These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Regulation of excitation by GABA neurotransmission: focus on metabolism and transport.
    Author: Madsen KK, Larsson OM, Schousboe A.
    Journal: Results Probl Cell Differ; 2008; 44():201-21. PubMed ID: 17579816.
    Abstract:
    The vast majority of excitatory synapses in the central nervous system (CNS) utilize glutamate as the neurotransmitter. The level of excitation appears to be under regulatory control by the major inhibitory neurotransmitter GABA, which is synthesized from glutamate by its decarboxylation catalysed by glutamate decarboxylase (GAD). The inactivation of GABA is brought about by high affinity GABA transporters located in the presynaptic GABAergic neurons as well as surrounding astrocytes and subsequently GABA may be metabolized by GABA-transaminase (GABA-T) ultimately allowing the carbon skeleton to enter the tricarboxylic acid (TCA) cycle for oxidative metabolism. In the presynaptic GABAergic neuron, GABA taken up seems, however, preferentially to enter the vesicular GABA pool and hence it is recycled as a transmitter. It has become clear that compounds acting as inhibitors at either the transporters or GABA-T are capable of regulating the inhibitory tonus thus controlling excitation. This has led to development of clinically efficatious antiepileptic drugs. This paper shall review recent progress in targeting these pharmacological entities.
    [Abstract] [Full Text] [Related] [New Search]