We hypothesized that pretreatment with chronic cervical dorsal rhizotomy (CDR; C(3)-C(6)) would reveal ineffective crossed spinal pathways to phrenic motoneurons. Anesthetized CDR (1 week post-rhizotomy) and control rats were spinally hemisected at C(2), and phrenic potentials were evoked by stimulating the ventrolateral funiculus contralateral and rostral to hemisection. Phrenic potentials contralateral to the stimulating electrode were evoked at lower stimulus currents (CDR=640 +/- 46 microA; control=900 +/- 50 microA; P<0.05) and potential amplitude was significantly greater in CDR versus control rats (P<0.05). The serotonin receptor antagonist methysergide (4 mg/kg, i.v.) had no effect on the crossed phrenic potential amplitude (91+/-17% of control at 800 microA; P>0.05). Thus, CDR enhances crossed phrenic pathways but serotonin receptor activation is not necessary to maintain this effect.