NDLI: Presymptomatic and symptomatic ALS SOD1(G93A) mice differ in adenosine A1 and A2A receptor-mediated tonic modulation of neuromuscular transmission

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Presymptomatic and symptomatic ALS SOD1(G93A) mice differ in adenosine A1 and A2A receptor-mediated tonic modulation of neuromuscular transmission

Content Provider	PubMed Central
Author	Nascimento, Filipe Sebastião, Ana M. Ribeiro, Joaquim A.
Abstract	Amyotrophic lateral sclerosis (ALS) is a disease leading to neuromuscular transmission impairment. A2A adenosine receptor (A2AR) function changes with disease stage, but the role of the A1 receptors (A1Rs) is unknown and may have a functional cross-talk with A2AR. The role of A1R in the SOD1(G93A) mouse model of ALS in presymptomatic (4–6 weeks old) and symptomatic (12–14 weeks old) phases was investigated by recording endplate potentials (EPPs), miniature endplate potentials (MEPPs), and quantal content (q.c.) of EPPs, from Mg2+ paralyzed hemidiaphragm preparations. In presymptomatic mice, the A1R agonist, N 6-cyclopentyladenosine (CPA) (50 nM), decreased mean EPP amplitude, MEPP frequency, and q.c. of EPPs, an effect quantitatively similar to that in age-matched wild-type (WT) mice. However, coactivation of A2AR with CGS 21680 (5 nM) prevented the effects of CPA in WT mice but not in presymptomatic SOD1(G93A) mice, suggestive of A1R/A2AR cross-talk disruption in this phase of ALS. DPCPX (50 nM) impaired CGS 21680 facilitatory action on neuromuscular transmission in WT but not in presymptomatic mice. In symptomatic animals, CPA only inhibited transmission if added in the presence of adenosine deaminase (ADA, 1 U/mL). ADA and DPCPX enhanced more transmission in symptomatic mice than in age-matched WT mice, suggestive of increase in extracellular adenosine during the symptomatic phase of ALS. The data documents that at the neuromuscular junction of presymptomatic SOD1(G93A) mice, there is a loss of A1R-A2AR functional cross-talk, while in symptomatic mice there is increased A1R tonic activation, and that with disease progression, changes in A1R-mediated adenosine modulation may act as aggravating factors during the symptomatic phase of ALS.
Related Links	http://dx.doi.org/10.1007/s11302-015-9465-4
Ending Page	480
Page Count	10
Starting Page	471
File Format	PDF
ISSN	15739538
e-ISSN	15739546
Journal	Purinergic Signalling
Issue Number	4
Volume Number	11
Language	English
Publisher	Springer Netherlands
Publisher Date	2015-12-01
Access Restriction	Open
Rights Holder	Springer Netherlands
Subject Keyword	Cell Biology Molecular Biology Cellular and Molecular Neuroscience Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Molecular Biology Cellular and Molecular Neuroscience

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