Serotonin, gasping, autoresuscitation, and SIDS--a contrarian view.

摘要

in their study in the Journal of Applied Physiology, Erikson and Sposato (4) induced anoxic apnea in neonatal Pet-1 knockout (KO) and wild-type mice at postnatal day (P) 4.5 and P9 and examined the subsequent quality of gasping and autore-suscitation while the animals breathed room air. Pet-1 KO mice lack -70% of the usual number of serotonergic neurons, and they have brain tissue serotonin (5-HT) levels that are - 15% of the normal value (6). Both the onset of gasping and the restoration of eupnea were delayed once anoxic apnea developed in the Pet-1 KO animals compared with wild-type animals. However, the actual number of gasps and quality of gasping was remarkable similar in wild-type and mutant animals. Finally, the prolonged latency in the onset of gasping and in the restoration of eupnea was less pronounced in Pet-1 KO animals on P9 compared with Pet-1 KO animals on P4.5 (the Pet-1 KO animals seemed to be "outgrowing" the abnormalities of autoresuscitation), although the older Pet-1 KO animals did not initiate gasping or restore eupnea as quickly as similar age wild-type animals. Three issues, the function of serotonin in autoresuscitation, the function of serotonin in gasping, and the relevance of these studies to sudden infant death syndrome (SIDS), deserve comment.