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Just wondering if anyone had some ideas about the question in the title. I'm just wondering why some papers use embryonic cultures of specific brain regions for neurones to test the effects of knockouts/mutations on synaptic plasticity (for example, long term potentiation, LTP) instead of adult cultures?

Many thanks

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  • $\begingroup$ Could you edit your question to include a definition for LTP? $\endgroup$ – Michael_A Dec 14 '16 at 22:21
  • $\begingroup$ @Michael_A I think adding a definition for LTP to the question isn't necessary for the OP, but I made a clarifying edit that LTP is a type of synaptic plasticity and added a link to wikipedia for anyone who is unsure. These edits are pending. I also previously spelled out the abbreviations in OP, and it looks like that edit was accepted just after your comment. $\endgroup$ – Bryan Krause Dec 14 '16 at 23:05
  • $\begingroup$ @BryanKrause, nice. My request was a nudge to help keep this interesting question as accessible as possible. $\endgroup$ – Michael_A Dec 15 '16 at 5:30
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Some suggestions, there may be more:

1) The knockout may not be viable to adulthood (the animals die). Perhaps heterozygotes are viable, but to test the full knockout you need a homozygote.

2) Even if the knockout is viable to adulthood, the brain may develop adaptations to the knockout that aren't specific to the knockout itself: up- or down-regulation of certain channels, for example.

3) Plasticity is upregulated in developing brains compared to adult brains, so the effects may be more pronounced in the young tissue.

4) Younger tissue cultures better - you can keep cells alive longer, more easily.

Also good to note is that undifferentiated stem cells tend to be "neuron-default" - that is, if you just culture embryonic stem cells and you don't do anything special to them, they will tend to generate neuron-like cells. In the adult, neurons are always going to be alongside other types of cells: glia, vascular tissue, etc.

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