User:Tkadm30/Notebook/Endocannabinoids: Difference between revisions

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* http://www.ncbi.nlm.nih.gov/pubmed/22959887
* http://www.ncbi.nlm.nih.gov/pubmed/22959887
* http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2219532/
* http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2219532/
* http://www.ncbi.nlm.nih.gov/pubmed/21288475
CB1 signaling and memory:  
CB1 signaling and memory:  
* http://www.ncbi.nlm.nih.gov/pubmed/24648181
* http://www.ncbi.nlm.nih.gov/pubmed/24648181

Revision as of 05:27, 30 September 2014

Notes

Hypothesis

  1. DHA may potentiate synaptic plasticity (and cognition) via retrograde CB1 signaling.

Model

  1. Use omega 3 (DHA) fatty acids as substrate for docosahexaenoylethanolamide (DHEA) hydrolysis
  2. Protect the hippocampus and neurons from stress induced damage.
  3. CB1: A synaptogenic receptor

Documentation

Protocol:

CB1 signaling and memory:

DHA:

Anandamide signaling:

FAAH (fatty acid amide hydrolase):

Introduction to fatty amides:

Keywords

hippocampus, anandamide, FAAH, fatty acids, THC, neurogenesis, synaptogenesis