Biomedical subjects

S M Ross

Publications and source records attributed to S M Ross.

At least 91 records · Page 5Linked to original sources

PubMed1977

Potentiation of tricyclic antidepressant toxicity by physostigmine in mice.

Subtoxic doses of physostigmine have been found to potentiate the convulsive toxicity and lethality of amitriptyline and imipramine in CD1 and B6A mice. Neostigmine failed to potentiate the toxicity and lethality of imipramine. Physostigmine tended to protect mice against atropine-induced lethality. These data suggest the site of toxicity of this drug-drug interaction between the tricyclic antidepressants and physostigmine may be occurring in the CNS through a mechanism distinct from the anticholinergic actions of the antidepressants.

Amitriptyline↗

PubMed1977

Warning signals and alerting: effects on differential classical conditioning.

Three experiments were carried out to investigate the effects of a nondifferential warning signal on differential classical conditioning. In Experiment 1, a 500-msec warning interval was found to result in good differential conditioning performance at an interstimulus interval (ISI) of 500 msec in which differential conditioning did not otherwise occur. The second experiment demonstrated the warning effect with both visual and auditory conditioned stimuli, thus ruling out the possibility that the warning effects were due to eye movements. Experment 3 showed that a warning signal and an increased ISI were functionally equivalent, as demonstrated by conditioning performance and the similar effects obtained when the ISI and warning-interval conditions were switched from optimal to nonoptimal and vice versa.

Acoustic Stimulation↗

PubMed1975

Stimulus input recruitment and stimulus trace decay factors in the trace conditioning deficit of severely retarded young adults.

Trace and delay classical eyelid conditioning procedures were used to investigate the relative contributions of conditioned stimulus input recruitment and trace decay processes to the trace conditioning deficit of severely and profoundly retarded subjects. The study included both trace and delay conditioning groups at interstimulus intervals of 500 and 950 msec. The conditioned stimulus durations were 50 msec for the 500-msec interstimulus interval trace group and 500 msec for the 950-msec interstimulus interval trace group. The "empty" interval between conditioned stimulus offset and the onset of the unconditioned stimulus was 450 msec for both trace conditioning groups. After 250 conditioning trials, there was no difference between the two trace groups, and both were significantly below the delay groups in final level of responding. These results suggest that stimulus trace decay rather than input recruitment, as manipulated by varying conditioned stimulus duration, accounts for the poor trace conditioning performance demonstrated by these subjects.

Adolescent↗

PubMed1975