Strychnine eliminates reciprocation and augmentation of respiratory bursts of the in vitro frog brainstem

Abstract

We have recorded rhythmic bursts of efferent action potentials from nerves of respiratory muscles in the frog ( Rana pipiens), using a modified in vitro preparation, in which the brainstem lies in situ in the ventral half of the skull. The burst in the sternohyoid branch of the hypoglossal nerve (Hsh) was augmenting, and alternated with a relatively brief augmenting burst in the main branch of the hypoglossal nerve (Hm). The laryngeal branch of the vagus nerve (Xl) displayed a biphasic burst, beginning before peak activity of Hsh and spanning the Hm burst. The spatio-temporal patterns of these bursts closely resemble those recorded from the same nerves in intact and in decerebrate frogs, indicating that the bursting rhythm of this in situ preparation constitutes fictive breathing. The nature of neurotransmission responsible for burst reciprocity and augmentation was investigated by applying the glycine receptor blocker, strychnine. Low levels of strychnine (1 and 5 M) increased the frequency of fictive breathing without changing the shape or timing of Hsh, Hm and Xl bursts; at higher doses (10 and 20 M) the bursts in all nerves abruptly changed shape and timing to become synchronous and decrementing. The strychnine-induced changes were associated with the appearance of a prominent peak (10–20 Hz) on the spectral analysis of the nerve discharge, possibly indicating a fundamental change in neurogenesis of the respiratory pattern. We conclude that the burst augmentation and reciprocation discharge characteristics of fictive breathing in the frog require strychnine-sensitive inhibitory networks.