User:Tkadm30/Notebook/Astrocytes: Difference between revisions

Revision as of 16:23, 27 May 2015

Adenosine and cannabinoids connection
1. DHA modulation of ATP response is controlled via the (use-dependent) inhibition of ionotropic P2X7 receptors:
  1. http://www.ncbi.nlm.nih.gov/pubmed/17099292
  2. http://www.ncbi.nlm.nih.gov/pubmed/12351710
Astrocytes mediated synaptic plasticity :
Exocytosis of ATP
1. Downregulation of glutamatergic synaptic transmission
2. P2X7 receptor activation induce exocytosis of ATP [1]
3. non-exocytotic glutamate release
4. http://www.ncbi.nlm.nih.gov/pubmed/15371507

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 __TOC__
-=== Astrocytic activity promote persistent synaptic plasticity in the hippocampus. ===
-DHA (docosahexaenoic acid) supplementation enhance synaptic plasticity and cognition by regulating BDNF expression and glutamate release from astrocytic metabotropic glutamate receptors. <cite>Wu-2008</cite> <cite>Martin-2011</cite>
-Furthermore, BDNF expression may requires Adenosine receptors (A2a) activation to induce long-term potentiation (LTP). <cite>Duster-2014</cite>
-Thus, BDNF-induced synaptogenesis is enhanced by DHA supplementation to neurons, while endogenous cannabinoids may
-protect neurons from glutamate excitoxicity and inflammation. <cite>Kim-2013</cite> <cite>Kim-2011</cite>
-=== Astrocytic promoters of synaptic plasticity ===
-# DHA conjugate in the hippocampus is N-docosahexaenoyl ethanolamine (DHEA; synaptamide).
-# DHA synthesis is produced by astrocytes from α-linolenic acid (ALA), a polyunsaturated (n-3) fatty acid precursor.
-# DHEA subclass is N-acyl ethanolamines (NAE)
 === Astrocytes mediate activity-dependent LTP via purinergic signaling receptors ===