%0 Journal Article
%T Elucidating the Role of AII Amacrine Cells in Glutamatergic Retinal Waves
%A Alana Firl
%A Jiang-Bin Ke
%A Joshua H. Singer
%A Lei Zhang
%A Marla B. Feller
%A Peter G. Fuerst
%J The Journal of Neurosience
%D 2015
%R 10.1523/JNEUROSCI.3291-14.2015
%X Spontaneous retinal activity mediated by glutamatergic neurotransmission¡ªso-called ¡°Stage 3¡± retinal waves¡ªdrives 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 ¦Á-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 ¦Á-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 ¦Á-RGCs and anti-correlated with that of OFF ¦Á-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 I h, 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
%U http://www.jneurosci.org/content/35/4/1675