated by Phosphorylation in Acutely Dissociated Guinea-Pig Hippocampal Neurons. The Journal of Physiology, 420, 207-221. [14] Corda, M.G. and Guidotti, A. (1983) Modulation of GABA Receptor Binding by Ca2+. Journal of Neurochemistry, 41, 277-280.
http://dx.doi.org/10.1111/j.1471-4159.1983.tb11840.x [15] Aguayo, L.G., Espinoza, F., Kunos, G. and Satin, L.S. (1998) Effects of Intracellular Calcium on GABAA Receptors in Mouse Cortical Neurons. Pflugers Archiv, 435, 382-387.
http://dx.doi.org/10.1007/s004240050527 [16] Chen, P.S., Toribara, T.Y. and Warner, H. (1990) Microdetermination of Phosphorus. Analytical Chemistry, 28, 1756- 1758.
http://dx.doi.org/10.1021/ac60119a033 [17] Bradford, M.M. (1976) A Rapid and Sensitive Method for the Quantitation of Microgram Quantities of Protein Utilizing the Principal of Protein-Dye Binding. Analytical Biochemistry, 72, 248-254.
http://dx.doi.org/10.1016/0003-2697(76)90527-3 [18] Menzikov, S.A. (2013) Neuronal Multifunctional ATPase. Biophysical Reviews and Letters, 8, 213-227.
http://dx.doi.org/10.1142/S1793048013300065 [19] Yingst, D.R. (1988) Modulation of the Na, K-ATPase by Ca and Intracellular Proteins. Annual Review of Physiology, 50, 291-303.
http://dx.doi.org/10.1146/annurev.ph.50.030188.001451 [20] Powis, D.A. and Wattus, G.D. (1981) The Stimulatory Effect of Calcium on Na, K-ATPase of Nervous Tissue. FEBS Letters, 126, 285-288.
http://dx.doi.org/10.1016/0014-5793(81)80262-1 [21] Tsakiris, S., Koromilas, C. and Schulpis, K.H. (2001) Reduced Mg2+-ATPase Activity in the Hypoglycemic Adult Rat Brain. Zeitschrift fur Naturforschung C-A. Journal of Biosciences, 56, 912-914. [22] Vasic, V., Jovanović, D., Krstić, D., Nikezić, G., Horvat, A., Vujisić, L., et al. (1999) Prevention and Recovery of CuSO4-Induced Inhibition of Na+/K+-ATPase and Mg2+-ATPase in Rat Brain Synaptosomes by EDTA. Toxicology Letters, 110, 95-103.
http://dx.doi.org/10.1016/S0378-4274(99)00144-7 [23] De Koninck, Y. and Mody, I. (1996) The Effects of Raising Intracellular Calcium on Synaptic GABAA Receptor-Channels. Neuropharmacology, 35, 1365-1374.
http://dx.doi.org/10.1016/S0028-3908(96)00063-9 [24] Li, L., Wang, Y., Ma, K.T., Cheng, H.J., Zhao, L. and Si, J.Q. (2013) The Effect of Niflumic Acid and Blocker of Calcium Channel on the Desensitization of Gamma Aminobutyric Acid-Activated Current. Zhongguo Ying Yong Sheng Li Xue Za Zhi, 29, 128-132. [25] Obrietan, K. and van den Pol, A.N. (1995) GABA Neurotransmission in the Hypothalamus: Developmental Reversal from Ca2+ Elevating to Depressing. The Journal of Neuroscience, 7, 5065-5077. [26] Akopian, A., Gabriel, R. and Witkovsky, P. (1998) Calcium Released from Intracellular Stores Inhibits GABAA-Me- diated Currents in Ganglion Cells of the Turtle Retina. Journal of Neurophysiology, 80, 1105-1115. [27] Stelzer, A., Kay, A.R. and Wong, R.K. (1988) GABAA-Receptor Function in Hippocampal Cells Is Maintained by Phosphorylation Factors. Science, 241, 339-341.
http://dx.doi.org/10.1126/science.2455347 [28] Jassar, B.S., Ostashewski, P.M. and Jhamandas, J.H. (1997) GABAA Receptor Modulation by Protein Tyrosine Kinase in the Rat Diagonal Band of Broca. Brain Research, 775, 127-133.
http://dx.doi.org/10.1016/S0006-8993(97)00892-5 [29] Hydén, H., Rapallino, M.V. and Cupello, A. (2000) Unraveling of Important Neurobiological Mechanisms by the Use of Pure, Fully Differentiated Neurons Obtained from Adult Animals. Progress in Neurobiology, 60, 471-499.
http://dx.doi.org/10.1016/S0301-0082(99)00035-0 [30] Simons, T.J. (1988) Calcium and Neuronal Function. Neurosurgical Review, 11, 119-129.
http://dx.doi.org/10.1007/BF01794675 [31] Taleb, O., Trouslard. J., Demeneix, B.A., Feltz, P., Bossu, J.L., Dupont, J.L. and Feltz, A. (1987) Spontaneous and GABA-Evoked Chloride Channels on Pituitary Intermediate Lobe Cells and Their Internal Ca Requirements. Pflügers Archiv, 409, 620-631.
http://dx.doi.org/10.1007/BF00584663 [32] Stelzer, A., and Wong, R.K. (1987) GABA Receptors of Isolated Guinea-Pig Hippocampal Neurons: Intra- and Extra-cellular Regulatory Factors. The Journal of Physiology (London), 394, 115-120. [33] Tapia, J.C., Espinoza, F. and Aguayo, L.G. (1997) Differential Intracellular Regulation of Cortical GABAA and Spinal Glycine Receptors in Cultured Neurons. Brain Research, 769, 203-210.
http://dx.doi.org/10.1016/S0006-8993(97)00672-0 [34] Abashidze, S., Jariashvili, T. and Kometiani, Z. (2001) The Effect of EGTA and Ca++ in Regulation of the Brain Na/K- ATP-ase by Noradrenaline. BMC Biochemistry, 2, 8.
http://dx.doi.org/10.1186/1471-2091-2-8 [35] Menzikov, S.A. and Menzikova, O.V. (2002) Effects of Orthovanadate and Genistein on the Plasma Membrane Cl-- ATPase Sensitive to GABAA-Ergic Ligands in the Bream (Abramis brama L.) Brain. Doklady Biological Sciences, 385, 334-336.
http://dx.doi.org/10.1023/A:1019952515746 [36] Farhat, G., Yamout, B., Mikati, M.A., Demirjian, S., Sawaya, R. and Fuleihan, G.E.H. (2002) Effect of Antiepileptic Drugs on Bone Density in Ambulatory Patients. Neurology, 58, 1348-1353.
http://dx.doi.org/10.1212/WNL.58.9.1348 [37] Cesur, Y., Yuca, S.A., Kaya, A., Yilmaz, C. and Bay, A. (2013) Vitamin D deficiency Rickets in Infants Presenting with Hypocalcaemic Convulsions. West Indian Medical Journal, 62, 201-204.