User:Tkadm30/Notebook/Endocannabinoids: Difference between revisions

Revision as of 05:15, 23 October 2014

DHA may potentiate synaptic plasticity (and cognition) via retrograde CB1 signaling.
1. DHA activate the NMDA receptor and upregulate the release of glutamate. 1
2. Hippocampal CA3 synapses facilitate synaptic plasticity, thus learning is enhanced. 1
  1. Induction of Long-Term Potentiation/Persistent synaptic plasticity (LTP). (Pathway)
Synaptic activation of GABA(B) receptor by endocannabinoids promotes synaptic function and learning. (activity-dependent synaptogenesis) [reference needed]

The Promoter: omega 3 (fish oil supplement) fatty acids
1. DHA (docosahexaenoic acid) conjugate (in the hippocampus?) is docosahexaenoyl ethanolamide (DHEA).
The Wet Blanket:
1. Role: Protect the hippocampus and neurons from glutamate excitoxicity.
2. CB1: A synaptogenic receptor? (most likely) 1 2 3
The Vector:
1. FAAH/anandamide hydrolysis of DHEA (a endocannabinoid like molecule)

Protocol:

Cannabinoids and hippocampal neurogenesis:

DHA:

Anandamide signaling:

FAAH (fatty acid amide hydrolase):

Introduction to fatty amides:

Synaptic Plasticity:

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

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 ## Hippocampal CA3 synapses facilitate synaptic plasticity, thus learning is enhanced. [http://cercor.oxfordjournals.org/content/21/11/2442.full 1]
 ### Induction of Long-Term Potentiation/Persistent synaptic plasticity (LTP). ([http://www.genome.jp/kegg-bin/show_pathway?hsa04720+2902 Pathway])
-# Synaptic activation of GABA(B) receptor by endocannabinoids promotes synaptic function and learning. (activity-dependent synaptogenesis)
+# Synaptic activation of GABA(B) receptor by endocannabinoids promotes synaptic function and learning. (activity-dependent synaptogenesis) [reference needed]
 === Model ===