The brainstem of adult rats in vivo can be conditioned for SD by superfusing with artificial cerebrospinal fluid (ACSF) in which 75% of the chloride ions were replaced by acetate and to which 10 mM KCl and 10 mM tetraethylammonium (TEA) were added. By contrast, immature rats up to 14 days after birth could be conditioned for SD by superfusing the brainstem with acetate-ACSF alone. Instead of this also short lasting periods of asphyxia were sufficient to condition the brainstem for SD in immature rats. Here we tested whether asphyxia conditions the adult rat brainstem as well for SDs.

Experiments were performed in sodium thiopentone-anesthetized rats (100 mg/kg, i.p.), paralyzed with pancuronium bromide (2–4 mg/kg/h i.v.) and artificially ventilated. We recorded SD-related DC deflections at two sites in the brainstem close to the caudal trigeminal nucleus (lateral spacing 1 mm), and in the cerebral cortex. Both at the cerebral cortex and at the brainstem local blood flow was continuously recorded by Laser Doppler probes together with arterial blood pressure and heart rate. Blood gases and acid-base balance values were checked prior, during and after each period of asphyxia. Asphyxia was performed by stopping the respiratory pump. SD were elicited by microinjections of 1 M KCl (micropipette, tip diam. 5 mm, 100 kPa, 1 s) in a region close to the trigeminal nucleus.

In the native brainstem a microinjection of KCl did not induce any SD-related DC deflections. Asphyxia for at most 1 min resulted in a negative DC deflection in the brainstem of 5.55.4 mV (n=10). A microinjection of KCl in an interval up to 2 min after restarting the respiratory pump did not induce SD as well. Superfusion of the brainstem with acetate-TEA-KCl-ACSF did not alter blood gases and acid-base balance values as well as cardiovascular parameters. Now, microinjections of 1 M KCl initiated propagating SDs (DC amplitude 24.110.8 mV, rise time 13.66.9 s; half-time duration 19.18.2 s, propagation velocity 3.3 mm/min, n=19, mean valuesstd. dev., respectively), and 1-min-asphyxia caused negative DC deflections of 22.99.8 mV (n=28). Microinjection of KCl in an interval up to 6 min after restarting the respiration and complete recovery of the DC potential did not initiate propagating SDs. During propagating SDs the local blood flow in the brainstem increased transiently by 53.610.9%, the blood flow in the cerebral cortex remained unchanged. Systemic administration of MK-801 (3 mg/kg, i.p.) blocked the microinjection-induced SDs, but not the asphyxia-related DC shifts.

In contrast to immature animals up to P14, in adult rats the conditioning of the brainstem with acetate-TEA-KCl-ACSF was a prerequisite to elicit SD. A transient asphyxia (duration = 1 min) failed to condition the brainstem for SD. Short lasting breathing arrest is not an adequate stimulus to trigger brainstem SDs and subsequent cardiovascular reactions.