Professor Bruce McEwen discusses the remodeling of dendrites, which are affected by BDNF, TPA, cell-adhesion molecules, and a number of other factors.

We know best for the hippocampus, and so I’ll talk about that. We know that the shrinkage of dendrites is produced by excitatory amino acids, which probably help to destabilize the cytoskeleton, but you need circulating glucocorticoids around, and you also need enough BDNF [brain-derived neurotrophic factor] around to make it possible for this to occur. We suspect that, at least in some parts of the brain, there’s another molecular system, called the tissue plasminogen activator [TPA], which is as it sounds, it helps in the blood clotting or in hydrolyzing blood clots, but these are also proteases that are released from nerve cells, and they probably work independently of their protease activity as signaling molecules. If you don’t have TPA, you don’t have stress-induced loss of spines of synapses in the hippocampus, and so the animal actually is resilient or resistant to the effects of stress – the short-term effects of stress – on memory. There’s another class of molecules called the cell adhesion molecules, and they are involved probably in facilitating signaling processes, they’re also perhaps involved in how sticky cells are – whether they will retract and be able to move – and this molecule is also essential for dendritic remodeling. I suspect there are many, many more molecules, so it isn’t simply something that is driven by your stress hormones alone. There are the stress hormones working in a permissive sense, along with a lot of other processes.

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