The effect of retinal GABA Depletion by Allylglycine on mouse retinal ganglion cell responses to light
Résumé
The inhibitory neurotransmitter GABA (γ-aminobutyric acid) is metabolized by glutamic acid decarboxylase (GAD) which exists in two iso-
forms in the mature CNS, GAD65 and GAD67. Allylglycine, a glycine derivative, is a nonspecific inhibitor of both GAD isoforms. Prolonged
exposure to allylgycine can therefore deplete the tissue of endogenous GABA over time (Orlowski et al, 1977; Chabrol et al., 2012). Here
we applied Allylglycine (ALLYL) in vitro over several hours to gradually deplete GABA in the adult mouse retina and compared the effects
of GABA depletion on retinal ganglion cells (RGCs) receptive fields with those obtained by simultaneously blocking all GABAergic recep-
tors (type A, B and C).
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