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Hoodia p57 order of GNAQ is critical to the growth potential of both plant cells and neurons, the latter especially, for generation of functional neurons. (D) The GNAQ is required for Ca2+ oscillations necessary to regulate neural development, synapse formation, and post-synaptic signaling, as described earlier. The Ca2+/CaM intracellular cascades are also discussed (data not presented). (E-E) For a detailed depiction of Ca2+/CaM intracellular signalling pathways in Drosophila, see SI Appendix.) (F) Drosophila GNAQ is essential for neuronal growth and activity. The Amoxicillin to buy over the counter Ca2+-sensitive cAMP pathway, Ca2+/CaM signal transduction, and voltage-gated potassium channels, specifically, are important for neuron function. In fact, these GNAQ-dependent oscillations appear to act through the NMDA receptor. role of CaM in controlling Ca2+ oscillations Drosophila has not yet been considered. To examine the role of NMDA receptor signaling within the control of CaM, we used CaMαG to isolate CaM receptors (caMKs). In the absence of CaMαG, caMKs were highly sensitive to CaM, indicating the influence of this subunit on Ca2+ oscillations. However, with CaM αG, oscillations did not extend to the membrane, whereas control experiments showed similar CaM oscillations under control conditions in the absence and presence of CaMKs. These data demonstrated the critical role of CaM in the Ca2+ oscillations of CaMKs (Fig. 6E and data not shown). Cummings (27) proposed that Ca2+ could play a major role in neuronal and postsynthetic growth regulation as demonstrated by the fact that endogenous Ca2+ ions act as "dopamine" and "neurotrophic" regulators of neurite growth. The importance Ca2+ for postsynaptic generation was recently proven by the observation of presence extracellular Ca2+ in synapses (28). contrast, the Ca2+/CaM intracellular signaling cascade, which is critical for cell-to-cell signalling, has been largely undefined. The role of calcium in controlling synaptic connectivity has only recently, however, been the focus of research. We propose that the CaM intracellular signal transduction cascade in both synapses and the nuclear membrane is a critical means of controlling Ca2+ oscillations in the CaM/CAM signal transduction machinery. We demonstrate that the NMDA receptor is important for Ca2+/CaM intracellular signaling in neural cells (Fig. 6F). Thus, a small proportion of GNAQ is sufficient to increase Ca2+ production. However, even transient elevations of GNAQ in hippocampal neurons caused excessive Ca2+ production, whereas inhibition of Ca2+/CaM production by NMDA was sufficient to block the growth effect of GNAQ (Fig. 6F). Thus, NMDA receptor blockade is sufficient to limit Ca2+ transmission, at least in part, by causing CaM activation. As described previously, Ca2+/CaM intracellular signaling is highly sensitive to extracellular Ca2+ level (30, 31). Thus, our observations in hippocampal neuron growth could be consistent with the fact that Ca2+ is required to support the CaM intracellular signaling pathway. Furthermore, the fact that GNAQ production is increased by NMDA receptor blockade in neurons likely is attributable to the blockage of Ca2+ transport into the cell, as suggested by presence of extracellular Ca2+ in neuronal subfields. We have previously shown that neuronal protein kinases, Cdk5 and p38LIP, contribute significantly to NMDA receptor-dependent Ca2+/CaM intracellular oscillations (12). Indeed, an increase in Ca2+ release from hippocampal neurons is accompanied by an activation of Cdk5 and p38LIP (13, 13). These results provide further evidence that increasing intracellular Ca2+ through NMDA receptor signaling is essential for Ca2+ oscillations in Drosophila. However, there is little, if any, evidence that these two proteins contribute significantly to the Ca2+/CaM intracellular signaling cascade in neuronal development. The presence of extracellular Ca2+ in neurons after transfection is most likely due to other Ca2+-sensitive channels within the cell, such as Kv8 cation channels, which we identified previously (32). In contrast, the requirement for Ca2+/CaM intracellular signaling in postsynaptic growth is unclear. Extracellular Ca2+ levels are high after NMDA receptor activation in hippocampal neurons, whereas a small contribution from extracellular Ca2+ to oscill.