Brainstem nitric oxide tissue levels correlate with anoxia-induced gaspingactivity in the developing rat

Gasping is an important mechanism for survival that appears to be developme ntally modulated by the glutamate-nitric oxide (NO) pathway. However, the t emporal characteristics of NO brain tissue levels during gasping are unknow n. We hypothesized that during anoxia-induced gasping, the gasping frequenc y would be closely correlated with caudal brainstem tissue NO concentration s in developing rats. Brainstem and cortical tissue NO levels were measured during anoxia using a voltammetric electrode in adult rats and 5-day-old p ups during control conditions and following pretreatment with the NMDA rece ptor antagonist MK-801 (1 mg/kg) or the neuronal NO synthase inhibitor 7-ni tro-indazole (7-NI; 100 mg/kg). In young animals, NO tissue levels followed a triphasic trajectory coincident with gasp frequency which was markedly a ltered by MK-801 and 7-NI, albeit with preservation of gasp frequency-NO ti ssue level relationships. In adult rats, 40-fold higher NO tissue levels oc curred and followed a monophasic trajectory coincident with gasp patterning . In the cortex, monophasic increases in NO levels occurred at all ages. We conclude that anoxia-induced gasping neurogenesis is modulated via NMDA-NO mechanisms in the developing rat. We postulate that higher NO brainstem co ncentrations may favor early autoresuscitation, but limit anoxic tolerance. Copyright (C) 2001 S. Karger AG, Basel.