thesis on high school defense mechanism

First discovered in 1989, Cystic Fibrosis (CF) is a genetically predetermined condition, its presences is lifelong and highly complex, which is why many CF sufferers and families develop various mechanisms in order to adapt to the condition (Tippingemail, Scholes, Cox, 2010).

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Mutations in the Disrupted-In-Schizophrenia 1 (DISC1) gene have been implicated in major psychiatric disorders. Although DISC1 functions in neurodevelopment have been extensively described, its role in glutamatergic synaptic transmission remains poorly understood. The main objective of this thesis is to define how DISC1 regulates glutamate release in the hippocampus, a brain structure that expresses high levels of DISC1 and has been associated with mental illnesses. To investigate the impact of DISC1 on neurotransmission, the synaptic vesicle (SV) cycle was examined at the hippocampal synapses using the synaptic tracer vGlut1-pHluorin under two independent genetic perturbation - RNAi and a DISC1 knockout mouse. Population imaging of these synapses revealed a significant reduction in SV exocytosis rates during synaptic stimulation. This reduction was accompanied by a decrease in presynaptic Ca2+ influx, an important determinant of SV release. Further, DISC1 was demonstrated to boost SV exocytosis by enhancing Ca2+ influx through the N-type voltage-gated Ca2+ channel. Based on these results, a working model whereby DISC1 promotes SV release through increasing Cav2.2-dependent presynaptic Ca2+ influx is proposed. These findings identify a novel mechanism by which a mental illness gene regulates glutamate release and highlight the possible role of aberrant glutamate release in the etiology of major psychiatric disorders.


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