칼슘/칼모듈린 의존성 세린 단백질 인산화효소 단백질, 카스킨, 활성존가소성, 시냅스전달, PTPσ
Table Of Contents
I. Introduction 1 1.1 Importance of synaptic adherence mechanism in synaptic transmission 1 1.2 Association between synaptic adhesion molecules in the brain and mental illness 2 1.3 AZ is associated with the synaptic adhesion molecule 5 1.4 The active zone participates in regulating synaptic transmission 8 1.5 Caskins participate in the synaptic function through interaction with other proteins 9 1.6 Caskins regulate the presynaptic function 11 II. Resources and Methods 13 2.1 Mouse strategy 13 2.2 Quantitative real-time reverse transcription PCR (qRT‐PCR) 13 2.3 Preparation of lentiviral expression vector 14 2.4 Western blotting 14 2.5 Mouse and rat hippocampal culture 15 2.6 Preparing of lentiviruses 16 2.7 Infection and transfection 16 2.8 Antibodies 17 2.9 Cultured neuron electrophysiology 17 2.10 Electron microscopy (EM) imaging 19 2.11 Coimmunoprecipitation 20 III. Result 22 3.1 Caskin2 and Caskin1/2 deficient cause abnormal synaptic transmission 22 3.2 Caskin1 deficient cultured hippocampal neurons did not affect the synaptic organization and transmission 22 3.3 Caskin2 deficient cultured hippocampal neurons disrupted excitatory synapse transmission 24 3.4 Caskin2 deletion reduces the number of readily releasable vesicles at excitatory presynaptic boutons 24 3.5 Caskin2 deletion induces abnormal structures in presynaptic nerve terminals 27 3.6 PTPσ interacts with and exclusively dephosphorylates Caskin2 29 3.7 Caskin2 specifically modulates glutamate receptor functions 31 3.8 The specific tyrosine residue of Caskin2 is associated with the dephosphorylation activity of PTPσ 33 IV. Figure 35 V. Discussion 50 VI. References 61 VII. 요약문 70