Inhibitory glycine receptors (GlyRs) are mainly expressed in the spinal cord and in the midbrain, where they control motor and sensory pathways. We describe here a fast potentiation of GlyR by intracellular Ca2+. This phenomenon was observed in rat spinal cord neurons and in transfected human cell lines. Potentiation develops in <100 ms, is proportional to Ca2+ influx, and is characterized by an increase in GlyR apparent affinity for glycine. Phosphorylation and G protein pathways appear not to be involved in the potentiation mechanism. Single-channel recordings in cell-attached and excised patches, as well as whole-cell data suggest the presence of a diffusible cytoplasmic factor that modulates the GlyR channel gating properties. Ca2+-induced potentiation may be important for rapid modulation of glycinergic synapses.
Fast potentiation of glycine receptor channels by intracellular calcium in neurons and transfected cells / Fucile, Sergio; DE SAINT JAN, D; PRADO DE CARVALHO, L; Bregestovski, P.. - In: NEURON. - ISSN 0896-6273. - 28:(2000), pp. 571-583. [10.1016/S0896-6273(00)00134-3]
Fast potentiation of glycine receptor channels by intracellular calcium in neurons and transfected cells
FUCILE, Sergio;
2000
Abstract
Inhibitory glycine receptors (GlyRs) are mainly expressed in the spinal cord and in the midbrain, where they control motor and sensory pathways. We describe here a fast potentiation of GlyR by intracellular Ca2+. This phenomenon was observed in rat spinal cord neurons and in transfected human cell lines. Potentiation develops in <100 ms, is proportional to Ca2+ influx, and is characterized by an increase in GlyR apparent affinity for glycine. Phosphorylation and G protein pathways appear not to be involved in the potentiation mechanism. Single-channel recordings in cell-attached and excised patches, as well as whole-cell data suggest the presence of a diffusible cytoplasmic factor that modulates the GlyR channel gating properties. Ca2+-induced potentiation may be important for rapid modulation of glycinergic synapses.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
