Skip to main content
. Author manuscript; available in PMC: 2013 Feb 1.
Published in final edited form as: Mol Cell Neurosci. 2011 Nov 30;49(2):158–170. doi: 10.1016/j.mcn.2011.11.004

Figure 9. ATP-induced NPY release and subsequent NPY Y1 receptor-mediated p44/42 ERK activation in GBCs underlies injury-induced neuroregeneration in the OE.

Figure 9

Schematic diagram showing: (A) Extracellular or injury-released ATP transiently inhibits p44/42 ERK via activation of purinergic receptors in the OE. We don’t know the cell types in which ATP transiently inhibits p44/42 ERK. Our data suggest that activation of purinergic receptors in GBCs by ATP produces transient inhibition of p44/42 ERK. (B) Extracellular or injury-released ATP induces NPY release from sustentacular (SC) and microvillous cells (MC) via activation of purinergic receptors. Released NPY activates p44/42 ERK in GBCs via NPY Y1 receptors and subsequently promotes basal cell proliferation. (C) Simultaneous application of ATP with polypeptide growth factors, such as NPY or FGF2 does not synergistically increase basal cell proliferation since growth factor-mediated activation of p44/42 ERK in GBCs is attenuated by purinergic receptor-mediated inhibition of p44/42 ERK.