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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

Modulation of the acoustic startle reflex in humans in the absence of anticipatory changes in the middle ear reflex

If a weak tone precedes an intense tone, then the acoustic startle eyeblink reflex elicited by the stronger stimulus is inhibited. It has been suggested that the leading stimulus gives rise to a protective middle ear reflex that attenuates the effective intensity of the second. This hypothesis was tested and disproved. In seven subjects intense tone bursts sufficient to elicit both intratympanic and eyeblink responses were presented sometimes alone and sometimes preceded at various lead times (25 to 400 msec) by a weak tone. The weak tone inhibited the amplitude of the eye blink to the strong tone, maximally at intervals of 100 to 200 msec, but was never seen to produce any of the anticipatory impedance changes that would be characteristic of middle ear reflex activity during the interval between the two stimuli.     

Effect of prior exposure to a lithium- and an amphetamine-paired flavor on the acoustic startle response in rats

The experiments reported here evaluated the hypothesis that an amphetamine-paired flavor elicits conditioned fear-arousal, whereas a lithium-paired flavor elicits conditioned nausea-disgust by examining the effect of prior flavor exposure on an acoustic startle reaction (ASR). Exposure to a lithium-paired flavor by intraoral infusion, either immediately prior to a startle session (Experiment 1) or during a startle session (Experiments 2 and 3), resulted in a blunted ASR. In contrast, intraoral infusion of an amphetamine-paired flavor resulted in a potentiated ASR. The blunted ASR produced by exposure to a lithium-paired flavor dramatically reversed to a potentiated ASR when rats were pretreated with the antiemetic drug ondansetron prior to the saccharin-lithium pairing (Experiment 3). The findings shed light on a mechanism by which rewarding drugs produce conditioned taste avoidance in rats.