Normal breathing requires preBotzinger complex neurokinin-1 receptor-expressing neurons

The normal breathing rhythm in mammals is hypothesized to be generated by n eurokinin-1 receptor(NK1R)-expressing neurons in the preBotzinger complex ( preBotc), a medullary region proposed to contain the kernel of the circuits generating respiration. If this hypothesis is correct, then complete destr uction of preBotC NK1R neurons should severely perturb and perhaps even fat ally arrest breathing. Here we show that specific and near complete bilater al (but not unilateral) destruction of preBotC NK1R neurons results in both an ataxic breathing pattern with markedly altered blood gases and pH, and pathological responses to challenges such as hyperoxia, hypoxia and anesthe sia. Thus, these similar to 600 neurons seem necessary for the generation o f normal breathing in rats.