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Results for “Startle Response”

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PubMed1996

NMDA receptors in the pontine brainstem are necessary for fear potentiation of the startle response.

The fear-potentiated startle model in rats is a valuable animal test for the investigation of the neural and neurochemical basis of fear. In this model, rats are trained to associate a neutral stimulus with an aversive stimulus, so that after conditioning the conditioned stimulus alone elicits a state of fear leading to an exaggerated acoustic startle response. The fear-potentiated startle model does not require instrumental responding for the indication of states of fear. The acoustic startle response is mediated by a simple brainstem circuit, with the caudal pontine reticular nucleus as an interface that receives input from startle-enhancing circuits. In the present study, we tested the hypothesis that N-methyl-D-aspartate (NMDA) receptors on neurones of the caudal pontine reticular nucleus are involved in the mediation of fear-potentiated startle. After fear-conditioning, we injected the NMDA receptor antagonist DL-2-amino-5-phosphonopentanoic acid (AP-5), into the caudal pontine reticular nucleus of awake rats and tested the effect on the expression of fear-potentiated startle. Injections of AP-5 (0.125-0.5 nmol) into the caudal pontine reticular nucleus dose dependently attenuated fear-potentiated startle without affecting the baseline amplitude of the acoustic startle response. The results suggests that, in the caudal pontine reticular nucleus, glutamate may mediate fear-potentiated startle via NMDA receptors.

2-Amino-5-phosphonovalerate↗
PubMed1990

[The startle response and epilepsy].

Startle responses (SR) are described as epileptic and non-epileptic attacks and their mechanisms are poorly understood. Long-loop reflexes and a satisfactory response to L-tryptophan treatment have only seldom been published in this condition. This prompted us to report a case with epilepsy and startle-induced tonic spasms, the latter refractory to all conventional medication except for L-tryptophan. Special emphasis is placed on the electrophysiological findings. Similar observations of non-habituation of SR in post-anoxic brain damage and in the case of startle epilepsy possibly suggest a deficit of cortical inhibition, probably in the supplementary motor area, rather than brain stem dysfunction in both instances.

Adult↗
PubMed1986

Cerebellar vermis: essential for long-term habituation of the acoustic startle response.

The acoustic startle response in rats shows both short-term habituation, which recovers in seconds or minutes, and long-term habituation, which is effectively permanent. Lesions of the cerebellar vermis significantly attenuated long-term habituation without affecting the short-term process or altering initial response levels. In this response system the cerebellar vermis is part of an essential circuit for long-term habituation.

Acoustic Stimulation↗
PubMed1992

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 twofold 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.

Acoustic Stimulation↗
PubMed1993

Effects of bilateral lesions of auditory cortex in mice on the acoustic startle response.

The acoustic startle response (ASR) was used to investigate the effects of auditory cortical lesions on a brain stem-mediated auditory behavior. The ASRs were obtained longitudinally from young adult C57BL/6J mice before bilateral ablation of auditory cortex, 1 day after ablation, and 1 month later. Control mice received lesions of nonauditory cortex. For some mice, averaged brain stem-evoked responses (ABR) were obtained, and these indicated no effects of lesions on auditory sensitivity. One month after surgery, mice with auditory cortex ablations were statistically indistinguishable from controls on all suprathreshold measures of ASR. However, 1 day after ablation of auditory cortex, experimental animals (but not controls) exhibited a change in ASR amplitude (but not threshold or latency). When a noise burst of 80 dB SPL was used to elicit the ASR, the amplitude was diminished, but with a 110 dB stimulus, amplitude was enhanced. The findings can be interpreted in one of two ways: temporary interference with modulation of the ASR normally performed by auditory cortex; or a general effect of auditory cortex ablation on brain stem auditory circuits not specific to the ASR. In any event, if auditory cortex plays a modulatory role with regard to the ASR, it is apparently nonessential and/or readily compensated for after ablation.

Acoustic Stimulation↗
PubMedDate not supplied

Effects of 6-hydroxydopamine and alpha-methyl-para-tyrosine on the acoustic startle response in rats.

The acoustic startle response was measured in rats after depletion of central catecholamines either chronically (through intraventricular injection of 6-hydroxydopamine) or acutely (through intraperitoneal injections of alpha-methyl-para-tyrosine). Chronic depletion resulted in an augmented startle response which could not be attributed to a failure of habituation or enhanced sensitization, while acute depletion depressed startle amplitude. The results were interpreted as evidence that catecholamines normally exert a facilitatory influence on the startle response and that the enhanced response seen in the chronically lesioned animal reflects the potentiation of the role of catecholamine-containing neurons through the development of denervation supersensitivity. This interpretation is consistent with other observations which suggest that catecholamines play a general role in modulating thresholds to aversive events.

Acoustic Stimulation↗
PubMed2003

Rat strain-dependent effects of repeated stress on the acoustic startle response.

Amplitude and habituation of the acoustic startle response were assessed in four recombinant inbred (RI) rat strains. One group from each strain underwent repeated restraint stress, the last session of which was 24h before startle testing while, a second group from each strain was not stressed prior to testing. Additionally, prepulse inhibition of the acoustic startle response, and anxiety behavior in the elevated plus-maze were assessed in separate, non-stressed groups of each strain. In the non-stressed condition, these RI strains differed significantly from each other on all behaviors measured. In the two RI strains that showed the greatest habituation of the startle response, repeated stress resulted in significantly lower acoustic startle amplitude than that seen in non-stressed controls of those strains. In the strains showing low levels of habituation, repeated stressed increased the level. Neither genotype-dependent levels of startle amplitude, prepulse inhibition of the startle response, nor anxiety in the plus-maze were closely related to the effect of stress on either startle amplitude or habituation. The results suggest that genotype-dependent habituation of the startle response may be important in determining whether stress will alter startle amplitude.

Acoustic Stimulation↗
PubMed2004

Effects of buspirone and alprazolam treatment on the startle-potentiated startle response.

The startle potentiated startle (SPS) paradigm has been reported to be an effective procedure for studying the conditioned enhancement of acoustic startle in the absence of electric shocks or extinction. This study examines the effects of two anxiolytic treatments, buspirone and alprazolam, on this SPS effect. Subjects were tested in the SPS paradigm 2 days a week (Monday and Thursday) for 10 weeks. Each startle test session consisted of 10 Noise Alone trials (115 dB acoustic noise burst presented for 40 ms) and 10 Light+Noise trials (115 dB acoustic stimuli presented during the latter 40 ms of a 3,540 ms period in which a 15-watt light was illuminated). Although there was no difference in startle amplitude on Noise Alone trials when compared to Light+Noise trials initially, by the end of the first test session and continuing throughout the duration of the experiment, startle amplitude on Light+Noise trials was significantly (approximately 50-75%) greater than on Noise Alone trials. After five control (i.e., no injection) SPS test sessions, once-weekly drug challenges were conducted over the course of 7 weeks. In these weekly drug challenges, subjects received acute treatment with various doses of the benzodiazepine anxiolytic alprazolam (0.25, 0.5, 1.0 mg/kg) or the novel anxiolytic buspirone (1.0, 2.0, 4.0 mg/kg); subjects also received vehicle treatment (0.5% methylcellulose) on one treatment day. All treatments were administered intraperitoneally (i.p.), 15 min before the start of startle testing. Consistent with previous reports, buspirone increased and alprazolam decreased startle amplitude on the Noise Alone trials; these effects were dose-related. Both agents reduced the magnitude of the SPS effect when it was expressed as the Light+Noise startle amplitude minus the Noise Alone startle amplitude. These findings are similar to the effects of these treatments in the traditional shock-based fear-potentiated startle paradigm.

Acoustic Stimulation↗
PubMed1995

Changes in the acoustic startle response and prepulse inhibition of acoustic startle in rats after local injection of pertussis toxin into the ventral tegmental area.

The effect of local injection of pertussis toxin (PTX) into the ventral tegmental area (VTA) on acoustic startle in rats was investigated. The PTX treatment caused only minor effects of its own on the acoustic startle response (ASR) or prepulse inhibition (PPI) of acoustic startle. However, systemic treatment with the indirect DA receptor agonist, amphetamine (2 mg/kg, SC) caused a significant increase in ASR magnitude and a significant disruption of PPI in PTX-treated rats while no such effects were observed in sham-treated rats. Treatment with the direct DA receptor agonist, apomorphine (2 mg/kg, SC), caused a significant disruption of PPI, an effect that was observed in both PTX- and sham-treated rats. Treatment with the 5-HT1A receptor agonist, 8-OH-DPAT (0.5 mg/kg, SC), did not affect PPI in either group but caused a marked increase in ASR magnitude in sham-treated rats. Interestingly, this effect was blocked in PTX-treated rats. The present results suggest that local injection of PTX into the VTA causes an increased sensitivity to the behavioural effects of psychostimulants on acoustic startle and may also suggest that intact midbrain 5-HT1A receptors are essential for the effect of 5-HT1A agonists on acoustic startle.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2005

Auditory startle response in firefighters before and after trauma exposure.

OBJECTIVE: Although previous psychophysiological studies have revealed heightened muscular and autonomic responses in individuals with posttraumatic stress disorder (PTSD), these studies have not permitted inferences about whether the abnormal responses are a vulnerability factor or are acquired following trauma. The present study reports the first prospective psychophysiological investigation, to the authors' knowledge, of posttraumatic stress responses by prospectively evaluating the auditory startle response in firefighters before and after trauma exposure. METHOD: Orbicularis oculi (eye blink) electromyograms and skin conductance responses to 15 100-dB acoustic startle stimuli were assessed in 84 trainee firefighters before trauma exposure. After commencement of active duty, 35 firefighters were reassessed within 4 weeks of exposure to a traumatic event, and 36 firefighters were reassessed as a comparison group that was not exposed to trauma. RESULTS: In the trauma-exposed group, pretrauma physiological activity was predictive of posttrauma acoustic startle responses. Pretrauma skin conductance response to startle was also predictive of posttraumatic stress severity. CONCLUSIONS: These results provide initial support for elevated startle response being a vulnerability factor for posttraumatic stress responses.

Acoustic Stimulation↗
PubMed2003

Increased auditory startle response and reduced prepulse inhibition of startle in transgenic mice expressing a double mutant form of amyloid precursor protein.

Prepulse inhibition (PPI), a form of sensorimotor gating, occurs when an auditory startle response is markedly inhibited by a preceding sub-threshold stimulus (prepulse). Deficits in PPI have been demonstrated in patients with certain psychiatric disorders, such as schizophrenia, and in laboratory animals following specific pharmacological manipulations. Patients with Alzheimer's disease (AD) have not been tested in PPI, but have been shown to have abnormal sensory gating in another paradigm. Transgenic (Tg) CRND8 mice, which model Alzheimer's disease, carry the Swedish and Indiana familial Alzheimer's disease mutations of the human amyloid precursor protein gene and show age-related increases in beta-amyloid (Abeta) production, as well as plaque deposition. The present experiment investigated auditory startle threshold and PPI in TgCRND8 mice at various ages. In two longitudinal studies, PPI was examined in male TgCRND8 mice and non-transgenic (non-Tg) controls at 6-8 weeks of age (pre-plaque), and every 2 weeks thereafter until all mice were at least 16 weeks old (post-plaque). In a cross-sectional study, three different age sets of nai;ve TgCRND8 and non-Tg mice were tested: 10-12, 12-14, and 15-17 weeks old. In all three studies, TgCRND8 mice consistently and robustly demonstrated an enhanced response to a range of auditory startle stimuli compared to non-Tg mice. In addition, the TgCRND8 mice exhibited modest reductions in PPI, compared to non-Tg controls. These PPI deficits were present at pre- and post-plaque time points and did not appear to intensify with age; thus, they do not seem to correlate with the known neuropathology of TgCRND8 mice.

Acoustic Stimulation↗
PubMed1984

Acoustic startle responses of protein malnourished rats.

Acoustic startle responses were measured as part of a systematic attempt to determine if early protein malnutrition leads to a general hyperreactivity to aversive stimulation. In Experiment 1 startle responses transduced by floor movements were not reliably influenced by protein restriction in the preweaning or postweaning periods. The magnitude of the startle response, however, was positively correlated with body weight, partly as a consequence of the transduction method. Thus, differences in body weight might have obscured diet-related differences in startle amplitude. In Experiment 2 startles were recorded as electromyographic responses of the neck muscles and were larger in rats fed the low protein diet postweaning, especially in rats switched from high to low protein conditions at weaning. There was no indication that rats subjected to preweaning protein malnutrition were hyperreactive to aversive stimulation. In Experiment 1 it was also found that mean startle amplitudes were larger in young adults, 60 or 90 days old, than in 35-day-old rats, partly because there was less habituation in the adults.

Age Factors↗
PubMedDate not supplied

Effect of voluntary muscle contraction on the startle response to auditory stimuli.

Startle reflex responses were studied in 15 normal human subjects using weak (88 dB) and strong (114 dB) auditory stimuli in the orbicularis oculi, masseter, sternocleidomastoid, trapezius, deltoid, biceps, forearm flexors and quadriceps muscles. With the subjects in the relaxed state, no consistent responses were seen with the weak stimuli, and with the strong stimuli responses were only present in orbicularis oculi muscles. When the above muscles were in a state of voluntary contraction, the strong stimuli produced complex responses which were not always excitatory in nature, with muscle relaxation being noted in a number of stimulation sequences. Repetitive weak and strong stimuli were used to study habituation effects in the orbicularis oculi muscles. The repetitive strong stimuli produced a wide range of response patterns, indicating a high inter-individual variability in habituation. In two subjects, no habituation effects were present. Our study supports the high intra-individual variability of the startle response, and suggests that this response is affected by the state of muscle contraction at the time of stimulation. Startle response is more easily elicited in a state of muscular contraction. Future studies of startle reflex should take this into consideration.

Acoustic Stimulation↗
PubMed2006

Startle responses elicited by whiplash perturbations.

The human startle response produces muscle contractions throughout the body but the most brisk and synchronized contractions appear in the neck muscles. This response, which is greatest with the first exposure to a startling stimulus, could produce excessive and inappropriately directed muscle contractions that could explain the higher incidence of whiplash injuries in people who are unprepared for the collision. This study seeks neurophysiological evidence of startle responses in the neck muscles of 120 healthy subjects exposed to between 1 and 16 rear-end impacts or forward perturbations of different speeds. Startle responses were quantified by the synchronous electromyographic (EMG) activity between 10 and 20 Hz in bilaterally homologous sternocleidomastoid, scalene and cervical paraspinal neck muscles. Coherence analyses of EMGs from the left and right muscles were used to estimate synchrony for: (i) the first unexpected trial, (ii) subsequent habituated trials, and (iii) the superposition of habituated trials and a loud acoustic stimulus (40 ms, 124 dB sound). The peak in coherent EMG activity between contralateral muscle pairs in the 10-20 Hz bandwidth was related to startle. Synchrony in this bandwidth was observed between the left and right muscles during the first impact or whiplash-like perturbation. This synchrony decreased significantly in the habituated trials, but reappeared when the loud acoustic stimulus was introduced. Its presence in the first trial indicates that startle is part of the neuromuscular response to an unexpected rear-end impact. This startle component of the neuromuscular response could play a role in the aetiology of whiplash injuries.

Acceleration↗
PubMed1995

Conditioned pleasure attenuates the startle response in rats.

The acoustic startle response of rats was found to be attenuated if elicited in the presence of a conditioned stimulus predicting reward. During conditioning, animals received a total of 21 pairings of light with palatable food and sucrose solution, whereas controls received food and sucrose in the absence of light. The amplitude of the acoustic startle response was significantly reduced in the presence of light in conditioned animals, but not in controls. It is assumed that a conditioned response to light is the activation of a central state of pleasure. We therefore suggest that "pleasure-attenuated startle" reflects a mechanism by which a defensive or aversive response is attenuated during a pleasant, hedonic state.

Acoustic Stimulation↗
PubMed2006

The auditory startle response in post-traumatic stress disorder.

Post-traumatic stress disorder (PTSD) patients are considered to have excessive EMG responses in the orbicularis oculi (OO) muscle and excessive autonomic responses to startling stimuli. The aim of the present study was to gain more insight into the pattern of the generalized auditory startle reflex (ASR). Reflex EMG responses to auditory startling stimuli in seven muscles rather than the EMG response of the OO alone as well as the psychogalvanic reflex (PGR) were studied in PTSD patients and healthy controls. Ten subjects with chronic PTSD (>3 months) and a history of excessive startling and 11 healthy controls were included. Latency, amplitude and duration of the EMG responses and the amplitude of the PGR to 10 auditory stimuli of 110 dB SPL were investigated in seven left-sided muscles. The size of the startle reflex, defined by the number of muscles activated by the acoustic stimulus and by the amplitude of the EMG response of the OO muscle as well, did not differ significantly between patients and controls. Median latencies of activity in the sternocleidomastoid (SC) (patients 80 ms; controls 54 ms) and the deltoid (DE) muscles (patients 113 ms; controls 69 ms) were prolonged significantly in PTSD compared to controls (P < 0.05). In the OO muscle, a late response (median latency in patients 308 ms; in controls 522 ms), probably the orienting reflex, was more frequently present in patients (56%) than in controls (12%). In patients, the mean PGR was enlarged compared to controls (P < 0.05). The size of the ASR response is not enlarged in PTSD patients. EMG latencies in the PTSD patients are prolonged in SC and DE muscles. The presence of a late response in the OO muscle discriminates between groups of PTSD patients with a history of startling and healthy controls. In addition, the autonomic response, i.e. the enlarged amplitude of the PGR can discriminate between these groups.

Acoustic Stimulation↗
PubMed1992

The auditory startle response in the Steele-Richardson-Olszewski syndrome and Parkinson's disease.

The startle response to an unexpected auditory stimulus was studied in eight patients with a clinical diagnosis of the Steele-Richardson-Olszewski syndrome (SRO), 11 patients with idiopathic Parkinson's disease (PD) and 12 normal subjects. The patients with PD were studied 'on' at the time of maximal effect of their treatment; five of these patients were also studied in their 'off' state without treatment. The auditory startle response was absent in three patients with SRO: in the remaining five the latency to onset of earliest electromyography activity (EMG) of the auditory startle response was delayed and few muscles (orbicularis oculi, sternocleidomastoid and rectus abdominis) were recruited in the response. In PD the auditory startle response was similar to that recorded in normal subjects, both in terms of the pattern of muscles recruited and the amplitude of the EMG responses, but the latency of responses in orbicularis oculi and sternocleidomastoid muscles were significantly delayed. This result was not influenced by treatment with L-dopa. In patients with SRO the finding of an abnormal startle response is consistent with loss of neurons in the lower pontine reticular formation. This region is intimately involved in the startle response in animal studies. In patients with PD the late auditory startle response might be related to withdrawal of facilitatory input to brainstem centres and reticulospinal pathways from basal ganglia. The similarity of the responses in patients when 'on' and 'off' suggests these pathways are not under potent dopaminergic control.

Adult↗