The effect of GABA and the GABA-uptake-blocker NO-711 on the b-wave of the ERG and the responses of horizontal cells to light

Abstract

An increase in the extracellular GABA concentration decreases the b-wave; an impairment of the function of ACs increases the b-wave. These conditions are discussed in the context of the lack of consistent changes to the b-wave during therapy with vigabatrin.

A Ni2+-sensitive component of the ERG b-wave from the isolated bovine retina is related to E-type voltage-gated Ca2+ channels

“…A stimulation of the b-wave amplitude was found using the GABA-uptake blocker NO-711 [12]. GABAergic horizontal or amacrine cells modulate the b-wave amplitude through on-bipolar cells indicating that the release of GABA is partially reduced when triggering of GABA release by E/Rtype Ca 2+ channels is blocked by Ca 2+ channel antagonists.…”

Propofol modulates inner retina function in Beagles

“…Our findings could be a reflection of such GABA A receptor behavior. Recently, b‐wave increase in rabbits was achieved by using the GABA‐uptake blocker NO711 to block the influence of AI amacrine cells on the axon terminal of rod bipolar cells 41 …”

Modelling the topography of absolute defects in patients exposed to the anti-epileptic drug vigabatrin and in normal subjects using automated static suprathreshold perimetry of the entire 80° visual field

“…The topography of the visual field itself results from the regional asymmetries in the slopes of the density of the various retinal cells with increasing eccentricity [39][40][41][42]. It is also possible, therefore, that the toxic effect resulting directly from vigabatrin, or from the increased GABA level secondary to vigabatrin, or from a combination of both, becomes manifest only in regions where the population of the affected cell type [42][43][44][45] reaches a critical lower limit. However, the pathophysiology of vigabatrin-induced retinal damage is unknown.…”