This is about a 5 minute stretch about neuroplasticity in the hippocampus:
III. The Hippocampus
- As we talked about on Wednesday, the hippocampus is a major target of stress hormones. However, cortisol is not the only hormone that affects the hippocampus.
- Cortisol- We have already talked about how cortisol leads to hippocampal atrophy. What does this mean? Basically, the hippocampus shrinks.
- Chronic (or even acute) exposure to high levels of cortisol can cause death of dendrites in the CA3 region or the hippocampus. The hippocampus has 4 major layers (CA1-4).
- Cortisol in the dendate gyrus stops neurogenesis. Neurogenesis is the production of new neurons. This process continues as we age and is thought to be involved in some of the more general forms of plasticity discussed earlier.
- These two changes can lead to memory deficits- underscores the importance of the hippocampus for learning and memory.
- Estrogen and Progesterone- I mentioned on Wednesday that they had protective effects…
- When given in appropriate amounts, these hormones have been shown to increase the number of synapses (cell connections) in the CA1 region of the hippocampus.
- This synaptogenesis seems to occur via the NMDA receptor (N-methyl-D-aspertate).
- NMDA is a glutamate receptor and is thought to be the major way to affect plasticity via the growth of new synapses.
- Estrogen upregulates production of NMDA
- How does it work? In the post-synaptic cell, the NMDA receptor will only become active if both the pre and postsynaptic cells are active at the same time. By acting as a coincidence detector in this way, NMDA helps in the formation of neural networks.
- Reversible atrophy in CA3
- This occurs mainly in ground squirrels and in other small rodent like mammals.
- This occurs during hibernation.
- This is very similar to the atrophy seen as a result of stress. However, this occurs much faster and is generally thought to be reversible.
- The mechanism of this is not really understood.