GABA and glycine in the developing brain

GABA and glycine are major inhibitory neurotransmitters in the CNS and act on receptors coupled to chloride channels. During early developmental periods, both GABA and glycine depolarize membrane potentials due to the relatively high intracellular Cl− concentration. Therefore, they can act as excitatory neurotransmitters. GABA and glycine are involved in spontaneous neural network activities in the immature CNS such as giant depolarizing potentials (GDPs) in neonatal hippocampal neurons, which are generated by the synchronous activity of GABAergic interneurons and glutamatergic principal neurons. GDPs and GDP-like activities in the developing brains are thought to be important for the activity-dependent functiogenesis through Ca2+ influx and/or other intracellular signaling pathways activated by depolarization or stimulation of metabotropic receptors. However, if GABA and glycine do not shift from excitatory to inhibitory neurotransmitters at the birth and in maturation, it may result in neural disorders including autism spectrum disorders.

[1]  Y. Ben-Ari,et al.  Giant synaptic potentials in immature rat CA3 hippocampal neurones. , 1989, The Journal of physiology.

[2]  D. Richter,et al.  Inactivation of the Glycine Transporter 1 Gene Discloses Vital Role of Glial Glycine Uptake in Glycinergic Inhibition , 2003, Neuron.

[3]  Hiroki Toyoda,et al.  Cl− uptake promoting depolarizing GABA actions in immature rat neocortical neurones is mediated by NKCC1 , 2004, The Journal of physiology.

[4]  Molly V. Lucas,et al.  Oxytocin enhances brain function in children with autism , 2013, Proceedings of the National Academy of Sciences.

[5]  Xavier Leinekugel,et al.  Giant Depolarizing Potentials: the Septal Pole of the Hippocampus Paces the Activity of the Developing Intact Septohippocampal ComplexIn Vitro , 1998, The Journal of Neuroscience.

[6]  E. Cherubini,et al.  GABA-mediated giant depolarizing potentials as coincidence detectors for enhancing synaptic efficacy in the developing hippocampus. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[7]  Adam J Pawson,et al.  The Concise Guide to Pharmacology 2013/14: Ligand-Gated Ion Channels , 2013, British journal of pharmacology.

[8]  H. Betz Glycine receptors: heterogeneous and widespread in the mammalian brain , 1991, Trends in Neurosciences.

[9]  E. Cherubini,et al.  Role of giant depolarizing potentials in shaping synaptic currents in the developing hippocampus. , 2006, Critical reviews in neurobiology.

[10]  R. Khazipov,et al.  Maternal Oxytocin Triggers a Transient Inhibitory Switch in GABA Signaling in the Fetal Brain During Delivery , 2006, Science.

[11]  T. Smart,et al.  GABA Potency at GABAA Receptors Found in Synaptic and Extrasynaptic Zones , 2012, Front. Cell. Neurosci..

[12]  Amene Shahrokhi,et al.  Oxytocin-Mediated GABA Inhibition During Delivery Attenuates Autism Pathogenesis in Rodent Offspring , 2014, Science.

[13]  H. Luhmann,et al.  Activation of glycine receptors modulates spontaneous epileptiform activity in the immature rat hippocampus , 2014, The Journal of physiology.

[14]  E. Cherubini,et al.  Developmental Changes in Spontaneous GABAA‐mediated Synaptic Events in Rat Hippocampal CA3 Neurons , 1994, The European journal of neuroscience.

[15]  L. Nguyen,et al.  Glycine receptors and brain development , 2013, Front. Cell. Neurosci..

[16]  E. Cherubini,et al.  In the developing rat hippocampus a tonic GABAA‐mediated conductance selectively enhances the glutamatergic drive of principal cells , 2007, The Journal of physiology.

[17]  Urs Gerber,et al.  β‐Alanine and taurine as endogenous agonists at glycine receptors in rat hippocampus in vitro , 2002 .

[18]  J. A. Payne,et al.  The K+/Cl− co-transporter KCC2 renders GABA hyperpolarizing during neuronal maturation , 1999, Nature.

[19]  Y. Ben-Ari,et al.  GABA: an excitatory transmitter in early postnatal life , 1991, Trends in Neurosciences.

[20]  Y. Ben-Ari,et al.  A randomised controlled trial of bumetanide in the treatment of autism in children , 2012, Translational Psychiatry.

[21]  A. Konnerth,et al.  Long-term potentiation and functional synapse induction in developing hippocampus , 1996, Nature.

[22]  H. Yamasue,et al.  Clinical and neural effects of six-week administration of oxytocin on core symptoms of autism. , 2015, Brain : a journal of neurology.

[23]  K. Obata,et al.  Excitatory and inhibitory actions of GABA and glycine on embryonic chick spinal neurons in culture , 1978, Brain Research.

[24]  L. M. Prida,et al.  Heterogeneous populations of cells mediate spontaneous synchronous bursting in the developing hippocampus through a frequency-dependent mechanism , 2000, Neuroscience.

[25]  R. Khazipov,et al.  GABA: a pioneer transmitter that excites immature neurons and generates primitive oscillations. , 2007, Physiological reviews.

[26]  G. Buzsáki,et al.  Correlated Bursts of Activity in the Neonatal Hippocampus in Vivo , 2002, Science.

[27]  A. VanDongen,et al.  Activation Mechanisms of the NMDA Receptor , 2009 .

[28]  E. Cherubini,et al.  Strychnine‐sensitive glycine responses of neonatal rat hippocampal neurones. , 1991, The Journal of physiology.

[29]  Evdokia Anagnostou,et al.  Oxytocin Increases Retention of Social Cognition in Autism , 2007, Biological Psychiatry.

[30]  Mari A. Virtanen,et al.  Glycine Transporter-1 Controls Nonsynaptic Inhibitory Actions of Glycine Receptors in the Neonatal Rat Hippocampus , 2014, The Journal of Neuroscience.

[31]  S. Gasparini,et al.  Silent synapses in the developing hippocampus: lack of functional AMPA receptors or low probability of glutamate release? , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[32]  K. Obata Transmitter sensitivities of some nerve and muscle cells in culture. , 1974, Brain research.

[33]  E. Cherubini,et al.  Glutamate controls the induction of GABA-mediated giant depolarizing potentials through AMPA receptors in neonatal rat hippocampal slices. , 1999, Journal of neurophysiology.

[34]  J. Gaiarsa,et al.  The allosteric glycine site of the N-methyl-D-aspartate receptor modulates GABAergic-mediated synaptic events in neonatal rat CA3 hippocampal neurons. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[35]  Thoralf Opitz,et al.  Synchronous Oscillatory Activity in Immature Cortical Network Is Driven by GABAergic Preplate Neurons , 2001, The Journal of Neuroscience.

[36]  E. Cherubini,et al.  The Depolarizing Action of GABA Controls Early Network Activity in the Developing Hippocampus , 2011, Molecular Neurobiology.

[37]  Y. Ben-Ari,et al.  Modulation of GABA‐mediated Synaptic Potentials by Glutamatergic Agonists in Neonatal CA3 Rat Hippocampal Neurons , 1991, The European journal of neuroscience.

[38]  H. Matsuzaki,et al.  Developmental changes in KCC1, KCC2, and NKCC1 mRNA expressions in the rat brain. , 2002, Brain research. Developmental brain research.

[39]  Heiko J. Luhmann,et al.  Refuting the challenges of the developmental shift of polarity of GABA actions: GABA more exciting than ever! , 2012, Front. Cell. Neurosci..

[40]  E. Cherubini,et al.  Spontaneous recurrent network activity in organotypic rat hippocampal slices , 2005, The European journal of neuroscience.

[41]  P. Bregestovski,et al.  Excitatory GABA: How a Correct Observation May Turn Out to be an Experimental Artifact , 2012, Front. Pharmacol..

[42]  J. A. Payne,et al.  Cation-chloride cotransporters in neuronal development, plasticity and disease , 2014, Nature Reviews Neuroscience.

[43]  Christian Rosenmund,et al.  Synapses as Therapeutic Targets for Autism Spectrum Disorders: An International Symposium Held in Pavia on July 4th, 2014 , 2014, Front. Cell. Neurosci..