Abstract
A neural model is described of how spontaneous retinal waves are formed in infant mammals, and how these waves organize activity-dependent development of a topographic map in the lateral geniculate nucleus, with connections from each eye segregated into separate anatomical layers. The model simulates the spontaneous behavior of starburst amacrine cells and retinal ganglion cells during the production of retinal waves during the first few weeks of mammalian postnatal development. It proposes how excitatory and inhibitory mechanisms within individual cells, such as Ca2+-activated K+ channels, and cAMP currents and signaling cascades, can modulate the spatiotemporal dynamics of waves, notably by controlling the after-hyperpolarization currents of starburst amacrine cells. Given the critical role of the geniculate map in the development of visual cortex, these results provide a foundation for analyzing the temporal dynamics whereby the visual cortex itself develops.
Highlights
This article describes a neural model of how spontaneous retinal waves are formed in infant mammals, and how these waves organize activity-dependent development of a topographic map in the lateral geniculate nucleus, or LGN, with connections from each eye segregated into separate anatomical layers of the LGN (Figure 1)
The model includes two key cell types: starburst amacrine cells (SACs) and retinal ganglion cells (RGCs) that interact through time
Model SACs occupy the first layer, where they are laterally connected to each other with isotropic distance-dependent Gaussian weighting functions. Anatomical data estimate their effective input radius at approximately 100mm [9]. This lateral communication approximates the function of transmission via nicotinic acetylcholine receptors during early development, which are thought to be a critical mediator of waves and thereby retinogeniculate development [8,19] Spontaneous activity within the SACs is generated using a Poisson process
Summary
This article describes a neural model of how spontaneous retinal waves are formed in infant mammals, and how these waves organize activity-dependent development of a topographic map in the lateral geniculate nucleus, or LGN, with connections from each eye segregated into separate anatomical layers of the LGN (Figure 1). The new model goes beyond earlier modeling efforts by explicitly accounting for the role of intracellular mechanisms such as Ca2+-activated K+ channels, cAMP, and afterhyperpolarization currents (AHPs) in controlling spatiotemporal properties of retinal waves [5]. These results include novel predictions concerning how these intracellular mechanisms regulate retinal waves. Our model advances current knowledge by simulating how single-cell currents may give rise to emergent dynamical network properties, such as wave velocity, shape, and periodicity
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