RT Journal Article
SR Electronic
T1 Elucidating the Role of AII Amacrine Cells in Glutamatergic Retinal Waves
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 1675
OP 1686
DO 10.1523/JNEUROSCI.3291-14.2015
VO 35
IS 4
A1 Alana Firl
A1 Jiang-Bin Ke
A1 Lei Zhang
A1 Peter G. Fuerst
A1 Joshua H. Singer
A1 Marla B. Feller
YR 2015
UL http://www.jneurosci.org/content/35/4/1675.abstract
AB 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 α-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 α-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 α-RGCs and anti-correlated with that of OFF α-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.