Sensitization of the acoustic startle reflex by footshock.

Administration of footshock (500-ms duration, 0.2–2.4 mA) increased the amplitude of the startle reflex for a long time after its presentation. The effect occurred with a single footshock, although its magnitude and consistency across animals were greater with 5 or 10 footshocks presented 1/s. The facilitatory effect came on within 2–4 min with a 0.6-mA shock, peaking in about 10 min and then dissipating over the next 40 min. Stronger shocks also increased startle, but with a more delayed onset of facilitation (8–20 min). Footshocks increased startle in rats not previously given startle-eliciting stimuli, indicating sensitization rather than dishabituation. The facilitatory effect may not be attributable to a rapid conditioning to the experimental context, because a change in lighting conditions from shock presentation to testing did not attenuate shock sensitization. This excitatory effect of shock on startle may represent the unconditioned effect of shock that can become associated with a neutral stimulus to support classical fear conditioning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Reflex-inhibiting stimuli and the refractory period of the acoustic startle reflex in the rat.

Previous studies show that if acoustic startle stimuli are presented in pairs, then the reaction to the 2nd stimulus (S2) is reduced, with the size of the refractory decrement determined by the interstimulus interval and the relative intensity of the 1st stimulus (S1). If a neutral stimulus (p) is presented just prior to S1, then the reaction to S1 is similarly inhibited, revealing the phenomenon of prestimulus inhibition. In 2 experiments with male albino Holtzman rats (N = 24) it was found that suppression of the reflex to S2 by S1 was unaffected by prestimulus inhibition of S1 (i.e., reflex amplitudes associated with S2 were identical in pS1-S2 series and S1-S2 series). In contrast, a reduction in the intensity of S1 relative to S2 did reduce the effect of S1 on S2. These data indicate that prestimulus inhibition of the reflex to S1 does not result because the preliminary stimulus attenuates the sensory impact of S1. The inhibitory process may be presumed to have a central locus. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Modification of the rat's startle reaction by termination of antecedent acoustic signals.

Conducted 4 experiments with 24 male albino rats relating inhibition and facilitation of the startle response, elicited by an intense auditory stimulus, to the offset of a 70-db continuous acoustic signal. Data indicate that if the antecedent signal terminated 10-1000 msec before the startle-eliciting stimulus, the amplitude of the startle response was reduced. If offset occurred less than 10 msec prior to the startle-eliciting stimulus, the response latency was reduced. Results are consistent with previous research employing weak antecedent acoustic signal onset. The overall configuration of the results suggests that activity in brain centers mediating the startle reflex may be an early component of the orienting reflex arc. (19 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Modification of the rat's startle reaction by an antecedent change in the acoustic environment.

Conducted 3 experiments with 6 male albino rats each in which inhibition and facilitation of the startle response, elicited by an intense auditory signal, was related to a change of the frequency characteristic of a 70-db continuous acoustic signal. Data indicated that if a frequency change occurred in the acoustic environment 64 msec before the startle-eliciting stimulus, the amplitude of the startle response was reduced; if frequency change occurred 4 msec prior to the startle-eliciting stimulus, the response latency was reduced. Results extend the generality of previous research employing weak antecedent acoustic signal onset and offset. Results indicate that neural mechanisms mediating the startle reflex may be activated by any change in the acoustic environment and that these mechanisms may be a component of the orienting reflex arc. (21 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Temporal integration in the acoustic startle reflex of the rat.

Exposed 6 male albino rats to 6,900 Hz tone pulses with durations of .25-64 msec. and intensities of 80-125 db. re .0002 dyne/cm2. Startle amplitudes increased with duration in a manner suggestive of an exponential function distorted by the failure of the auditory system to reflect faithfully prolonged intense sounds. 5 other male albino rats were exposed to pairs of 1-msec pulses at 125 db., having interpulse intervals ranging 1-11 msec. For pulses separated by 3 msec. or more, response amplitudes demonstrated a decaying exponential summation function with a time constant of 3 msec. Results are in accord with established principles of reflex function and organization. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

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 (8–26 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-freqency 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. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Conditioned brain-stimulation reward attenuates the acoustic startle reflex in rats.

The acoustic startle reflex (ASR) in rats is attenuated by a light paired with food or, in humans, by "pleasant" pictures. Rats were trained to barpress for lateral hypothalamus (LH) stimulation. ASR amplitudes were then measured at 4 intensities, with or without a light. Control rats that did not receive brain-stimulation reward (BSR) showed initially lower ASR amplitudes than did rats exposed to BSR, but both groups responded similarly with or without light. Next, experimental rats were given BSR in the presence of light but not in its absence. After conditioning, ASR amplitudes were reduced, and ASR thresholds were raised by a mean of 2.6 dB in the light but remained at preconditioning levels without light. No such change was found for control rats or rats with placements outside the LH. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Olfactory bulbectomy enhances sensitization of the acoustic startle reflex produced by acute or repeated stress.

The effects of olfactory bulbectomy on the acoustic startle reflex and shock-induced sensitization of the startle reflex were examined in 3 experiments. In Experiment 1, bulbectomized animals showed a modest increase in baseline startle responding following surgery, and normal acquisition of fear-potentiated startle, but a pronounced increase in baseline startle responding during the course of conditioning relative to sham-operated controls. In Experiments 2 and 3, bulbectomized animals showed shock-induced sensitization of the startle reflex to shock intensities that did not produce sensitization in sham and unoperated controls. These data suggest that olfactory bulbectomy results in an increased vulnerability to stressors, which may be mediated by a disinhibition of the amygdala or other structures involved in mediating stress and anxiety. Thus, the olfactory bulbectomy model of depression may share some similarities with other stress-induced models of depression. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

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 explicitly 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. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Modulation of the acoustic startle reflex by infusion of corticotropin-releasing hormone into the nucleus reticularis pontis caudalis

The amplitude of the acoustic startle reflex can be modulated by exposure to aversive stimuli or other conditions which evoke a state of fear. The neurotransmitters involved in this modulation are currently being investigated. Unilateral local infusion of corticotropin-releasing hormone (CRH; 0, 10, 20, 40 and 80 ng) into the nucleus reticularis pontis caudalis (PnC), an obligatory synapse in the acoustic startle reflex, significantly elevated startle amplitude in a dose-dependent manner. The facilitation of startle began immediately following infusion, reached asymptote approximately 20-25 min later, and persisted throughout the remaining 60 min test session. This CRH-enhanced startle effect was blocked by infusion of the CRH antagonist, alpha-helical CRH9-41, immediately prior to CRH infusion. These results support an involvement of CRH at the level of the PnC in modulating the acoustic startle reflex.     

Lesions of the bed nucleus of the stria terminalis block sensitization of the acoustic startle reflex produced by repeated stress, but not fear-potentiated startle

1. The effects of lesions of the bed nucleus of the stria terminalis (BST) on the acquisition of conditioned fear were examined. In Experiment 1, BST lesions did not block acquisition of fear-potentiated startle to an explicit visual conditioned stimulus (CS) over 20 days of training. However, BST lesions blocked a gradual elevation in baseline startle also seen over the course of training. 2. The gradual increase in baseline startle was replicated in Experiment 2 without the presence of an explicit CS, using unoperated subjects. Experiment 2 showed that the elevation was due to repetitive exposure to shock, because unshocked control subjects did not show any elevation over sessions. 3. In Experiment 3, lesions of the BST did not disrupt rapid sensitization of the startle reflex by footshock, showing that different neural substrates underlie sensitization of startle by acute and chronic exposure to footshock. 4. These data indicate that the BST, despite its anatomical continuity with the amygdala, is not critically involved in the acquisition of conditioned fear to an explicit CS. Nevertheless, the BST is involved in mediating a stress-induced elevation in the startle reflex. This suggests that the BST and the CeA, which constitute part of the "extended amygdala" have complementary roles in responses to stress.     

Enhancement of acoustic startle by electrical stimulation of the amygdala.

The present study demonstrated that electrical stimulation of the amygdala enhanced the acoustic startle response. A 25-ms train of 0.1-ms pulses initiated 5 ms before the onset of a 20-ms noise burst significantly increased startle at currents from 40 to 400 μA. Electrode placements just medial to the amygdala (in the pathway connecting the amygdala to the brain stem) increased startle with the lowest currents. Startle was also increased in all animals with stimulation in the central, medial, and intercalated nuclei of the amygdala. Stimulation in areas surrounding the amygdaloid complex was ineffective. In a second experiment, paired pulses with interpulse intervals between 0.1 and 20.0 ms delivered to the amygdala demonstrated that the stimulated axons had a distribution of refractory periods between 0.6 and 1.0 ms. This suggests that the population of neurons which subserves the enhancement of acoustic startle is fairly homogeneous and has small, myelinated axons. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Emotion, attention, and the startle reflex.

This theoretical model of emotion is based on research using the startle-probe methodology. It explains inconsistencies in probe studies of attention and fear conditioning and provides a new approach to emotional perception, imagery, and memory. Emotions are organized biphasically, as appetitive or aversive (defensive). Reflexes with the same valence as an ongoing emotional state are augmented; mismatched reflexes are inhibited. Thus, the startle response (an aversive reflex) is enhanced during a fear state and is diminished in a pleasant emotional context. This affect–startle effect is not determined by general arousal, simple attention, or probe modality. The effect is found when affects are prompted by pictures or memory images, changes appropriately with aversive conditioning, and may be dependent on right-hemisphere processing. Implications for clinical, neurophysiological and basic research in emotion are outlined. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Circadian modulation of the rat acoustic startle response.

The acoustic startle response (ASR) of male rats was measured during several sessions over a 24-hr period in both a light–dark cycle and a constant-dark condition. Each session consisted of 10 trials each at 80, 90, 100, 110, and 120 dB white noise. The results indicate robust daily and circadian modulation of ASR amplitude that consist of an approximately 2-fold nocturnal increase at eliciting-stimuli intensities above 80 dB. Similar results were observed in female rats in constant-dark conditions. To determine whether daily changes in auditory thresholds were responsible for the observed modulation, ASR reflex modification procedures were used. These procedures were designed to measure auditory thresholds at frequencies of 10 and 40 kHz at several times of day. The results suggest a lack of significant circadian differences in auditory thresholds at these frequencies. This study demonstrates a novel role of the rat circadian system in the modulation of ASR amplitude. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Affective individual differences and startle reflex modulation.

Potentiation of startle has been demonstrated in experimentally produced aversive emotional states, and clinical reports suggest that potentiated startle may be associated with fear or anxiety. To test the generalizability of startle potentiation across a variety of emotional states as well as its sensitivity to individual differences in fearfulness, the acoustic startle response of 17 high- and 15 low-fear adult Ss was assessed during fear, anger, joy, sadness, pleasant relaxation, and neutral imagery. Startle responses were larger in all aversive affective states than during pleasant imagery. This effect was enhanced among high fear Ss, although follow-up testing indicated that other affective individual differences (depression and anger) may also be related to increased potentiation of startle in negative affect. Startle latency was reduced during high- rather than low-arousal imagery but was unaffected by emotional valence. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Circadian modulation in the rat acoustic startle circuit.

The acoustic startle reflex (ASR) in rats exhibits robust circadian modulation, with ASR amplitudes greater during subjective night. To identify the location of this modulation, startle reactions were evoked either acoustically or electrically via electrodes implanted in the primary ASR circuit. Startle amplitudes were compared at different times in the circadian cycle. In constant environmental conditions, startle amplitudes were greater in subjective night for acoustically evolved and for electrically evoked reactions from the ventral lateral lemniscus and medial longitudinal fasciculus. The results show that at least 1 site of circadian modulation must occur at some point in the circuit after the last brainstem synapse in the caudal pontine reticular formation, at the level of spinal interneurons or motoneurons or at the neuromuscular junction. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Attention and schizophrenia: Impaired modulation of the startle reflex.

The startle reflex (SR) elicited by abrupt stimuli can be modified by attention to nonstartling stimuli that shortly precede the startle-eliciting stimulus. The present study of 15 recent-onset, relatively asymptomatic schizophrenic outpatients and 14 demographically matched normal control Ss demonstrated that attentional modulation of SR is impaired in schizophrenic patients. Specifically, the control group exhibited greater startle eye-blink modification following to-be-attended prestimuli than following to-be-ignored prestimuli, whereas the patients failed to show the attentional modulation effect. These results suggest traitlike attentional deficits in schizophrenia because the patients were relatively asymptomatic. The measurement of attentional modulation of SR may provide a nonverbal, reflexive, state-independent marker of the vulnerability to schizophrenia. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Protection against impulse-type industrial noise by utilizing the acoustic reflex.

"This experiment was designed to investigate the practicality of externally eliciting the acoustic reflex to protect the ear from industrial impulse noise. Ten subjects were exposed to 100 impacts of the recorded noise of a mechanical drop hammer during a 10-minute period. The noise was presented at a 120-db. average SPL. Subjects listened to the same noise under three conditions… . eliciting the acoustic reflex prior to an impact may be an effective means of protecting the ear against industrial impulse noises. The advantages of AR protection over protection provided by earplugs are discussed." (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Facilitation and inhibition of the acoustic startle reflex in the rat after a momentary increase in background noise level

Small increments in background noise were shown to increase the amplitude of a subsequently elicited acoustic startle reflex (ASR) in rats by as much as 100% under optimal conditions. Increment lead time (5-160 ms) and level (1.5-15 dB), initial noise level (30-70 dB), startle level (95-125 dB), number of test days (1-5), and drug condition (diazepam or saline ip) were varied in 6 experiments. Prepulse facilitation (PPF), measured by difference scores, was greatest for intermediate increments (3 dB) and lead times (20-40 ms) and was replaced by prepulse inhibition (PPI) for higher values, especially in the later test days. Diazepam reduced baseline ASR and diminished PPI, but it did not affect PPF. These data argue against hypotheses that attribute PPF of this sort to either temporal integration within the ASR pathways or to the elicitation of a nonspecific arousal reaction by the prepulse.     

Effects of inferior colliculus lesions on the acoustic startle response.

"Nonspecific" electrolytic lesions (with respect to subdivision) of the mouse inferior colliculus (IC) resulted in the attenuation of acoustic startle response (ASR) amplitudes of the 1st postoperative day, but ASR amplitudes increased to above baseline levels 1 wk later. Lesions of the IC central nucleus (CN) also attenuated ASR amplitudes on the 1st postsurgery day, but startle amplitudes recovered to baseline levels 1 wk after surgery. Lesions of the IC lateral nucleus (LN) or dorsal cortex (DC) resulted in elevation of startle amplitudes above baseline 7 days after surgery and produced enhanced ASR amplitudes to repeated stimuli. 14 days after the surgery, lesion effects on startle amplitudes remained the same as those on Day 7 for each lesion condition. The present findings implicate the ICLN and ICDC as inhibitory modulators of the ASR, but indicate only a minor role for the ICCN. (PsycINFO Database Record (c) 2010 APA, all rights reserved)