Synapse, the contact between neurons, is a complex system composed of a multitude of molecular machinery.
It has been well documented that migration of cortical neurons is a complex process that includes radial glia-dependent and glia-independent steps (LoTurco & Bai, 2006).
Motor neuron death in ALS is a complex process, and may involve multiple pathways including formation of protein aggregates, axonal transport defects, oxidative damage, mitochondrial defects, and alterations in calcium homeostasis [6].
Each neuron is actually a complex switching device, but in this review, we introduce only the simplest cellular model, that neurons are binary switches, either quiescent or activated.
For the LSWT-PCNN-based method, it is also more time consuming than the proposed method, because the PCNN neuron is very complex and it needs iterative operation to obtain pleasing fusion results.
As we begin to explore the function, connectivity and plasticity of the nervous system we need to recognize this needs a much more granular analysis of molecular identity, since even the presumed functionally relatively simple primary sensory neuron, is extraordinarily complex and diverse.
As the calculations for one model neuron are complex, the digital simulation of large networks is not efficient using existing simulation systems.
The damage to neurons is based on a complex interplay of multiple factors.
Our results illustrated that although the target specificity of neurons is in fact complex and diverse, yet they are strongly affected by their genetic and molecular compositions.
Thus, the developmental history of the midbrain GABAergic neurons is complex and involves contributions from adjacent brain regions, especially the r1.
