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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Adenosine Signaling through A1 Receptors Inhibits Chemosensitive Neurons in the Retrotrapezoid Nucleus

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Author(s):
James, S. D. [1] ; Hawkins, V. E. [1] ; Falquetto, B. [2, 1] ; Ruskin, D. N. [3] ; Masino, S. A. [3] ; Moreira, T. S. [4] ; Olsen, M. L. [5] ; Mulkey, D. K. [1]
Total Authors: 8
Affiliation:
[1] Univ Connecticut, Dept Physiol & Neurobiol, Storrs, CT 06269 - USA
[2] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, Sao Paulo - Brazil
[3] Trinity Coll Hartford, Dept Psychol, Neurosci Program, Hartford, CT - USA
[4] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, Sao Paulo - Brazil
[5] Virginia Polytech Inst & State Univ, Sch Neurosci, Blacksburg, VA 24061 - USA
Total Affiliations: 5
Document type: Journal article
Source: ENEURO; v. 5, n. 6 NOV-DEC 2018.
Web of Science Citations: 2
Abstract

A subset of neurons in the retrotrapezoid nucleus (RTN) function as respiratory chemoreceptors by regulating depth and frequency of breathing in response to changes in tissue CO2/H+ The activity of chemosensitive RTN neurons is also subject to modulation by CO2/H+-dependent purinergic signaling. However, mechanisms contributing to purinergic regulation of RTN chemoreceptors are not entirely clear. Recent evidence suggests adenosine inhibits RTN chemoreception in vivo by activation of Al receptors. The goal of this study was to characterize effects of adenosine on chemosensitive RTN neurons and identify intrinsic and synaptic mechanisms underlying this response. Cell-attached recordings from RTN chemoreceptors in slices from rat or wild-type mouse pups (mixed sex) show that exposure to adenosine (1 mu M) inhibits chennoreceptor activity by an Al receptor-dependent mechanism. However, exposure to a selective Al receptor antagonist (8-cyclopentyL-1,3-dipropylxanthine, DPCPX; 30 nM) alone did not potentiate CO2/H+-stimulated activity, suggesting activation of Al receptors does not limit chennoreceptor activity under these reduced conditions. Whole-cell voltage-clamp from chemosensitive RTN neurons shows that exposure to adenosine activated an inward rectifying K+ conductance, and at the network level, adenosine preferentially decreased frequency of EPSCs but not IPSCs. These results show that adenosine activation of Al receptors inhibits chemosensitive RTN neurons by direct activation of a G-protein-regulated inward-rectifier K+ (GIRK)-like conductance, and presynaptically, by suppression of excitatory synaptic input to chemoreceptors. (AU)

FAPESP's process: 14/04866-5 - Role of P2Y1 receptors within the C1 neurons controlling breathing and blood pressure
Grantee:Bárbara Falquetto
Support Opportunities: Scholarships abroad - Research Internship - Doctorate
FAPESP's process: 15/23376-1 - Retrotrapezoid nucleus, respiratory chemosensitivity and breathing automaticity
Grantee:Thiago dos Santos Moreira
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 16/22069-0 - Amelioration of the brainstem vascular imbalances in an spontaneously hypertensive rats with exercise
Grantee:Thiago dos Santos Moreira
Support Opportunities: Regular Research Grants