Presynaptic action of barbiturates in the frog spinal cord.

The action of pentobarbital on primary afferents of the isolated frog spinal cord was analyzed with sucrose gap and intracellular recordings techniques. Pentobarbital in concentrations generally considered to be in the anesthetic range greatly prolonged presynaptic inhibition and also depolarized primary afferents. The depolarization was accompanied by an increase in excitability and resulted from activation of gamma-aminobutyric acid receptors, possibly by a direct action on these receptors, since the depolarization was reversibly blocked by gamma-aminobutyric acid, but not by glycine, antagonists, and magnesium ions. Furthermore, dorsal root ganglion cells exhibited a reduced sensitivity to both gamma-aminobutyric acid and pentobarbital after a "desensitizing" dose of gamma aminobutyric acid. The prolongation of presynaptic inhibition and the activation of gamma-aminobutyric acid receptors on primary afferents by pentobarbital should act to reduce the amount of transmitter released from the first synapse in sensory pathways.