Recent evidence suggests that neurons within the ventromedial medulla give rise to an inhibitory pathway(s) which projects directly upon the sympathetic preganglionic neuropil. The present investigations were initiated to determine the effects of interrupting this pathway on the expression of a learned autonomic response, defensively conditioned cardioacceleration in the pigeon. Experiment I included two groups. Each experimental animal was trained concomitantly with a sham-operated control, and all birds received 100 trials of conditioning. Each conditioning trial consisted of a 6-sec light presentation followed immediately by a 0.5-sec foot shock. The first experimental group included birds with lesions involving the rostral medullary raphe nuclei (RMR), while the second included birds sustaining lesions of the caudal pontine raphe region (CPR). The principal findings were that (a) RMR-lesioned birds exhibited heart rate increases significantly greater than CPR-lesioned and control birds, (b) heart rate changes in CPR- lesioned birds were not significantly different from control values, and (c) RMR and CPR lesions did not affect base line heart rates significantly. Experiment II was undertaken to determine whether the elevated responsivity following RMR lesions represented a performance increment or an actual enhancement of associative learning. RMR- lesioned animals and their paired controls received 60 trials of sensitization training (explicitly unpaired lights and foot shocks) followed by 60 trials of conditioning. The primary result was that, independent of the training paradigm, RMR-lesioned animals, had significantly greater heart rate increases than control animals. In summary, the “lability” of heart rate changes following RMR lesions apparently is a performance effect and does not represent an enhancement of associative learning. Additionally, the data are consistent with the hypothesis that lesions of this midline medullary region disrupt a descending pathway important for the phasic reflex modulation of chronotropic cardiac responses to exteroceptive stimuli.