Reduction of streptomycin-induced acute and chronic toxicities.

The acute and chronic toxicities of streptomycin sulfate (SS) and of the streptomycin hydrochloride-calcium chloride complex (SCC) were compared. The LD50 determined in mice was significantly higher for SCC than for SS. Chronic toxicity was evaluated by recording the nystagmus induced by damped torsion pendulum in rabbits. SS and SCC treatments (200 mg/kg intramuscularly of absolute streptomycin base) decreased the duration, the maximal frequency, and the total number of beats of nystagmus. However, SCC-induced changes were significantly lower than SS-induced ones. The extent of the lesion in the crista ampullaris was evaluated by light and electron microscopy and was correlated with the electrophysiological findings. Because the authors also demonstrated that there are no differences in the antibacterial effects of these salts, SCC may have a place in long-term streptomycin treatment.

Effects of synaptic drugs on turtle optokinetic nystagmus and the spike responses of the basal optic nucleus.

Behavioral and electrophysiological measures were used to elucidate the retinal modulation of oculomotor control in the turtle. Eye movements were recorded following intravitreal applications of 2-amino-4-phosphonobutyrate (APB) and the GABA antagonists picrotoxin and bicuculline. Visual responses of single basal optic nucleus (BON) neurons of the accessory optic system were studied in parallel experiments. The effectiveness of APB, a glutamate analog thought to act selectively on the retinal ON pathway, was assessed independently by recording electroretinograms or ganglion cell activity. Injections of APB into the turtle's eye reduced or blocked the injected eye's ability to drive horizontal optokinetic nystagmus, as also observed in rabbit and cat (Knapp et al., 1988; Yucel et al., 1989). Single-unit recordings from the BON during APB superfusion (50-200 microM APB) of the contralateral retina demonstrated that these cells, which are direction-sensitive and respond to the offset of light flashes, have their responses to moving stimuli blocked by APB. During the APB effect, GABA antagonists were applied to the same eye. Although moderate doses of APB were sufficient to block optokinetic or BON light responses, the addition of GABA blockers still elicited a spontaneous temporal-to-nasal nystagmus (Ariel, 1989) or visually responsive yet direction-insensitive responses from BON cells (Schuerger et al., 1990). These results are discussed in terms of the retinal output to pathways involved in oculomotor control of optokinetic nystagmus.