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Activation of adenosine A2A receptor on GABAergic inputs to 2nd‐order neurons of peripheral chemoreceptors in the NTS
Author(s) -
Zhang Weirong,
Mifflin Steve
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1026.26
Subject(s) - adenosine , cgs 21680 , gabaergic , agonist , chemistry , inhibitory postsynaptic potential , adenosine a2a receptor , neuroscience , receptor , adenosine a1 receptor , adenosine receptor , medicine , endocrinology , biology , biochemistry
Hypoxia elevates extracellular adenosine level in the NTS. Both adenosine A1 and A2A receptors exist in the NTS. Unlike inhibitory A1 receptor, activation of adenosine A2A receptor usually has a facilitation effect on neural function. In this project, we studied the effect of A2A receptor activation on GABAergic inputs to second‐order NTS neurons. Whole‐cell recordings were performed in NTS neurons in brainstem slices. Second‐order neurons were identified following DiA labeling of carotid bodies. Recordings were performed with CNQX but no TTX to study action potential‐dependent spontaneous pre‐synaptic GABA release (sIPSCs). In 3/7 NTS neurons, application of A2A receptor agonist CGS 21680 at 100 nM induced a significant increase in the frequency of sIPSCs (155±12% of control, p<0.05) without a significant change of the amplitude (95±3% of control, p>0.05). In the other 4/7 NTS neurons, CGS 21680 did not induce a significant change in sIPSCs frequency (93±4% of control, p>0.05). In 3 of these 4 neurons, CGS 21680 induced a significant decrease in sIPSCs amplitude (86±2% of control, p<0.05). The results indicate a heterogeneous and complex function of adenosine A2A receptor in the NTS. The lack of response in some neurons may be due to a lack of receptor on certain GABAergic neurons or indirect mechanisms involving other neurochemicals and ion channels. This work is supported by AHA BGIA 0865269F and NIH HL88052.