Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2848079 | Respiratory Physiology & Neurobiology | 2008 | 8 Pages |
Hyperthermia prolongs the laryngeal chemoreflex (LCR). Under normothermic conditions, adenosine antagonists shorten and adenosine A2A (Ad-A2A) agonists prolong the LCR. Therefore, we tested the hypothesis that SCH-58261, an Ad-A2A receptor antagonist, would prevent thermal prolongation of the LCR when injected unilaterally within the nucleus of the solitary tract (NTS). We studied decerebrate piglets aged 4–13 days. We elicited the LCR by injecting 0.1 ml of water into the larynx and recorded integrated phrenic nerve activity. The laryngeal chemoreflex was prolonged when the body temperature of each piglet was raised ∼2.5 °C, and SCH-58261 reversed the thermal prolongation of the LCR when injected into the NTS (n = 13), but not when injected in the nucleus ambiguus (n = 9). Injections of vehicle alone into the NTS did not alter the thermal prolongation of the LCR (n = 9). We conclude that activation of adenosine receptors, perhaps located on GABAergic neurons in the NTS, contributes to thermal prolongation of the LCR.