Eggers Laboratory

What mechanisms create the long timecourse of inhibitory neurotransmitter release in the retina?

 

Previous results (Eggers et al, 2006) showed that the timecourse of GABA and glycine release underlying light-evoked inhibition onto bipolar cells was very slow, relative to the initial light stimulus.  In other systems, prolonged, asynchronous release often results from a large build-up of Ca²⁺ in the presynaptic neuron.  However, as the light-evoked release of GABA and glycine requires transmission through synapses upstream from the amacrine cells, it is possible that this prolonged release is not due to inherent release properties of the amacrine cells.  To test this idea we are directly activating amacrine cell inputs to bipolar cells with electrical stimulation.  This will allow us to test the mechanisms responsible for this slow release. 

How is inhibition differently regulated by rod and cone pathways in the retina?

Visual information is separated into parallel pathways of ON, OFF and rod signaling at the bipolar cell dendrites. Inhibition to bipolar cell axon terminals has also previously been shown to vary between these pathways.  However, as these recordings were made in dark-adapted retinas where rod signals are most active, it is not clear what roles cone pathways vs. rod pathways play in this inhibition.  Previous studies have also suggested that the timecourse of inhibition might match the timecourse of excitation to bipolar cells.  This would suggest that the timecourse of inhibition should change when BCs transition between receiving slow rod-mediated excitation and faster cone-mediated excitation.  To address these questions we are recording light–evoked and spontaneous inhibitory currents to determine how inhibition changes between dark and light adapted rod and cone bipolar cells.