Because ChR2 expression can be Pazopanib targeted in specific types of cells, optogenetic stimulation allows potential therapeutic strategies to be investigated for neuroscience research and applications. A lot of studies that utilized ChR2 for in vivo dopaminergic neuron stimulation successfully induced dopamine release in brain and conditioned animal behaviors. An optogenetic approach can thus be an effective tool for the dopaminergic regulation of cells, which could be an alternative model for the controlled release of dopamine in the Parkinson’s animal model. Various techniques, including neuroimaging, microdialysis, and electrochemical methods, have been developed for detecting dopamine levels. Compared to off-line neuroimaging and microdialysis methods, electrochemical detection provides higher temporal resolution in real time. To further improve the selectivity and sensitivity of dopamine sensing, various approaches using surface modifications on the sensing electrode have been developed. The surface can be modified using self-assembled monolayers, which provide a simple, convenient, and flexible method for functionalizing the chemical properties of the electrode-electrolyte interface. Moreover, various nanomaterial-based modifications, such as those using gold nanoparticle can provide larger effective areas for sensitivity enhancement to have low detection limit for dopamine recording. To better understand the optogenetic regulation of dopamine release from PC12 cells, the present study evaluates dopamine release from ChR2-tranfected PC12 cells using a surface-modified dopamine sensing electrode under various optogenetic stimulation schemes. Nasopharyngeal carcinoma is a head and neck malignant tumor rare throughout most of the world but common in Southeast Asia, especially in Southern China. Epstein-Barr virus, environmental factors, and genetic susceptibility play important roles in the pathogenesis of NPC pathogenesis, the EBV in particular has been implicated in the molecular abnormalities leading to NPC. The molecular pathogenesis of NPC includes abnormal expression and alteration of dominant oncogenes and recessive oncogenes/tumor-suppressor genes and alterations in signaling pathways such as the Akt pathway, mitogen-activated protein kinases, and the Wnt signaling pathway. Therefore, further elucidation of the molecular mechanism underlying NPC is essential for the development of new effective therapeutic agents. Eukaryotic translation initiation factor 4E plays a critical role in initiating translation of mRNAs, and up-regulating the expression of tumor relevant proteins, which are involved in activation of proto-oncogenes, angiogenesis, autocrine growth stimulation, cell survival, invasion and communication with the extracellular environment. Overexpression of eIF4E has been found in many types of tumors and cancer cell lines, but not in typical benign lesions.