1. Our purpose was to define whether a region of medulla could be iden
tified that is critical for the expression of gasping. 2. Decerebrate,
vagotomized, paralysed and ventilated adult rats were used. The patte
rn of phrenic activity was reversibly altered from eupnoea to gasping
by exposure to hypoxia or anoxia. 3. Gasping was irreversibly eliminat
ed following unilateral electrolytic lesions of the lateral tegmental
field of the medulla. The eupnoeic rhythm continued after these lesion
s. 4. Injections of kainic acid into the lateral tegmental field also
eliminated gasping. Phrenic activity in eupnoea was not altered. 5. Le
sions outside the lateral tegmental field caused marked changes in the
eupnoeic rhythm, including expiratory apnoea. Upon exposure to hypoxi
a or anoxia, gasping was still induced. 6. This region for the neuroge
nesis of gasping in rats is identical to the region that serves a comp
arable function in cats. Moreover, it overlaps with the 'pre-Botzinger
' complex which has been described for the in vitro brainstem preparat
ion of the neonatal rat. Our results raise doubts that this complex pl
ays a role in the neurogenesis of eupnoea.