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Glycine Receptors and Glycinergic Synaptic Input at the Axon Terminals of Mammalian Retinal Rod Bipolar Cells
Author(s) -
Cui Jinjuan,
Ma YuPing,
Lipton Stuart A.,
Pan ZhuoHua
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2003.052092
Subject(s) - glycine receptor , axon , strychnine , biophysics , glycine , inhibitory postsynaptic potential , neuroscience , inner plexiform layer , reversal potential , chemistry , axon hillock , patch clamp , biology , retina , electrophysiology , biochemistry , amino acid
We investigated the properties of glycine receptors and glycinergic synaptic inputs at the axon terminals of rod bipolar cells (RBCs) in rats by patch‐clamp recording. Glycine currents recorded from isolated axon terminals were larger than those from isolated somata/dendrites; this was confirmed by puffing glycine onto these two regions in retinal slices. The current density at terminal endings was more than one order of magnitude higher than the density at somatic/dendritic regions. Glycine currents from isolated terminals and isolated somata/dendrites showed similar sensitivity to picrotoxinin blockade. Single‐channel opening recorded from isolated terminals and somata/dendrites displayed a similar main‐state conductance of ≈46 pS. Application of glycine effectively suppressed depolarization‐evoked increases in intracellular Ca 2+ at the terminals. In the presence of GABA A and GABA C antagonists, strychnine‐sensitive chloride currents were evoked in RBCs in retinal slices by puffing kainate onto the inner plexiform layer. No such currents were observed if the recorded RBCs did not retain axon terminals or if Ca 2+ was replaced by Co 2+ in the extracellular solution. The currents displayed discrete miniature‐like events, which were partially blocked by tetrodotoxin. Consistent with early studies in the rabbit and mouse, this study demonstrates that glycine receptors are highly concentrated at the axon terminals of rat RBCs. The pharmacological and physiological properties of glycine receptors located in the axon terminal and somatic/dendritic regions, however, appear to be the same. This study provides evidence for the existence of functional glycinergic synaptic input at the axon terminals of RBCs, suggesting that glycine receptors may play a role in modulating bipolar cell synaptic transmission.