Abstract
It has been well-known that the electrical activity of the central nervous system is facilitated by relatively lower doses of central depressants. Many reports were presented to support the facilitatory mechanism in the brain of exprimental animals at lower dose levels of barbiturates: lowering of stimulation threshold for the recruiting response by King (1) and' Domino (2), increase in amplitude of the somatosensory evoked potential recorded from the internal capsule by King et al. (3), and increase in amplitude of the evoked potential recorded from the auditory cortex by Pradhan and Galambos (4). Nakai (5) and Nakai and Takaori (6) showed that pentobarbital sodium, chloralose and chlorpromazine increased the magnitude of the cortical potential evoked by click stimuli and accelerated the manifestation of the ensuing rhythmic after-discharges, while urethane and ethyl alcohol even in small doses reduced the amplitude of the evoked potential.
The role of the inferior colliculus as a relay nucleus for the auditory pathway was investigated electrophysiologically by Ades and Brookhart (7) and Thurlow et al. (8). However, there is scarcely any systematic study concerning the effects of central depressants on the evoked potential in the inferior colliculus. It is considered that the effect of central depressants on the collicular acoustic potential may differ from that on the cortical one. The difference may give some clue for the elucidation of the central auditory mechanism.
