Two halogenated cyclobutanes, one anesthetic and one not, were compared on receptor-specific pathways in isolated neonatal rat spinal cord. The anesthetic 1-chloro-1,2,2-trifluorocyclobutane depressed the monosynaptic reflex (glutamate non-NMDA receptors) and abolished a slow ventral root potential (glutamate NMDA, non-NMDA and tachykinin receptors). This compound slightly enhanced the muscimol-evoked dorsal root potential (GABAA) but reversibly depressed the dorsal root potential elicited by dorsal root stimulation. The non-anesthetic 1,2-dichlorohexafluorocyclobutane increased monosynaptic reflex, depressed slow ventral root potential approximately 50%, had little effect on muscimol-evoked dorsal root potential, and irreversibly depressed dorsal root-evoked dorsal root potential. Hypoxia accounts for slow ventral root potential depression, but not monosynaptic reflex enhancement. In this preparation and for this pair of compounds, anesthetic properties are related to blockade of transmission at glutamate synapses, with a small component of GABAA enhancement. Monosynaptic reflex increase may be related to the non-anesthetic cyclobutane's convulsant and anti-anesthetic properties.