WB for Fodrin/Spectrin

Stress in vivo, and CRH application in vitro, cause dendritic spine loss in hippocampal pyramidal neurons. This loss of spines, and subsequent synapses, is likely the underlying mechanism through which severe stress disrupts learning and memory. CRH, in combination with neuronal activity and NMDA receptor activation, recruits the actin destabilizing protein, calpain, to break down the actin cytoskeleton resulting in spine loss. Identifying the downstream signaling from CRH receptors could reveal potential therapeutic targets for diseases such as post-traumatic stress disorder (PTSD), anxiety, and depression.Calpain is a calcium activated protease recently identified as a key play in CRH-induced spine actin destabilization. There is no immunocytochemistry for activated calpain, but the hallmark measure of activated calpain is the presence and accumulation of its cleaved substrate, spectrin. Spectrin is an actin-associated scaffolding protein that confers stability to cellular structures. In the brain, spectrin is known as fodrin. The cleaved form of spectrin is known as the spectrin break down product (SBDP).