The central nervous system, which includes the spinal cord, retina, and brain, is derived from the neural tube. The neural tube is formed of a sheet of cells called the neuroepithelium. During embryonic development, neuroepithelial cells function as neural stem cells: they renew themselves while undergoing interkinetic nuclear movements along the apico-basal axis during the cell cycle, and they produce postmitotic cells that function as newborn neurons. Neuroepithelial cells exhibit a robust increase in nucleoplasmic [Ca(2+)] in response to G protein-coupled receptor activation during S-phase when the nucleus is located in the basal region of the cell. This Ca(2+) rise is caused by the release of Ca(2+) from intracellular Ca(2+) stores, and the Ca(2+) release in turn activates Ca(2+) entry from the extracellular space, which is called capacitative (or store-operated) Ca(2+) entry. The Ca(2+) release and store-operated Ca(2+) entry are essential for DNA synthesis during S-phase. The activity of this store-operated Ca(2+) signaling system declines in parallel with the decreasing proliferative activity of neuroepithelial cells. When exiting the cell cycle, the cells lose the apical process where gap junctions are located. Following the loss of gap junction coupling, the postmitotic cells show a high input resistance, which allows them to be readily depolarized. The Ca(2+) response to the excitatory neurotransmitter glutamate appears and develops during neuronal differentiation. The glutamate-induced Ca(2+) rise increases transiently during natural cell death (apoptosis). The rise in Ca(2+) levels mediated by voltage-gated Ca(2+) channels also develops during neuronal differentiation. Thus, when neuroepithelial cells differentiate into neurons, a transition from a store-operated system to a voltage-operated system occurs in the main Ca(2+) signaling system. This transition may reflect a change in the mode of intercellular communication from a stored Ca(2+)-dependent mode to a plasma membrane potential-dependent mode.
Copyright © 2012 Elsevier Inc. All rights reserved.