User:Tkadm30/Notebook/DHA: Difference between revisions
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'''DHA supplementation may promote persistent synaptic plasticity in the hippocampus:''' | '''DHA supplementation may promote persistent synaptic plasticity in the hippocampus:''' | ||
* DHA supplementation may enhance activity-dependent synaptic plasticity and cognition by regulating BDNF expression and glutamate release from hippocampal astrocytes. Furthermore, BDNF expression may requires adenosine A2A receptor activation to induce long-term potentiation (LTP). Thus, BDNF-induced synaptogenesis is enhanced by DHA supplementation to neurons, while DHEA may protect neurons from glutamate excitoxicity and inflammation. | * DHA supplementation may enhance activity-dependent synaptic plasticity and cognition by regulating BDNF expression and glutamate release from hippocampal astrocytes. Furthermore, BDNF expression may requires adenosine A2A receptor activation to induce long-term potentiation (LTP). Thus, BDNF-induced synaptogenesis is enhanced by DHA supplementation to neurons, while DHEA may protect neurons from glutamate excitoxicity and inflammation. | ||
* DHA may increase CREB function by upregulation of | * DHA may increase CREB function by upregulation of mature BDNF levels. | ||
* ATP-induced CREB phosphorylation mediate synaptic plasticity and LTP through cAMP response element (CRE)-mediated gene induction. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2538603/ PMC] [https://www.ncbi.nlm.nih.gov/pubmed/22593004 PMID] | * ATP-induced CREB phosphorylation mediate synaptic plasticity and LTP through cAMP response element (CRE)-mediated gene induction. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2538603/ PMC] [https://www.ncbi.nlm.nih.gov/pubmed/22593004 PMID] | ||
* DHA is neuroprotective and controlled by the P2RX7 receptor. [https://www.ncbi.nlm.nih.gov/pubmed/25504554 PMID] | * DHA is neuroprotective and controlled by the P2RX7 receptor. [https://www.ncbi.nlm.nih.gov/pubmed/25504554 PMID] | ||
Revision as of 07:25, 12 August 2015
DHA (docosahexaenoic acid)
DHA supplementation may promote persistent synaptic plasticity in the hippocampus:
- DHA supplementation may enhance activity-dependent synaptic plasticity and cognition by regulating BDNF expression and glutamate release from hippocampal astrocytes. Furthermore, BDNF expression may requires adenosine A2A receptor activation to induce long-term potentiation (LTP). Thus, BDNF-induced synaptogenesis is enhanced by DHA supplementation to neurons, while DHEA may protect neurons from glutamate excitoxicity and inflammation.
- DHA may increase CREB function by upregulation of mature BDNF levels.
- ATP-induced CREB phosphorylation mediate synaptic plasticity and LTP through cAMP response element (CRE)-mediated gene induction. PMC PMID
- DHA is neuroprotective and controlled by the P2RX7 receptor. PMID
DHEA (N-docosahexaenoyl ethanolamide)
- Ethanolamide metabolite of DHA.
- Derivative of anandamide.
- A novel endocannabinoid with antiglutamatergic and neuroprotective effects that induce synaptogenesis in vivo. PMC
