Stress Components
This section elaborates on the cellular mechanisms underlying inflammation and the stress response. There are different components to the stress response, one which is direct, neurohormone, and the other is indirect, neuroimmune. This section elaborates on both and the nature of both in different psychiatric and autoimmune populations.
It also elaborates on how cellular level inflammatory and stress responses are initiated by the phosporylation of transfer factors and their associated proteins (e.g. AP-1, NK-κΒ, TRAF2&6, ERK, MAPK, CaMK, PKA, PKC, etc.). For instance as cited on page Inflammatory v.s. Anti-inflammatory Protein Expression, NK-κΒ (p65 and p50) protein binds to cell surface proteins TRAF2 and 6 to facilitate activations of pro-inflammatory cytokines, TNF-α and IL-1. Activation of HPA associated glucocorticoids (GCs) and anti-inflammatory cytokine, IL-10, help to inhibit inflammatory process expression by strengthening IκBα’s role in degrading NK-κΒ. This serves to inhibit the inflammatory process.
Interestingly, protein synthesis also occurs in the brain. The protein, CaMKII, is expressed post-synaptically between the sensory thalamus and the lateral nucleus of the amygdala. Its expression activates two subunits of the NMDA receptor, NR2Α and NR2Β, during the retrieval of fear conditioning (Moriya et al., 2000; Rodrigues et al., 2004). This suggests a role for Ca2+/calmodulin-dependent protein kinase II (CaMKII) and the extracellular signal-regulated kinase/mitogen-activated protein kinase cascade (ERK/MAPK) during long term fear conditioning consolidation (Duvarci et al., 2005; Schafe et al., 2000). Therefore underlying inflammatory and chronic stress responses are protein synthesis, which influence the later expression of cytokine and neurotransmitter receptors in various locations in the body as well as in the brain and central nervous system. Future study of the actions of these proteins may reveal the nature of the corresponding activity in bodily tissue and in the brain respectively.
References
Duvarci, S., Nader, K., & LeDoux, J.E. (2005). Activation of ERK/MAPK cascade in the amygdala is required for memory reconsolidation of auditory fear conditioning. Eur J Neurosci, 21(1), 283-9.
Moriya, T., Kouzu, Y. et al., (2000). Close linage between CaMKIIα/β and NMDA-2A receptors in the lateral amygdala and significance for retrieval of auditory fear conditioning. Eur J Neurosci, 12(9), 3307-14.
Rodrigues, S.M., Farb, C.R., et al., (2004). Pavlovian fear conditioning regulates Thr286 autophosphorylation of CaMKII at lateral amygdala synapses. J Neurosci, 24(13), 3281-8.
Schafe, G.E., Atkins, C.M. et al., (2000) Activation of ERK/MAPK in the amygdala is required for memory consolidation of Pavlovian fear conditioning. J Neurosci, 20(21), 8177-87.