Rationale: In adult rats, bilateral ablation of preBotzinger Complex(preBotC) neurokinin 1 expressing (NK1R) neurons leads to a progressive and irreversible disruption in breathing pattern, initially during sleep, eventually resulting in an ataxic breathing pattern during wakefulness. Objectives: Here we determine whether ablation of fewer preBotC NKIR neurons leads to a persistent pattern of disordered breathing during sleep but not during wakefulness. Methods: Adult male Sprague Dawley rats (n=12) were instrumented to record diaphragmatic, abdominal and neck EMG, and EEG. Fourteen days later, a second surgery was performed to stereotaxically microinject into the preBotC on one side, the toxin saporin conjugated to substance P (SP-SAP), which selectively ablates NK1R neurons. Main Results: Post-injection, rats were monitored within a plethysmograph until they were sacrificed (days 21-51). At day 6-9 post-unilateral SP-SAP injection, respiratory pattern during sleep, particularly REM sleep, became increasingly disordered, characterized by an increase in frequency of central sleep apnea (CSA) and hypopneas (36.8±7.4 episodes/hour of REM vs 6±2.0 pre-injection control; p<0.05), while breathing during resting wakefulness remained stable. Unlike bilateral SP-SAP injected rats, an ataxic breathing pattern did not develop during wakefulness. Rats that were monitored up to 51 days post-SP-SAP injection continued to have sleep disordered breathing (SDB); breathing during wakefulness remained relatively stable. Histological analysis of the ventrolateral medulla confirmed that NKIR neurons within the preBotC on the injected but not on the contralateral side of the medulla were ablated. Conclusions: Gradual loss of preBotC NK1R neurons may be an underlying factor of SDB, in particular of CSA.