Our laboratory has characterized bidirectional signalling between neurons and glial cells in the mammalian retina. We find that light-evoked neuronal activity elicits Ca2+ increases in Müller cells, specialized glial cells of the retina. A flickering light stimulus evokes an increase in the occurrence of Ca2+ transients in Müller cells. Addition of adenosine greatly potentiates this light-evoked Ca2+ response. The purinergic antagonist suramin and the ATP hydrolysing enzyme apyrase block the glial Ca2+ response, indicating that neuron to glia signalling in the retina is mediated by ATP release from neurons and activation of glial purinergic receptors. Glia to neuron signalling has also been observed. Müller cell stimulation can evoke a hyperpolarization in neighbouring ganglion cells lasting tens of seconds. The hyperpolarization is blocked by the A1 adenosine receptor antagonist DPCPX and is reduced by ecto-ATPase and ectonucleotidase inhibitors, indicating that the hyperpolarization is mediated by glial release of ATP which is converted to adenosine by ecto-enzymes, leading to the activation of neuronal adenosine receptors. The existence of bidirectional purinergic signalling between neurons and glia suggests that glial cells participate in information processing in the retina.
- Bidirectional signalling between neurons
- Glia-neuron interactions in retina
- Glial to neuron signalling
- Light-evoked glial responses
- Neuron to glia signalling