Functional properties of GABA receptors of AII amacrine cells of the rat retina.

Amacrine cells are a highly diverse group of inhibitory retinal interneurons that sculpt the responses of bipolar cells, ganglion cells, and other amacrine cells. They integrate excitatory inputs from bipolar cells and inhibitory inputs from other amacrine cells, but for most amacrine cells, little is known about the specificity and functional properties of their inhibitory inputs. Here, we have investigated GABA receptors of the AII amacrine, a critical neuron in the rod pathway microcircuit, using patch-clamp recording in rat retinal slices.

Inhibitory inputs to an inhibitory interneuron: Spontaneous postsynaptic currents and GABA receptors of A17 amacrine cells in the rat retina.

Amacrine cells constitute a large and heterogeneous group of inhibitory interneurons in the retina. The A17 amacrine plays an important role for visual signalling in the rod pathway microcircuit of the mammalian retina. It receives excitatory input from rod bipolar cells and provides feedback inhibition to the same cells.

Different glutamate sources and endogenous co-agonists activate extrasynaptic NMDA receptors on amacrine cells of the rod pathway microcircuit.

The NMDA receptors (NMDARs) expressed by AII and A17 amacrine cells, the two main inhibitory interneurons of the rod pathway microcircuit in the mammalian retina, are exclusively extrasynaptic, activated by ambient levels of glutamate, and molecularly distinct, with AII and A17 amacrines expressing GluN2B- and GluN2A-containing receptors, respectively. This important sensory microcircuit thus provides a unique model to study the activation and function of extrasynaptic NMDARs. Here, we investigated the sources of glutamate and the endogenous co-agonists (d-serine or glycine) that activate these distinct populations of NMDARs.

Excitability is increased in hippocampal CA1 pyramidal cells of Fmr1 knockout mice.

Fragile X syndrome (FXS) is caused by a failure of neuronal cells to express the gene encoding the fragile mental retardation protein (FMRP). Clinical features of the syndrome include intellectual disability, learning impairment, hyperactivity, seizures and anxiety. Fmr1 knockout (KO) mice do not express FMRP and, as a result, reproduce some FXS behavioral abnormalities.