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D S Leitner

Publications and source records attributed to D S Leitner.

11 recordsLinked to original sources
PubMed1993

Parameters affecting gap detection in the rat.

The present research used a startle amplitude reduction paradigm to investigate the ability of the rat's auditory system to track rapidly changing acoustic transients. Specifically examined was the ability of brief gaps in otherwise continuous noise to reduce the amplitude of a subsequently elicited acoustic startle reflex. The duration of the gap, time between gap offset and startle elicitation (the interstimulus interval or ISI), and rise-fall characteristics of the gap were systematically varied. Consistent with previous research, gaps reliably reduced startle amplitude. Gaps 2 msec long were reliably detected, and a 50-msec ISI resulted in the greatest amplitude reduction. Gaps presented at short ISIs produced amplitude reduction that followed a different time course than did gaps presented at longer ISIs. These results may reflect differences in the length of time available for the processing of the stimulus and may involve two different processes.

Acoustic Stimulation↗
PubMed1990

Augmentation of the rat's acoustic startle reflex by nonreflexogenic stimuli.

The size of the rat's acoustic startle reflex was augmented by brief acoustic clicks (which did not themselves elicit startle) presented several milliseconds before the reflex-eliciting stimulus (RS). The same clicks presented after the RS gave relatively weak augmentation that was present in the 1st, but not the 2nd, testing session. Brief footshocks set to 75% of each animal's flinch threshold augmented startle when presented both before and after the RS in both testing sessions. Augmentation by a leading footshock increased with shock intensity and was unaffected by the intensity of the RS. Augmentation by a trailing footshock increased with shock intensity and also with the intensity of the RS. Reflex size is not fixed at the time of reflex elicitation but can be augmented by a later nonreflexogenic stimulus. Reflex augmentation may be caused by the 2nd member of a stimulus pair discharging elements of the reflex pathway that were partially activated by the 1st.

Acoustic Stimulation↗
PubMed1989

Multisensory deficits in rats produced by acute exposure to cold swim stress.

Cold swim stress and morphine administration produce analgesia. Whether this was accompanied by changes in other senses was investigated. Analgesia was assessed with a tail-flick test; the sensitivity of the other senses was assessed using the ability of mild sensory stimuli (prestimuli) to inhibit the amplitude of a subsequently elicited acoustic startle response. In Experiment 1, auditory prestimuli were used. In Experiment 2, visual prestimuli were used. In each experiment, rats were exposed to cold-water swims followed by behavioral testing, warm swims followed by testing, and testing alone. This was repeated, substituting morphine injections followed by testing, vehicle injections followed by testing, or testing alone. Both cold swim stress and morphine produced reliable analgesia. Only cold swim stress interfered with the ability of the stimuli to inhibit startle. This reflects decreased sensitivity to auditory and visual stimulation caused by cold swim stress, which suggests that the resultant sensory deficits are more global than is currently believed.

Afferent Pathways↗
PubMed1989

Effect of in utero cocaine exposure on startle and its modification.

The effect of prenatal cocaine on acoustic sensorineural reactivity was assessed using reflex modification procedures in infants born to mothers with cocaine abuse (C-exposed). Reflex modification was tested using a controlled eyeblink-eliciting tap to the glabella presented either alone or with a 90-dB SPL tone. The results from 19 C-exposed infants were compared to 19 healthy matched drug-free infants. ANOVA comparison of the two groups showed C-exposed infants were more reactive in general, as indicated by a larger glabellar reflex, and more responsive to auditory stimuli, as indicated by an increased blink when the tone accompanied the tap (p less than 0.05). These data suggest that in utero cocaine exposure may have a direct effect on sensorineural processing and may place these infants at risk for cognitive and/or neurological sequelae.

Blinking↗
PubMed1988

Inhibition of acoustic startle in the rat by a footshock prestimulus: effects of morphine and naloxone.

In a series of three experiments, we investigated the ability of footshock to inhibit the rat's acoustic startle response. Based on the mean thresholds obtained from a flinch-jump test, 8 rats were tested in a startle inhibition procedure with prestimulus intensities of 0.1, 0.2, 0.4, and 0.8 mA. Subjects were presented with a series of startle-eliciting noise bursts, preceded by a 300-ms footshock of one of the four intensities. Control trials consisting of the noise alone were also included. Startle amplitude was measured during the 100 ms immediately following the noise onset. Footshock reliably inhibited startle at all intensities; inhibition was near maximum at 0.2 mA. Morphine administration reliably interfered with the inhibition at all intensities, and this was reversed by naloxone administration. These data suggest that morphine may have a more general effect than is currently believed.

Acoustic Stimulation↗
PubMed1985

Role of the inferior colliculus in the inhibition of acoustic startle in the rat.

Fifteen rats were tested for amplitude reduction of the acoustic startle response using auditory and visual prestimuli. Eight subjects then received large lesions of the inferior colliculus, and the remaining subjects served as normal controls. All animals were reassessed on a post-test identical to the pre-test. In addition, all subjects were tested for latency reduction of startle using auditory prestimuli. There were no significant differences between groups on the pre-test for startle amplitude, visual amplitude reduction, or auditory amplitude reduction, nor did the control group differ significantly on these measures from pre-test to post-test. After surgery, the lesion group displayed a large, significant increase in startle amplitude. Auditory prestimuli were no longer effective in reducing startle amplitude in this group, but visual prestimuli still produced reliable amplitude reduction. Both groups displayed reliable latency reduction to auditory prestimuli; the groups were not significantly different from each other on this measure. These data support the proposition that the inferior colliculus is part of a neural circuit for startle amplitude reduction by auditory prestimuli.

Acoustic Stimulation↗
PubMed1984

Potentiation of cold swim stress analgesia in rats by diazepam.

It was hypothesized that diazepam (DZP) would attenuate the analgesia produced by cold swim stress because of its anxiolytic and biochemical anti-stress properties. In fact, it had the opposite effect. Administered alone, neither DZP nor its vehicle affected the nociceptive thresholds of rats, as assessed by a flinch-jump test. In combination with cold swim stress, DZP elevated nociceptive thresholds significantly more than did the stressor alone. This was true whether DZP was injected before or after exposure to the stressor, or whether or not DZP administration was acute or chronic.

Analgesia↗
PubMed1982

Optic nerve regeneration in goldfish under light deprivation.

Regeneration following bilateral optic nerve crush was studied in groups of goldfish housed either on a standard diurnal cycle or under total light deprivation. Unoperated fish were included in each deprivation condition. Regeneration was only slightly delayed in the surgical group housed under light deprivation (68-81 days), compared to fish undergoing regeneration on the diurnal cycle (59-63 days). Visual capacity, as judged by days to meet criterion on a visual pattern discrimination task, was unrelated to deprivation condition, but significantly lessened in fish having regenerated optic nerves. These results are discussed in terms of visual acuity following optic nerve regeneration and mechanisms of axonal reconnection.

Animals↗