Working hypothesis and aims
Trauma-related LTP/LTD disbalance in favor of potentaion and excessive excitation of glutamate receptors generated when arousing experiences occur in conjunction with memory-related activation of the hippocampus and amigdala. Traumatic memories connected to the amplification of mechanism LTP, when new information is unable to induce reliable LTD, which reverses synaptic plasticity formed during previous emotional learning experiences.
MHC class I and CD3-zeta play a key role in these changes. We assume that the composition of glutamate receptors and CD3-zeta expression in T-cells can be used as the model reflecting for LTP/LTD balance in CNS.
The work includes the learning of following parameters:
1. The Expression in T-cells: glutamate receptors, CD3-zeta.
2. Glutamate level in plasma
3. Cytokines levels in plasma:
1. interferon-γ that can induce some components of class I MHC (9).
2. tumor necrosis factor-α that influences the AMPAR expression and plays a role in LTP reduction (10).
Groups (of 20 people each) will make patients with a priori various degree of LTP/LTD balance: healthy people and PTSD patients.
People suffering PTSD, frequently have conditions when they again, brightly and deeply experience event injuring them. The memoirs painted by painful emotions, seize attention of the person and then it seems to him as if he again experiences injuring event and sees it as real.
We assume, that it is connected to the unable to induce reliable LTD, and that the composition of glutamate receptors and CD3-zeta expression in T-cells such people should differ from healthy.
Used method: enzyme- linked immunosorbent assay (ELISA), FACS
