, 2008 and Huberman et al , 2003) or whether it can act in an ins

, 2008 and Huberman et al., 2003) or whether it can act in an instructive way to guide neural circuit formation through specific spatiotemporal see more patterns of neural activity (Feller, 2009 and Huberman et al., 2008). These

issues have been investigated in some detail in the mammalian visual system, where retinal ganglion cell (RGC) projections to the dorsal lateral geniculate nucleus (dLGN) and superior colliculus (SC) form two sensory maps, one reflecting eye of origin and the other retinotopic location (Huberman et al., 2008). Molecular factors are clearly involved in forming these neural circuits, directing RGC axons whether to cross at the optic chiasm (Petros et al., 2008) and where to branch in the dLGN and SC (Huberman et al., 2008 and McLaughlin and O’Leary, 2005). Evidence concerning the role of neuronal activity in early selleck chemicals visual map development is more equivocal, failing to distinguish whether neuronal activity acts in a passive way to promote cell survival and neurite outgrowth, or in an instructive way to guide neural circuit formation through specific spatiotemporal patterns of neural activity (Crair, 1999, Stellwagen and Shatz, 2002 and Huberman

et al., 2003). This fundamental question has been difficult to answer because manipulations that change the spatiotemporal pattern of ongoing spontaneous neuronal activity typically also alter the activity of individual neurons (their overall spike rate, or burst frequency, etc.). This completely confounds changes in interneuronal activity patterns with changes in single-neuron activity levels, making it impossible to distinguish between a passive and active role for neuronal activity in visual map development (Chalupa, 2009 and Feller, 2009). As in many parts of the developing brain and spinal cord (Meister et al., 1991, Bekoff et al., 1975 and Feller, 1999), coordinated waves

of spontaneous neuronal Linifanib (ABT-869) activity are found in the retina of all mammalian species examined (Wong, 1999 and Warland et al., 2006), well before the onset of sensory experience. Maps for eye of origin and retinotopy emerge in neonatal mice in the first week after birth, a period in which spontaneous retinal activity is mediated by nicotinic acetylcholine receptors containing the β2 subunit (β2-nAChRs; Feller et al., 1996 and Bansal et al., 2000). Genetic and pharmacologic manipulations that impair β2-nAChR-mediated retinal waves cause deficits in visual system development, including defects in retinotopy and eye segregation (Stellwagen and Shatz, 2002, Chandrasekaran et al., 2005, Mrsic-Flogel et al., 2005, Rossi et al., 2001, Grubb et al., 2003, McLaughlin et al., 2003, Penn et al., 1998, Pfeiffenberger et al.

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