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J R Ison

Publications and source records attributed to J R Ison.

At least 19 recordsLinked to original sources
PubMed1992

Impoverished stimulus input does not simulate the slowed visual kinetics of retinal damage.

In the rat with normal sight, the acoustic startle reflex to a sound burst is suppressed when the sound is preceded by a brief light pulse. This effect of light in the rat with retinal damage is reduced and peak suppression is seen at a greater delay. Both observations are expected consequences of the loss of visual sensitivity that should accompany photoreceptor loss. However, in an early stage of retinal damage, the peak of the suppressive effect is so delayed that at long lead times the light flash is a more effective stimulus in the rat with the damaged retina than in the normal rat. Two experiments tested the hypothesis that this crossing over of the two groups is a secondary consequence of a nonspecific loss of visual sensitivity in the visually impaired rat. If the hypothesis is correct, reductions in the intensity or duration of the light flash and the degree of dark adaptation should model the effect in normal rats. The overall amount of reflex suppression was diminished with these manipulations, but none diminished the temporal development of reflex suppression to a degree sufficient to produce the paradoxical crossover effect characteristic of retinal damage. These data indicate that decrements in the speed of visual processing are not secondary to the changes in sensitivity that accompany retinal damage, but should be viewed as a separate and independent form of visual impairment.

Animals↗
PubMed1991

Echoic memory in the rat: effects of inspection time, retention interval, and the spectral composition of masking noise.

Memory for tones (1100 vs. 2330 Hz) was studied in 4 rats (Rattus norvegicus), as affected by the durations of both target tones (30 to 620 ms) and noise-filled retention intervals (0 to 480 ms). With a 0-ms delay, performance was near asymptotic with the 30-ms tone, but the memory of this brief tone suffered a massive decrement at retention intervals as brief as 60 ms; in contrast, memory for the 340-ms tone was stable for at least 240 ms. If the retention interval was filled by band-stop noise (with targets presented in the spectral gap), then the rat's memory for brief tones was superior to that obtained with the standard broad-band noise filler, and band-stop noise was better than a band-pass noise that had the tones embedded in the region of its spectral energy. These findings are consistent with the hypotheses that auditory memory in the rat consists of a transient sensorylike echoic store and a short-term store more resistant to the effects of retroactive interference.

Animals↗
PubMed1991

Temporal resolution of gaps in noise by the rat is lost with functional decortication.

In Experiment 1 (n = 8), the rat's ability to detect brief gaps in white noise was measured by gap-produced inhibition of an acoustic startle reflex, elicited 100 ms after the gap. After bilateral application of KCl to the cortex, gaps as long as 15 ms provided no reflex inhibition; in contrast, the inhibitory threshold was between 2 and 4 ms in the saline control condition. In Experiment 2 (n = 13), noise pulses of 40, 50, or 70 dB were presented 20-500 ms before the startle stimulus, and in Experiment 3 (n = 5) noise offsets occurred so that the startle stimulus was presented at the end of a 2-30-ms gap. Noise pulses and offsets both inhibited reflex expression equally in saline- and KCl-treated animals. Differences between the normal (saline) functions of noise offsets and gaps suggest additional sensory processing with the longer lead time. The loss of gap sensitivity after KCl application indicates that gap processing, unlike pulses and offsets, depends on cortical mechanisms.

Animals↗
PubMed1991

Modulation of noise-potentiated acoustic startle via the benzodiazepine--gamma-aminobutyric acid receptor complex.

Diazepam (DZ), an anxiolytic benzodiazepine (BZD) compound, attenuated the facilitation of the acoustic startle response by background noise. In Experiment 1, using a cumulative dosing paradigm, the effect of DZ on noise potentiation was found to be dose related. In Experiment 2, using a between-animals exposure design, the effect of DZ on noise potentiation was attenuated by coexposure to the central-type BZD receptor antagonist RO 15-1788, which itself was without effect. Using a cumulative dosing design in Experiment 3, RO 15-1788 was found to reverse the effect of DZ, whereas the peripheral-type BZD receptor ligand RO 54864 was without effect. The differences in the effect of cumulative exposure versus single dose exposure to RO 15-1788 were interpreted as indicative of either an intrinsic effect of the antagonist after repeated exposure or an influence of background noise itself on the BZD-gamma-aminobutyric acid receptor complex.

Acoustic Stimulation↗
PubMed1991

Potentiation of acoustic startle behavior in the rat (Rattus norvegicus) at the onset of darkness.

In Experiment 1 (N = 8), a 20-ms light pulse, given at various times before a noise burst, inhibited reflex expression with a single trough at a lead time of 70 ms, whereas a dark pulse facilitated the reflex with two peaks at 40 and 160 ms. In Experiment 2 (N = 18) facilitation by dark onset had a single peak, and inhibition by light onset a single trough; thus, the double peak of the dark pulse may result because inhibition from light onset at the end of the dark pulse was briefly impressed on the facilitatory effect of dark onset. In Experiment 3 (N = 12), diazepam (2.5 mg/kg, but not 1 mg/kg) eliminated dark facilitation but not light inhibition. These diazepam data reveal a basic similarity, perhaps identity, of the mechanisms responsible for the effect of dark onset and those producing reflex facilitation by Pavlovian fear conditioning and prolonged background noise, because all are moderated by a GABAergic system.

Animals↗
PubMed1991

Intraretinal grafting restores visual function in light-blinded rats.

In seeing rats light flashes inhibit acoustic startle reflexes at short lead times. In contrast, visually impaired (light-blinded) rats show an early phase of exaggerated reflex expression, revealing the presence of pathological visual processing, and then an aberrant late phase of delayed inhibition. Grafting fetal retinal cells into the damaged retina entirely removed reflex facilitation and restored a modest degree of properly timed and statistically significant reflex inhibition. This restoration of visually-mediated behaviour, observed in two independent groups, reveals that intraretinal grafts provide useful information to blinded hosts.

Acoustic Stimulation↗
PubMed1990

Facilitation and inhibition of the human startle blink reflexes by stimulus anticipation.

The cutaneous eyeblink has 2 electromyographic components, 1 unilateral and early (R1) and 1 bilateral and late (R2), which are served by different neural pathways. These 2 reactions were measured when the eliciting stimulus was expected or relatively surprising. Forewarning was varied in 3 ways: Subjects received notice that the stimulus was about to occur on some trials (Experiment 1); delivered the stimulus to themselves on some trials (Experiments 2 & 3); or experienced a series of trials in which a tone was paired with the eliciting stimulus, followed by tone-alone trials interspersed with test trials (Experiment 4). In each case, forewarning enhanced R1 amplitudes while depressing R2 but reduced the latency of both components. This mixed pattern of effects reveals that the preparatory state provoked by forewarning focuses excitatory and inhibitory processes simultaneously on different reflex pathways: inhibition central and excitation peripheral.

Adult↗
PubMed1990

Inhibition of the cutaneous eyeblink reflex by unilateral and bilateral acoustic input: the persistence of contralateral antagonism in auditory processing.

The eyeblink reflex elicited by a cutaneous stimulus is inhibited by weak auditory stimuli that are heard just before the blink. It has been shown that monaural prestimuli produce more reflex depression than binaural prestimuli do, suggesting that reflex modification is sensitive to the outcome of antagonistic connections between contralateral auditory inputs. We examined the time course of this antagonism by giving unilateral versus bilateral pairs of noise pips 100 msec before the reflex eyeblink, with the noise pips separated by 0, 1, 4, or 8 msec. Unilateral stimuli were more effective in every condition, but their advantage diminished with increased delay between the two components. The extended bilateral and unilateral trends of increasing reflex depression with increased delay meet at about 15 msec; if this extrapolation is valid, 15 msec represents the upper limit on this system's retention of the location of a brief noise impulse. The rate of convergence of the two temporal functions reflects the decay of the antagonistic effect of one noise on its contralateral counterpart.

Adult↗
PubMed1990

Spectral frequency and the modulation of the acoustic startle reflex by background noise.

The rat's (Long-Evans) acoustic startle reflex to a high-frequency tone burst (10.5 kHz) was depressed by intense high-frequency band-pass noise (8-16 kHz) but enhanced by low frequency noise (1-2 kHz). However, contrary to the hypothesis that the depression of startle in intense background noise is produced by sensory masking, the reflex to a low-frequency tone burst (at 1 kHz) was depressed by both high- and low-frequency band-pass noise. Two additional hypotheses are offered to supplement sensory masking in order to explain the asymmetry in these data. The first is that the intratympanic reflex, which acts as a high pass filter on acoustic input, is elicited in intense backgrounds. The second is that acoustic startle reflexes elicited by intense low-frequency tones are in part elicited by their high-frequency distortion products and that these distortion products are then masked by high-frequency background noise.

Animals↗
PubMed1989

The acoustic startle response and disruption of aiming: I. Effect of stimulus repetition, intensity, and intensity changes.

Three experiments examined the disruption of perceptual motor performance by intense noise bursts. Subjects aimed a rifle at a fixed target for 15-s periods separated by 15 s of rest. This cycle was repeated 30 times in each of two series separated by a 15-min rest, each series containing five noise bursts. The noise bursts disrupted aiming for 1-2 s, an effect that increased with sound pressure level for 110, 120, and 130 dB stimuli. There was no difference between stimuli with energy centered on 250 Hz as opposed to 800 Hz. The effect diminished over the five bursts within the first series (but not to zero) and did not recover in the 15-min rest period. Some subjects received three days of testing; in these cases the effect of the noise bursts partially recovered after rest intervals of 24 hrs and then seven days. Other subjects received 15 trials with 110-dB stimuli, then five more trials with 130-dB stimuli. The disruption of aiming by 130 dB stimuli was not reduced by prior exposure to 110-dB stimuli.

Adult↗
PubMed1989

The acoustic startle response and disruption of aiming: II. Modulation by forewarning and preliminary stimuli.

Four experiments examined the disruption of rifle aim by intense noise bursts. In Experiment 1 a trigger pull was followed occasionally by a noise burst. Aiming was disrupted for 1-2 s, an effect that habituated within days and recovered between days. Expected stimuli were less disruptive than were unexpected stimuli. Experiment 2 demonstrated that weak auditory prestimuli 100 ms before unexpected intense sounds also reduced noise-produced errors. Experiment 3 showed that the intratympanic reflex had not played a protective role in this effect. Experiment 4 showed that a weak tactile prestimulus increased both a muscular measure of the acoustic startle reaction and the perturbing effect of the noise burst on motor performance. In general, conditions that affect the amplitude of the acoustic startle reflex similarly influence the disruptive effect of a noise burst on motor performance, but the two measures are not correlated in the detail necessary to suggest a causative relationship.

Adult↗
PubMed1986

Visual function measured by reflex modification in rats with inherited retinal dystrophy.

Developmental changes in visual function were studied in the Royal College of Surgeons (RCS) rat with inherited retinal degeneration by examining the inhibition of acoustic startle reflexes by visual prestimuli. Compared with a congenic strain of nondystrophic rat, the RCS rats showed an increase in the interstimulus interval between the inhibitory prestimulus and the eliciting stimulus that produced maximal inhibition, a result suggesting a decrease in the speed of processing. The amount of inhibition also decreased over time, which suggests a progressive loss of visual function. Simultaneous presentation of auditory and visual prestimuli was used to demonstrate that the changes in inhibition were related to alterations in visual function and that auditory function was not impaired in these rats. The results show that reflex modification is a suitable test for evaluating visual dysfunction in rats.

Acoustic Stimulation↗
PubMed1985

Cutaneous and auditory function in rats following methyl mercury poisoning.

Rats were given a total dose of 50 mg/kg (Exp. 1), 13.3 or 40 mg/kg (Exp. 2), or 40 mg/kg (Exp. 3) of methyl mercury chloride subcutaneously over a course of 5 days. At varying times after the toxic exposure, up to 1 year, their sensory functioning was assessed by reflex modulation methods: stimuli of interest were presented just before an intense tone which elicited the startle reflex, and stimulus reception was measured by the inhibitory control of the stimuli over the amplitude of the reflex. In Experiment 1 cutaneous prestimuli (electric shock to the tail) and brief acoustic transients (silent periods in noise) were less effective inhibitors of reflex activity in poisoned animals, compared to controls, indicating that the poisoned animals had impairments in cutaneous sensitivity and audition. In Experiment 2 the time course of sensory loss and subsequent recovery was studied. Impaired auditory function was shown further by a deficit in the effectiveness of weak noise pulses, and, in addition, the cutaneous deficit for weak tail shocks was accompanied by an exaggerated or hyperpathic response to more intense tail shocks. Experiment 3 confirmed the finding that the loss of sensitivity to weak shock was accompanied by an enhancement of the response to more intense shock. These data were related to peripheral neuropathy and shown to be analogous to certain clinical symptoms of Minamata disease reported in humans.

Acoustic Stimulation↗
PubMed1985

Impairment in auditory and visual function follows perinatal viral infection in the rat.

Acoustic startle reflexes are elicited by intense tone bursts but inhibited if weak bursts precede reflex elicitation. Rats were infected by intracerebral inoculation with lymphocytic choriomeningitis virus (LCMV) at birth. Compared to control animals, infected animals had higher elicitation and inhibition thresholds and showed recruitment at intense stimulus levels. Histopathology revealed both cochlear and retinal degeneration. Like some infectious agents in humans, perinatal exposure to LCMV in the rat yields a severe polysensory neuropathy.

Animals↗
PubMed1985

Genetic differences in avoidance learning by Rattus norvegicus: escape/avoidance responding, sensitivity to electric shock, discrimination learning, and open-field behavior.

The behaviors of rats selectively bred for either good or poor shuttle box avoidance learning were studied. The results of Experiment 1 indicated that the phenotypic difference in avoidance learning is not associated with differences in speed of escape or avoidance responding. Differences between the lines in frequency of intertrial responses (ITRs), which appear during training but not during pretest, suggest that ITRs in animals of the low-avoidance (SLA) line are more suppressed by electric shock than in animals of the high-avoidance (SHA) line. This result suggests that SLA animals may be more emotionally responsive than SHA animals. Experiment 2 demonstrated that the animals of the two lines do not differ in absolute sensitivity to electric shock, and Experiment 3 showed that the poor performance of the SLA line is not due to an inability to learn. Experiment 3 also provided evidence which suggests that the poor avoidance learning by SLA animals is due to their emotional reactivity. Observations of open-field behavior in Experiment 4 are consistent with this hypothesis. The major consistent correlate of the phenotypic difference in avoidance learning is greater emotionality or emotional reactivity in SLA than in SHA animals.

Animals↗
PubMed1979

Development of the acoustic startle response in the rat: ontogenetic changes in the magnitude of inhibition by prepulse stimulation.

Three experiments examined the development of the acoustic startle reflex and its modification by a preliminary stimulus in the infant rat during the 2nd and 3rd postnatal weeks. The 1st experiment employed a white noise S1 (20 msec, 70 dB), the 2nd a cutaneous S1 (.5 msec, .5 mA and 1.0 mA shock), and the 3rd identical S1-S2 pairs (20 msec, 10 kHz, 110 dB tones). The results demonstrate a similar maturation of the prepulse modification pattern over days in the 3 experiments, evidenced mainly in the growth of inhibition. The findings indicate peripheral and central mechanisms that are maturing during the period of life under observation and that contribute to the developmental patterns of modification.

Acoustic Stimulation↗
PubMed1979

Conditioning auditory stimuli and the cutaneous eyeblink reflex in humans: differential effects according to oligosynaptic or polysynaptic central pathways.

Electromyographic activity of orbicularis oculi muscles in humans was elicited by percutaneous electrical stimulation of the supraorbital brahcn of the trigeminal nerve. The reflex consists of an early brief ipsilateral R1 and a later prolonged consensual R2. The threshold for R1 was considerably elevated compared to that of R2. In one experiment brief acoustic stimuli, at 70 dB SPL, were presented at various intervals, from 5 to 800 msec, prior to the eliciting stimulus. In a second experiment similar stimuli, with intensities varying from 30 to 70 dB SPL, were given at the fixed lead time of 100 msec. In each experiment the preliminary acoustic stimulus enhanced R1 and depressed R2. Potentiation of R1 developed more rapidly than did depression of R2 and exhibited an early and a late peak, whereas depression had a single intermediate trough. Both effects linearly increased with increases in the intensity of the acoustic prepulse. These restuls are discussed in relation to the neuronal circuits responsible for the expression of the two reflex components.

Acoustic Stimulation↗