Modification of the rat's acoustic startle response by antecedent visual stimulation.

Male hooded and albino rats were exposed to a light flash followed at various temporal intervals by a startle-eliciting 117 db. (re 20 muN/m2) burst of white noise. The visual stimulus engendered startle response inhibition (maximally when the lead time was 64-250 msec) as well as startle response latency reduction (maximally when the lead time was 2-8 msec). The temporal functions for the effects of visual stimuli paralleled those previously reported for startle modification by acoustic events. Further study revealed that, given optimal lead times, inhibition is produced reliably by weaker visual stimuli (3 X 10-6 cd-sec/cm2) than latency reduction (3 X 10-4 cd-sec/cm2). This differential sensitivity to visual stimuli is also analogous to previously reported findings for events in the acoustic environment. It reveals that the neural mechanisms that mediate latency reduction and inhibition can be engaged by either acoustic or visual stimulation.     

Modification of the human glabella reflex by antecedent acoustic stimulation

The eyeblink elicited by a mechanically produced tap to the glabella was inhibited by a 50-msec, 80-dB SPL tone presented in the interval 50 to 800 msec prior to the tap, but maximal inhibition occurred when the lead interval was 100 msec. At this lead interval, the amount of inhibition was an increasing function of prestimulus intensity, but reliable inhibition was detected when prestimulus intensity was only 30 dB SPL. With a given inhibitory prestimulus, the amount of inhibition was independent of the intensity of the blink-eliciting tap. Monaural presentation of a prestimulus was found to produce more inhibition than the binaural presentation of that same prestimulus. The offset of an otherwise continuous binaural acoustic signal 100 msec prior to a tap inhibited the eyeblink, but more inhibition was found when offset occurred in only one ear.     

Potentiation of the acoustic startle response by a conditioned stimulus paired with acoustic startle stimulus in rats

The hypothesis that the standard acoustic startle habituation paradigm contains the elements of Pavlovian fear conditioning was tested. In a potentiated startle response paradigm, a startle stimulus and a light conditioned stimulus (CS) were paired. A startle stimulus then was tested alone or following the CS. Freezing behavior was measured to index conditioned fear. The startle response was potentiated on CS trials, and rats froze more in CS than in non-CS periods. In Experiment 1, response to a previously habituated, weak startle stimulus was potentiated. In Experiment 2, response to the same stimulus used as the unconditioned stimulus (US) in training was potentiated. This CS-potentiated response retarded the course of response decrements over training sessions as compared with an explictly unpaired control group. Conditioned fear is a standard feature of this habituation paradigm, serves to potentiate the startle response, and provides an associative dimension lacking in the habituation process per se.     

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.     

Measurement of acoustic startle response in mice

Apparatus for measurement of acoustic startle response in mice is described. The technique utilizes a spring suspended lever, commercially available strain-gauge transducer, and polygraph. Individual startle responses are recorded as upward (flexion) and downward (extension) pen deflections, the force of either component being linearly related to the amplitude of the vertical pen deflections. The apparatus, with minor modifications, may be used to measure startle responses in larger rodents.     

Inhibition of acoustic startle using different mechanoreceptive channels

In this experiment, we investigated the impact of vibrotactile prepulse frequency and intensity on the acoustically elicited startle response in humans. Mechanoreceptive channels differing in their sensitivity to transient stimulation have been identified in the skin. The Pacinian channel is optimally sensitive to vibrations at approximately 300 Hz and is specialized for the detection of stimulus transients, whereas the non-Pacinian I and III channels are optimally sensitive to vibrations at approximately 30 Hz. Vibrotactile prepulses with frequencies of 30 and 300 Hz and intensities of 95 and 130 mV were presented for 50 msec to the dominant hand of college students (N = 31), followed on some trials by a 95-dB broadband acoustic startle stimulus. The 300-Hz prepulses resulted in significantly more pronounced inhibition of startle magnitude, amplitude, and probability, whereas only the 30-Hz prepulses significantly facilitated blink latency. These results support the idea that the inhibition of acoustic startle is determined more by transient than by sustained aspects of vibrotactile prepulse stimuli. This study also demonstrates that different aspects of the startle response differentially reflect stimulus characteristics of the prepulse.     

Similar effects of attention directed to acoustic and tactile stimuli on prepulse inhibition of acoustic startle

Prepulse inhibition (PPI) is assumed to index automatic and controlled processing. In three experiments (n= 32, 22, and 30) participants were asked to judge the duration of a prepulse in comparison with a stimulus presented 4000 ms before the prepulse. A distracter was presented simultaneously with the prepulse to increase the cognitive demands of the task. PPI was assessed at stimulus onset asynchronies (SOAs) of 30-150 ms, and 420 ms. The prepulse was either a tone (60 dB) or a tactile stimulus (21 kPa), and startle was elicited by 95 dB white noise. Directing attention to the prepulse increased PPI at SOAs of 60 ms and longer in all experiments, but the sensory modality to which attention was directed played only a minor role. We conclude that directing attention to both acoustic and tactile prepulses increased PPI.     

Electrolytic,but not neurotoxic,lesions to the lateral tegmental tract increase acoustic startle amplitude and reduce startle stimulus-induced freezing

Startle amplitude and startle stimulus-induced freezing (an index of fear) were measured in a standard acoustic startle response (ASR) paradigm in male Sprague-Dawley rats. Groups with electrolytic lesions to the lateral tegmental tract (LTG) or with axon-sparing lesions to the area around LTG made with the neurotoxin NMDA were compared with vehicle-injected or sham operated control groups on these response measures. Replicating previous results (Leaton & Brucato, 2001), electrolytic lesions to LTG significantly reduced freezing and produced a persistent 300% increase in ASR amplitude compared with all other groups. The NMDA lesions had no effect on freezing or on ASR amplitude compared with the controls. In additional testing the rats with electrolytic lesions to LTG did not differ from controls in the acquisition or retention of context freezing using a footshock unconditioned stimulus. The data made a small, but necessary, step in further clarifying two pathways that modify ASR. The source of the descending pathway that provides tonic inhibition of the sensory input to the ASR circuitry is not within the LTG. The ascending pathway that carries the fear-inducing dimensions of the acoustic stimulus to the amygdala by way of the medial geniculate nucleus does not have an intermediate synapse in the area within LTG.     

The role of small changes in the acoustic environment in modifying the startle reflex.

When either the intensity or frequency spectrum of an approximately 70-db. SPL narrow-band noise was abruptly changed by a small amount, the rat's response to a startle stimulus presented 64 msec later was inhibited. When similar small frequency changes preceded the startle stimulus by ony 5 msec, the latency of the startle response was reduced, but even relatively large changes in intensity of the antecedent stimulus had no effect on response latency. These findings provide added support for the generalization that the neural processes associated with startle are engaged by small changes in the auditory environment. They also point to a measure of separation between the processes responsible for inhibition and those responsible for latency shift.     

Reflex modification by acoustic signals in newborn infants and in adults

This research asked whether the reflexive eyeblink elicited by a tap to the glabella (the flat region of skin between the eyebrows) is modified by acoustic signals which either precede or accompany the tap. Five experiments employing identical reflex modification procedures on neonates and adults suggest developmental differences in processing auditory stimuli. Neonates failed to exhibit reflex inhibition by either prior acoustic or tactile stimuli. Adults exhibited robust reflex inhibition to these same stimuli. Neonates, however, exhibited reliable reflex augmentation when mild (70 dB re: 0.0002 dyne/cm2) tones were presented simultaneously with the tap. For adults, tone intensities of at least 90 dB were necessary to obtain reliable reflex augmentation. The developmental processes implied by these findings are discussed.     

Stuttering and sensory gating: a study of acoustic startle prepulse inhibition

It was hypothesized that stuttering may be related to impaired sensory gating, leading to overflow of superfluous disturbing auditory feedback and breakdown of the speech sequence. This hypothesis was tested using the acoustic startle prepulse inhibition (PPI) paradigm. A group of 22 adults with developmental stuttering were compared with controls regarding the degree of PPI. No significant differences were found between the stuttering adults and the control group; the groups showed similar means and distribution. Likewise, no relation between the degree of PPI and the effect of altered auditory feedback on stuttering was found. In summary, the results of the study indicate that there is no relation between stuttering and PPI.