Physiological and pharmacological basis of GABA and glycine action on neurons of mudpuppy retina. II. Amacrine and ganglion cells

Intracellular recordings were obtained from amacrine and ganglion cells in the perfused retina-eyecup preparation of the mudpuppy. γ-Aminobutyric acid (GABA) and glycine (Gly) were added to the bathing medium and the GABA/Gly antagonists strychnine (Strych), picrotoxin (Picro), and bicuculline methiodide (BCC) were also applied. GABA/Gly caused a large decrease in input resistance (IR) in both amacrine and ganglion cells. The decreased IR was often more than 100 MΩ and constituted a large fraction of the input resistance of the cell. The GABA/Gly-mediated change in IR was not associated with a shift in membrane potential in amacrines, but caused a hyperpolarization in ganglion cells. GABA/Gly action on amacrine and ganglion cells was inverted to a depolarization by intracellular injections of Cl^- using KCl-filled micropipettes. This suggests that chloride is involved in mediating GABA/Gly action in both amacrine and ganglion cells. A comparison of selective GABA versus Gly sensitivity of ganglion cells showed a small population of on cells that were exclusively GABA sensitive and a small population of off cells that were exclusively Gly sensitive. The majority of amacrine and ganglion cells showed high sensitivity to both amino acids, though not always in equal proportion. All light responses of amacrine and ganglion cells were enhanced by Picro, BCC, and Strych associated with an increase in IR. These observations are consistent with the idea that in the inner retina GABA and Gly may be continuously (dark) released, and light-evoked inhibitory phenomena are superimposed on a tonic-release mechanism.