| First Author | Firl A | Year | 2015 |
| Journal | J Neurosci | Volume | 35 |
| Issue | 4 | Pages | 1675-86 |
| PubMed ID | 25632142 | Mgi Jnum | J:253661 |
| Mgi Id | MGI:6100883 | Doi | 10.1523/JNEUROSCI.3291-14.2015 |
| Citation | Firl A, et al. (2015) Elucidating the role of AII amacrine cells in glutamatergic retinal waves. J Neurosci 35(4):1675-86 |
| abstractText | Spontaneous retinal activity mediated by glutamatergic neurotransmission-so-called "Stage 3" retinal waves-drives anti-correlated spiking in ON and OFF RGCs during the second week of postnatal development of the mouse. In the mature retina, the activity of a retinal interneuron called the AII amacrine cell is responsible for anti-correlated spiking in ON and OFF alpha-RGCs. In mature AIIs, membrane hyperpolarization elicits bursting behavior. Here, we postulated that bursting in AIIs underlies the initiation of glutamatergic retinal waves. We tested this hypothesis by using two-photon calcium imaging of spontaneous activity in populations of retinal neurons and by making whole-cell recordings from individual AIIs and alpha-RGCs in in vitro preparations of mouse retina. We found that AIIs participated in retinal waves, and that their activity was correlated with that of ON alpha-RGCs and anti-correlated with that of OFF alpha-RGCs. Though immature AIIs lacked the complement of membrane conductances necessary to generate bursting, pharmacological activation of the M-current, a conductance that modulates bursting in mature AIIs, blocked retinal wave generation. Interestingly, blockade of the pacemaker conductance Ih, a conductance absent in AIIs but present in both ON and OFF cone bipolar cells, caused a dramatic loss of spatial coherence of spontaneous activity. We conclude that during glutamatergic waves, AIIs act to coordinate and propagate activity generated by BCs rather than to initiate spontaneous activity. |
