User:Tkadm30/Notebook/Astrocytes

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. [1] [2]

Furthermore, BDNF expression may requires Adenosine receptors (A2a) activation to induce long-term potentiation (LTP). [3]

Thus, BDNF-induced synaptogenesis is enhanced by DHA supplementation to neurons, while endogenous cannabinoids may protect neurons from glutamate excitoxicity and inflammation. [4] [5]

Astrocytic promoters of synaptic plasticity

1. DHA conjugate in the hippocampus is N-docosahexaenoyl ethanolamine (DHEA; synaptamide).
2. DHA synthesis is produced by astrocytes from α-linolenic acid (ALA), a polyunsaturated (n-3) fatty acid precursor.
3. DHEA subclass is N-acyl ethanolamines (NAE)

Astrocytes mediate activity-dependent LTP via purinergic signaling receptors

1. 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
2. Astrocytes mediated synaptic plasticity :
   1. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279365/
   2. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3915348/
   3. http://www.nature.com/tp/journal/v3/n1/full/tp2012136a.html
3. Exocytosis of ATP
   1. Downregulation of glutamatergic synaptic transmission
   2. P2X7 receptor activation induce exocytosis of ATP [6]
   3. non-exocytotic glutamate release
   4. http://www.ncbi.nlm.nih.gov/pubmed/15371507

Glutamate and astrocytes

• http://www.ncbi.nlm.nih.gov/pubmed/18226171