19.9C) corresponds with the observation that GABA is taken up by amacrine and Müller cells in the inner retina but exclusively by Müller cells in the outer retina. The subcellular distribution of the GABA transporter currents ( Fig. Other transporters, e.g., for GABA, are also electrogenic ( Figs. The driving force for the transport is the electrochemical sodium gradient across the plasma membrane generated by the Na +, K +-ATPase. 49 Sodium-dependent carriers allow uphill transport of substrates into the cells against a concentration gradient. 19.9A) a very negative membrane potential is essential for the efficient uptake of glutamate. The amplitude of the glutamate transporter currents is voltage-dependent ( Fig. 19.9A–B, E, G) and cellular depolarization. 48 The transport of an excess of sodium into the cell generates an inward current ( Figs. 46,47 EAATs mediate a cotransport of three sodium ions and one proton, and the countertransport of one potassium ion, with each glutamate anion. 44,45 In addition, EAAT2 (GLT1) and EAAT3 were found in human Müller cells. The major glutamate uptake carrier of Müller cells is the glutamate-aspartate transporter (GLAST, or excitatory amino acid transporter-1, EAAT1). By the uptake of neurotransmitters, Müller cells are involved in the regulation of the synaptic activity in the inner retina. Müller cells possess uptake and exchange systems for various neurotransmitters, including glutamate and GABA ( Fig. In the neuroretina, photoreceptor cells, neurons, and glial cells express high-affinity transporters for neurotransmitters. Precise “shaping” (i.e., control in time and space) of synaptic activity depends on the kinetics of the presynaptic neurotransmitter release and the reuptake of transmitter molecules into the cells. Schachat MD, in Ryan's Retina, 2018 Regulation of Synaptic Activity by Neurotransmitter Uptake