GABA may act as a self-limiting trophic factor at developing synapses.
Early in development, synapses with glycine or gamma-aminobutyric acid (GABA)-gated chloride channels exhibit the ability to depolarize postsynaptic cells. As the synapses mature and the gradient of chloride ions across the cell membrane is altered, these neurotransmitters signal an inhibitory response, hyperpolarizing the membrane and decreasing neuronal excitability. Kriegstein and Owens discuss how GABA-stimulated up-regulation of the expression of the potassium chloride cotransporter KCC2 may be the mechanism underlying this synaptic switch.
Kriegstein
A R
AR
Department of Neurology and Department of Pathology and at the Center for Neurobiology and Behavior, Columbia College of Physicians and Surgeons, New York, NY, USA. ark17@columbia.edu
Owens
D F
DF
D000818:Animals; D009414:Nerve Growth Factors / Q000502:physiology*; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D009414:Nerve Growth Factors; D005680:gamma-Aminobutyric Acid