Prospects of Using Platelets as Peripheral Marker to Study the Role of GABA in Autism


Literature indicated that platelets could be used as a model for neuronal receptors such as γ-amino butyric acid (GABA) and serotonin. Research work exhibited the presence of low levels of GABA and high levels of serotonin concentration in the platelets of autistic children as compare to their healthy counter parts. There are also other evidences pointing out to the significant role of GABA in autism such as association of g-band frequency with the cortical concentration of GABA and gabapentin (GABA analogue) specifically inhibits the cytosolic branched chain amino transferase (BCATc); an enzyme responsible to modulate glutamate availability for the synthesis of GABA.

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Khan, S. , Fatima-Shad, K. and Ghouse, H. (2014) Prospects of Using Platelets as Peripheral Marker to Study the Role of GABA in Autism. World Journal of Neuroscience, 4, 437-442. doi: 10.4236/wjns.2014.45049.

Conflicts of Interest

The authors declare no conflicts of interest.


[1] Kaneez, F.S. and Saeed, S.A. (2009) Investigating GABA and Its Function in Platelets as Compared to Neurons. Platelets, 20, 328-333.
[2] Shad, K.F. and Saeed, S.A. (2007) The Metabolism of Serotonin in Neuronal Cells in Culture and Platelets. Experimental Brain Research, 183, 411-416.
[3] Rolf, L.H., Haarmann, F.Y., Grotemeyer, K.H. and Kehrer, H. (1993) Serotonin and Amino Acid Content in Platelets of Autistic Children. Acta Psychiatrica Scandinavica, 87, 312-316.
[4] Rojas, D.C., Teale, P.D., Maharajh, K., Kronberg, E., Youngpeter, K., Wilson, L.B. and Hepburn, S. (2011) Transient and Steady-State Auditory Gamma-Band Responses in First-Degree Relatives of People with Autism Spectrum Disorder. Molecular Autism, 2, 11.
[5] Sweatt, A.J., Garcia-Espinosa, M.A., Wallin, R. and Hutson, S.M. (2004) Branched-Chain Amino Acids and Neurotransmitter Metabolism: Expression of Cytosolic Branched-Chain Aminotransferase (BCATc) in the Cerebellum and Hippocampus. Journal of Comparative Neurology, 477, 360-370.
[6] Raymond, G.V., Bauman, M.L. and Kemper, T.L. (1995) Hippocampus in Autism: A Golgi Analysis. Actaneuropathologica, 91, 117-119.
[7] Cserep, C., Szabadits, E., Szonyi, A., Watanabe, M., Freund, T.F. and Nyiri, G. (2012) NMDA Receptors in GABAergic Synapses during Postnatal Development. PloS One, 7, e37753.
[8] Hussman, J.P. (2001) Letters to the Editor: Suppressed GABAergic Inhibition as a Common Factor in Suspected Etiologies of Autism. Journal of autism and developmental disorders, 31, 247-248.
[9] Deutsch, S.I., Urbano, M.R., Neumann, S.A., Burket, J.A. and Katz, E. (2010) Cholinergic Abnormalities in Autism: Is There a Rationale for Selective Nicotinic Agonist Interventions? Clinical Neuropharmacology, 33, 114-120.
[10] Morales, M. and Bloom, F.E. (1997) The 5-HT3 Receptor Is Present in Different Subpopulations of GABAergic Neurons in the Rat Telencephalon. The Journal of Neuroscience, 17, 3157-3167.
[11] Berger, B., Gasper, P. and Verney, C. (1991) Dopaminergic Innervation of the Cerebral Cortex: Unexpected Differences between Rodents and Primates. Trends Neuroscience, 14, 21-27.
[12] Money, K.M. and Stanwood, G.D. (2013) Developmental Origins of Brain Disorders: Roles for Dopamine. Frontiers in Cellular Neuroscience, 7.
[13] Kang, Y., Zhang, X., Dobie, F., Wu, H. and Craig, A.M. (2008) Induction of GAB Aergic Postsynaptic Differentiation by α-Neurexins. Journal of Biological Chemistry, 283, 2323-2334.
[14] Graf, E.R., Zhang, X., Jin, S.X., Linhoff, M.W. and Craig, A.M. (2004) Neurexins Induce Differentiation of GABA and Glutamate Postsynaptic Specializations via Neuroligins. Cell, 119, 1013-1026.
[15] Tabuchi, K., Blundell, J., Etherton, M.R., Hammer, R.E., Liu, X., Powell, C.M. and Südhof, T.C. (2007) A Neuroligin-3 Mutation Implicated in Autism Increases Inhibitory Synaptic Transmission in Mice. Science, 318, 71-76.
[16] García-Cazorla, A., Oyarzabal, A., Fort, J., Robles, C., Castejón, E., Ruiz-Sala, P. and Agulló, S.B. (2014) Two Novel Mutations in the BCKDK (Branched-Chain Keto-Acid Dehydrogenase Kinase) Gene Are Responsible for a Neurobehavioral Deficit in Two Pediatric Unrelated Patients. Human Mutation, 35, 470-477.
[17] Oleskevich, S. and Lacaille, J.C. (1992) Reduction of GABAB Inhibitory Postsynaptic Potentials by Serotonin via Pre-and Postsynaptic Mechanisms in CA3 Pyramidal Cells of Rat Hippocampus in Vitro. Synapse, 12, 173-188.
[18] Fraser, D.D. and MacVicar, B.A. (1991) Low-Threshold Transient Calcium Current in Rat Hippocampal Lacunosum-Moleculare Interneurons: Kinetics and Modulation by Neurotransmitters. The Journal of Neuroscience, 11, 2812-2820.
[19] McMahon, L.L. and Kauer, J.A. (1997) Hippocampal Interneurons Are Excited via Serotonin-Gated Ion Channels. Journal of Neurophysiology, 78, 2493-2502.
[20] Piguet, P. and Galvan, M. (1994) Transient and Long-Lasting Actions of 5-HT on Rat Dentate Gyrus Neurones in Vitro. The Journal of Physiology, 481, 629-639.
[21] Feng, J., Cai, X., Zhao, J. and Yan, Z. (2001) Serotonin Receptors Modulate GABA (A) Receptor Channels through Activation of Anchored Protein Kinase C in Prefrontal Cortical Neurons. Journal of Neuroscience, 21, 6502-6511.
[22] Munsch, T., Freichel, M., Flockerzi, V. and Pape, H.C. (2003) Contribution of Transient Receptor Potential Channels to the Control of GABA Release from Dendrites. Proceedings of the National Academy of Sciences, 100, 16065-16070.
[23] Li, H., Lang, B., Kang, J.F. and Li, Y.Q. (2000) Serotonin Potentiates the Response of Neurons of the Superficial Laminae of the Rat Spinal Dorsal Horn to γ-Aminobutyric Acid. Brain Research Bulletin, 52, 559-565.
[24] Wang, D.S., Xu, T.L. and Li, J.S. (1998) 5-HT Potentiates GABA-and Glycine-Activated Chloride Currents on the Same Neurons in Rat Spinal Cord. Journal fur Hirnforschung, 39, 531-537.
[25] Xu, T.L., Pang, Z.P., Li, J.S. and Akaike, N. (1998) 5-HT Potentiation of the GABAA Response in the Rat Sacral Dorsal Commissural Neurones. British Journal of Pharmacology, 124, 779-787.
[26] Ghaziuddin, M., Ghaziuddin, N. and Greden, J. (2002) Depression in Persons with Autism: Implications for Research and Clinical Care. Journal of Autism and Developmental Disorders, 32, 299-306.
[27] Stewart, M.E., Barnard, L., Pearson, J., Hasan, R. and O’Brien, G. (2006) Presentation of Depression in Autism and Asperger Syndrome: A Review. Autism, 10, 103-116.
[28] Yan, Z. (2002) Regulation of GAB Aergic Inhibition by Serotonin Signaling in Prefrontal Cortex. Molecular Neurobiology, 26, 203-216.

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