AI Article Synopsis
- There is significant interaction between adenosine A(2A) receptors (A(2A)Rs) and brain-derived neurotrophic factor (BDNF), which is crucial for regulating synaptic transmission.
- A(2A)Rs not only help activate the BDNF receptor TrkB but also enhance the effects of BDNF, largely through the cAMP-PKA signaling pathway.
- The importance of A(2A)Rs in maintaining BDNF levels suggests potential therapeutic implications for conditions like Huntington's disease, where both BDNF and A(2A)Rs are compromised.
Article Abstract
In the last few years, accumulating evidence has shown the existence of an important cross-talk between adenosine A(2A) receptors (A(2A)Rs) and brain-derived neurotrophic factor (BDNF). Not only are A(2A)Rs involved in the mechanism of transactivation of BDNF receptor TrkB, they also modulate the effect of BDNF on synaptic transmission, playing a facilitatory and permissive role. The cAMP-PKA pathway, the main transduction system operated by A(2A)Rs, is involved in such effects. Furthermore, a basal tonus of A(2A)Rs is required to allow the regulation of BDNF physiological levels in the brain, as demonstrated by the reduced protein levels measured in A(2A)Rs KO mice. The crucial role of adenosine A(2A)Rs in the maintenance of synaptic functions and BDNF levels will be reviewed here and discussed in the light of possible implications for Huntington's disease therapy, in which a joint impairment of BDNF and A(2A)Rs seems to play a pathogenetic role.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5763899 | PMC |
| http://dx.doi.org/10.1100/tsw.2010.164 | DOI Listing |
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