Neurochemical Research

, Volume 33, Issue 8, pp 1459–1465 | Cite as

Post-translational Regulation of l-Glutamic Acid Decarboxylase in the Brain

Original Paper

Abstract

Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the central nervous system. GABA is converted from glutamic acid by the action of glutamic acid decarboxylase (GAD). There are two forms of GAD in the brain, GAD65 and GAD67, referring to a molecular weight of 65 and 67 kDa, respectively. Perturbations in GABAergic neurotransmission have been linked to a number of neurological disorders. Since GAD is the rate-limiting enzyme in controlling GABA synthesis, it is important to understand how GAD is regulated in the brain. It is known that GAD function can be regulated at the transcriptional/translational and post-translational levels. This review focuses briefly on the recent advances in revealing the post-translational regulation of GAD function including protein phosphorylation, palmitoylation and activity-dependent cleavage. The results from these studies have improved our understanding of the regulation of GAD function in the brain.

Keywords

Post-translational modification GAD65 GAD67 Phosphorylation Truncated GAD Calpain Palmitoylation 

Abbreviations

CSP

Cysteine string protein

GAD

Glutamic acid decarboxylase

HIP14

Huntingtin interacting protein 14

HSP70

Heat shock protein 70

IDDM

Insulin-dependent diabetes mellitus

PAT

Palmitoyl acyltransferase

PPT

Protein palmitoyl thioesterase

SPS

Stiff person syndrome

SV

Synaptic vesicles

VGAT

Vesicular GABA transporter

Notes

Acknowledgment

This work was supported by the National Institutes of Health (NS37851 to J-Y Wu).

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Copyright information

© Springer Science+Business Media, LLC 2008

Authors and Affiliations

  1. 1.Department of Basic Science, Charles E. Schmidt College of Biomedical ScienceFlorida Atlantic UniversityBoca RatonUSA

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