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Pathway-dependent modulation by P2-purinoceptors in the mouse retina

Authors


Dr M. Kaneda, as above.
E-mail: mkaneda@a5.keio.jp

Abstract

Adenosine trisphosphate (ATP) activates purinoceptors and acts as a neurotransmitter in the nervous system. In the retina, we previously reported that the immunohistochemical distribution of the subset of P2-purinoceptors differs between the ON and OFF pathways. Here, we investigated whether ATP activates P2-purinoceptors and modulates the physiological function of the mouse retina. We also examined if signal processing by P2-purinoceptors is pathway specific. Results showed that ATP activated both ON- and OFF-cholinergic amacrine cells. However, responses in OFF-cholinergic amacrine cells were greater than those in ON-cholinergic amacrine cells. Pharmacological studies in OFF-cholinergic amacrine cells showed that the response of OFF-cholinergic amacrine cells is mediated P2X2-purinoceptors. Further, ATP increased γ-aminobutyric acid (GABA)ergic inhibitory postsynaptic currents (IPSCs) in OFF- but not ON-cholinergic amacrine cells. The increase in GABAergic IPSCs was mediated by P2-purinoceptors. P2-purinoceptor-mediated signals suppressed OFF ganglion cells but activated ON ganglion cells. Our findings indicate that ATP physiologically modulates signal processing of the ON and OFF pathways in a pathway-specific manner through P2-purinoceptors.

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