Abstract
Sensory deafferentation resulting from the loss of photoreceptors during retinal degeneration (rd) is often accompanied by a paradoxical increase in spontaneous activity throughout the visual system. Oscillatory discharges are apparent in retinal ganglion cells in several rodent models of rd, indicating that spontaneous activity can originate in the retina. Understanding the biophysical mechanisms underlying spontaneous retinal activity is interesting for two main reasons. First, it could lead to strategies that reduce spontaneous retinal activity, which could improve the performance of vision restoration strategies that aim to stimulate remnant retinal circuits in blind patients. Second, studying emergent network activity could offer general insights into how sensory systems remodel upon deafferentation. Here we provide an overview of the work describing spontaneous activity in the degenerating retina, and outline the current state of knowledge regarding the cellular and biophysical properties underlying spontaneous neural activity.
Highlights
Oscillatory discharges are apparent in retinal ganglion cells in several rodent models of rd, indicating that spontaneous activity can originate in the retina
Blocking inhibition was found to increase spontaneous ganglion cell activity, suggesting that spontaneous ganglion cell spiking is primarily driven by excitatory input from presynaptic bipolar cells (Borowska et al, 2011; Menzler and Zeck, 2011). This issue was not clear cut as some spontaneous inhibitory inputs to ganglion cells persisted in the presence of glutamate receptor blockers (Borowska et al, 2011; Menzler and Zeck, 2011). While these inhibitory inputs alone were ineffective in driving significant rhythmic output from retinal ganglion cells (Menzler and Zeck, 2011), these findings suggested that an upstream element was active in the absence of glutamatergic signaling
Consistent with AII amacrine and ON cone bipolar cells being gap junction coupled in rd retinae, strongly modulating the membrane potential does not abolish spontaneous membrane oscillations (Borowska et al, 2011) and gap junction blockers significantly increase input resistance
Summary
Reviewed by: Rafael Linden, Federal University of Rio de Janeiro, Brazil Botir T. Sensory deafferentation resulting from the loss of photoreceptors during retinal degeneration (rd) is often accompanied by a paradoxical increase in spontaneous activity throughout the visual system. Oscillatory discharges are apparent in retinal ganglion cells in several rodent models of rd, indicating that spontaneous activity can originate in the retina. Understanding the biophysical mechanisms underlying spontaneous retinal activity is interesting for two main reasons. It could lead to strategies that reduce spontaneous retinal activity, which could improve the performance of vision restoration strategies that aim to stimulate remnant retinal circuits in blind patients. Studying emergent network activity could offer general insights into how sensory systems remodel upon deafferentation. We provide an overview of the work describing spontaneous activity in the degenerating retina, and outline the current state of knowledge regarding the cellular and biophysical properties underlying spontaneous neural activity
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