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The Journal of Neuroscience, April 30, 2008, 28(18):4777-4784; doi:10.1523/JNEUROSCI.4873-07.2008

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Development/Plasticity/Repair
Embryonically Expressed GABA and Glutamate Drive Electrical Activity Regulating Neurotransmitter Specification

Cory M. Root, Norma A. Velázquez-Ulloa, Gabriela C. Monsalve, Elena Minakova, and Nicholas C. Spitzer

Neurobiology Section, Division of Biological Sciences and Center for Molecular Genetics, Kavli Institute for Brain and Mind, University of California, San Diego, La Jolla, California 92093-0357

Correspondence should be addressed to Nicholas C. Spitzer at the above address. Email: nspitzer{at}ucsd.edu

Neurotransmitter signaling in the mature nervous system is well understood, but the functions of transmitters in the immature nervous system are less clear. Although transmitters released during embryogenesis regulate neuronal proliferation and migration, little is known about their role in regulating early neuronal differentiation. Here, we show that GABA and glutamate drive calcium-dependent embryonic electrical activity that regulates transmitter specification. The number of neurons expressing different transmitters changes when GABA or glutamate signaling is blocked chronically, either using morpholinos to knock down transmitter-synthetic enzymes or applying pharmacological receptor antagonists during a sensitive period of development. We find that calcium spikes are triggered by metabotropic GABA and glutamate receptors, which engage protein kinases A and C. The results reveal a novel role for embryonically expressed neurotransmitters.

Key words: GABA; glutamate; metabotropic receptors; calcium spikes; sensitive period; transmitter specification

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Received Oct. 27, 2007; revised Feb. 21, 2008; accepted March 26, 2008.

Correspondence should be addressed to Nicholas C. Spitzer at the above address. Email: nspitzer{at}ucsd.edu

This article has been cited by other articles:

				L. W. Chang and N. C. Spitzer Spontaneous Calcium Spike Activity in Embryonic Spinal Neurons Is Regulated by Developmental Expression of the Na+, K+-ATPase {beta}3 Subunit J. Neurosci., June 17, 2009; 29(24): 7877 - 7885. [Abstract] [Full Text] [PDF]

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