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PubMed1997

Startle responses in hereditary hyperekplexia.

BACKGROUND: Patients with hereditary hyperekplexia have excessive startle responses that are accompanied by transient stiffness and also continuous stiffness in infancy. A point of mutation has been identified for the major form of hereditary hyperekplexia in the gene encoding the alpha 1 subunit of the glycine receptor. OBJECTIVE: To measure startle reflexes and autonomic responses in the major form of hereditary hyperekplexia in the original Dutch pedigree. DESIGN: Startle reflexes and autonomic responses were examined by administering 3 series of 20 auditory stimuli at intervals of 10 seconds (90 and 113 dB) and 60 seconds (113 dB). SETTING: The Department of Neurology and Clinical Neurophysiology at the Leiden University Hospital, Leiden, the Netherlands. SUBJECTS: Nine patients with the major form of hyperekplexia and 20 healthy controls. Of the 9 patients, 5 took medication. The patients are part of the Dutch hyperekplexia pedigree. MAIN OUTCOME MEASURES: Startle responses were quantified with latency periods and areas of electromyographic bursts of the orbicular muscle of the eye, sternocleidomastoid and biceps muscles, and the thenar muscles. Autonomic reactions were measured with psychogalvanic responses and beat to beat changes of blood pressure and heart rate. RESULTS: The electromyographic bursts of the 4 muscles occurred in similar order in both patients and controls. The onset of the latency periods in the patient group was significantly (P < .001) prolonged in patients who took medication. Without medication, patients had shorter latency periods of the sternocleidomastoid muscle (P = .003) than controls. The electromyographic burst occurred significantly more often in patients than in controls (P < .001). The areas of the bursts were significantly larger in patients than in controls (P < .001); the degree of habituation was significantly stronger in patients than in controls (P < .001). The amplitude of the psychogalvanic response was increased in hyperekplexia, and the degree of habituation was significantly weaker in patients than in controls. Blood pressure and heart rate did not clearly react in either group. CONCLUSIONS: Motor startle responses are stronger and show more habituation in patients with hereditary hyperekplexia than in controls. The excessive responses include the psychogalvanic response. Increased responses do not necessarily indicate decreased habituation in hyperekplexia.

Acoustic Stimulation↗
PubMed2002

Prepulse inhibition of the startle response in risperidone-treated patients: comparison with typical antipsychotics.

Individuals with schizophrenia are known to show deficits in prepulse inhibition (PPI) of the startle response. PPI refers to a response suppression in reaction to a strong startling stimulus, if preceded briefly by a weak non-startling stimulus and represents a well-established animal model to investigate information processing deficits in schizophrenia. This study examined PPI of the startle acoustic response in schizophrenic patients given typical antipsychotics or a second generation atypical antipsychotic, risperidone, using a naturalistic between-subjects design. Two groups of male schizophrenic patients: (i) stable on a range of typical antipsychotics (n = 20), and (ii) stable on risperidone (n = 10) were tested for PPI (prepulse-to-pulse intervals: 30, 60, and 120 ms, prepulses 15 dB above the background) of the acoustic startle response, and compared with a group of healthy male subjects (n = 20). Patients on typical antipsychotics showed significantly less PPI with 30 and 60 ms prepulse trials than healthy subjects. Risperidone-treated patients did not differ from healthy subjects for PPI with any prepulse trials. Further longitudinal within-subject studies are now required to examine whether risperidone is superior to typical antipsychotics in improving information processing functions, as assessed by PPI of the acoustic startle response, in treatment-responsive male patients with schizophrenia.

Acoustic Stimulation↗
PubMed1998

Dependence on smoking and the acoustic startle response in healthy smokers.

Recent data from nicotine-dependent rats (14) and healthy smokers (18) would suggest that nicotine withdrawal modulates the acoustic startle reflex in a way similar to that of fear (5,20). We examined this directly using nonsmokers and healthy smokers who had no deprivation, brief deprivation (2-3 h), or prolonged deprivation (15 h). Groups differences in heart rate (HR), alveolar carbon monoxide (CO) levels, and desire and craving for cigarettes confirmed the presence of smoking withdrawal. However, there were no significant differences in the magnitude of the baseline startle response among the differently deprived smokers or between the smokers and the nonsmokers. Subsequent startle tests were carried out in the smokers during repeated sequences of preparing a cigarette for smoking (smoking cues) and then smoking. Whereas we did find statistically significant interactions of smoking deprivation with smoking cues and with renewed smoking, there was only weak confirmation of a priori predictions of motivational effects of smoking cues or of smoking. We conclude that smoking dependence may not affect the acoustic startle response itself; modulation seems to occur, but only after experience with the test situation. Discussed were possible mechanisms of this modulation in both humans and animals and further application of the startle response for providing interdisciplinary assessments of the motivational effects of nicotine withdrawal.

Acoustic Stimulation↗
PubMed1997

Control conditions in the fear-potentiated startle response paradigm.

In the present study, the fear-potentiated startle response paradigm was modified in order to investigate the decrease in control startle levels often observed after administration of anxiolytic drugs. The within-animal comparison of control startle amplitudes and fear-potentiated startle amplitudes normally used was replaced by a between-animal comparison. Moreover, the experimental design was extended with an additional control group, a no-shock group. The anxiolytics diazepam and chlordiazepoxide were used as pharmacological tools. The main findings were that both benzodiazepines dose-dependently reduced control startle amplitudes and no-shock startle amplitudes equally, suggesting that shock-associated contextual cues are not responsible for the drug-induced decrease in control startle amplitudes in the fear-potentiated startle response paradigm.

Animals↗
PubMed1994

Persistent stress-induced sensitization of adrenocortical and startle responses.

We assessed the functional adrenocortical and behavioral state of rats previously exposed to repeated stressor presentations. In Experiment 1, the whole-body startle response to threshold (91 dB) and suprathreshold (96 dB) stimuli was assessed in rats given 3 daily sessions (3DS) of 40, 2-mA tailshocks. The 3DS rats showed an exaggerated startle response to the threshold auditory stimulus 4 days poststressor compared to nonshocked controls (CON). An exaggerated startle response in stressed rats was not evident either 1 day or 10 days poststressor. In Experiment 2, adrenocortical sensitization and behavioral reactivity were assessed in rats exposed to 1 day (1DS) or 3 days of our stress regimen. Stressed rats exhibited elevated basal plasma corticosterone (CORT) levels 1 day poststressor which recovered by 9 days poststressor. Stressed rats also exhibited suppressed open-field activity 4 days poststressor. On the 10th day poststressor, rats were exposed to a single tailshock. The 1DS and 3DS rats showed both a sensitized and prolonged CORT response to stressor reexposure compared to control rats which received only the single tailshock. In addition, on the 11th day poststressor 3DS rats exhibited a moderate recapitulation of the elevated basal CORT levels seen after the initial stressor exposures. Thus, exposure to our stress regimen produces a chronic stress state in rats characterized by persistent behavioral and adrenocortical sensitization, as well as suppressed open-field activity and elevated basal CORT levels. Rats exhibiting a chronic stress state may be appropriate as a model for the study of stress-related psychophysiological illnesses, such as posttraumatic stress disorder.

Acoustic Stimulation↗
PubMed2001

The adenosine A2A agonist CGS 21680 reverses the reduction in prepulse inhibition of the acoustic startle response induced by phencyclidine, but not by apomorphine and amphetamine.

Systemic administration of the selective adenosine A2A agonist CGS 21680, at the highest dose tested (0.5 mg/kg), selectively reversed the reduction in prepulse inhibition (PPI) of the acoustic startle response induced by the NMDA antagonist phencyclidine (PCP), but not by the dopaminergic agonists apomorphine and amphetamine. CGS 21680 by itself was without effect on PPI, but did reduce the amplitude of the startle response. PCP also reduced startle amplitude, but there was no additive or synergistic effect between PCP and CGS 21680 on the startle response. CGS 21680 (0.5 mg/kg) blocked the locomotor activating effect of amphetamine, but this may have been secondary to a reduction in spontaneous locomotion induced by this compound. Taken together, these results indicate that stimulation of adenosine A2A receptors produce no consequence on dopamine agonist-induced disruption in PPI, but regulate the inhibitory effect of NMDA receptor blockade on PPI. This finding raises the possibility that adenosine A2A agonists possess antipsychotic-like properties.

Acoustic Stimulation↗
PubMed1994

Clozapine antagonizes phencyclidine-induced deficits in sensorimotor gating of the startle response.

Intense auditory stimuli elicit an involuntary startle response that is attenuated when the startling stimulus (the pulse) is preceded immediately by a low intensity stimulus (the prepulse). This phenomenon of prepulse inhibition (PPI) is utilized as a measure of sensorimotor gating and is significantly reduced in schizophrenic patients. Noncompetitive N-methyl-D-aspartate antagonists such as phencyclidine (PCP) and ((+)-D-aspartate 5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine) (dizocilpine, or MK-801) have been found previously to disrupt PPI in animals. The present investigation assessed the ability of several antipsychotic drugs to reverse PCP-induced deficits in PPI in rats. Animals were pretreated with either the atypical antipsychotic clozapine (0, 1.25, 2.5, 5.0 or 10.0 mg/kg), the D2 dopamine antagonist raclopride (0, 0.1 or 0.5 mg/kg), the D1 dopamine antagonist SCH23390 (0, 0.01 or 0.05 mg/kg) or the 5-hydroxytryptamine2 antagonists ritanserin (0 or 2.0 mg/kg) or ketanserin (0 or 1.0 mg/kg) and then were given PCP (1.0 mg/kg). After drug administration, animals were tested in startle chambers. PCP repeatedly and robustly decreased PPI without affecting base-line startle reactivity. Clozapine (5.0 mg/kg) antagonized this effect of PCP without altering PPI by itself. Raclopride, SCH23390, ritanserin and ketanserin were ineffective at reversing the PCP-induced deficit in PPI. As with PCP, 0.1 mg/kg of MK-801 disrupted PPI; this disruption also was antagonized by 5.0 mg/kg of clozapine. Thus, it appears that the ability of clozapine to reverse deficits in PPI produced by noncompetitive N-methyl-D-aspartate antagonists cannot be attributed to a sole antagonism of either D1 dopamine, D2 dopamine or 5-hydroxytryptamine2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗
PubMed2003

Comparison of video- and EMG-based evaluations of the magnitude of children's emotion-modulated startle response.

We investigated the reliability and validity of a video-based method of measuring the magnitude of children's emotion-modulated startle response when electromyographic (EMG) measurement is not feasible. Thirty-one children between the ages of 4 and 7 years were videotaped while watching short video clips designed to elicit happiness or fear. Embedded in the audio track of the video clips were acoustic startle probes. A coding system was developed to quantify from the video record the strength of the eye-blink startle response to the probes. EMG measurement of the eye blink was obtained simultaneously. Intercoder reliability for the video coding was high (Cohen's kappa = .90). The average within-subjects probe-by-probe correlation between the EMG- and video-based methods was .84. Group-level correlations between the methods were also strong, and there was some evidence of emotion modulation of the startle response with both the EMG- and the video-derived data. Although the video method cannot be used to assess the latency, probability, or duration of startle blinks, the findings indicate that it can serve as a valid proxy of EMG in the assessment of the magnitude of emotion-modulated startle in studies of children conducted outside of a laboratory setting, where traditional psychophysiological methods are not feasible.

Child↗
PubMed2002

Urocortin-deficient mice display normal stress-induced anxiety behavior and autonomic control but an impaired acoustic startle response.

Corticotropin-releasing hormone (Crh) plays an important role in modulating physiological and behavioral responses to stress. Its actions are mediated through two receptors, Crhr1 and Crhr2. Urocortin (Ucn), a Crh-related neuropeptide and the postulated endogenous ligand for Crhr2, is a potential mediator of stress responses. We generated Ucn-deficient mice using embryonic stem cell technology to determine its role in stress-induced behavioral and autonomic responses. Unlike Crhr1- or Crhr2-deficient mice, Ucn-deficient mice exhibit normal anxiety-like behavior as well as autonomic regulation in response to stress. However, the mutant mice display an impaired acoustic startle response that is not due to an obvious hearing defect. Thus, our results suggest that Ucn does not play an essential role in stress-induced behavioral and autonomic responses. Ucn may modulate the acoustic startle response through the Ucn-expressing neuron projections from the region of the Edinger-Westphal nucleus.

Alleles↗
PubMed1993

Microinjections of the metabotropic glutamate receptor agonist, trans-(+/-)-1-amino-cyclopentane-1,3-dicarboxylate (trans-ACPD) into the amygdala increase the acoustic startle response of rats.

The present study examined the effect of intraamygdaloid application of the metabotropic glutamate receptor agonist trans-ACPD on the acoustic startle response. Trans-ACPD led to a disruption of between-session habituation which is normally seen after repeated testing after injections of the vehicle into the amygdala. More specifically, a statistically significant increase of the magnitude of the startle response was observed 4 h after injection of 30 nmol of trans-ACPD into the central amygdaloid nucleus. The present findings suggest a role for the metabotropic glutamate receptor in the amygdala in the enhancement of the acoustic startle response.

Acoustic Stimulation↗
PubMed1997

Effect of acoustic stimulus characteristics on the startle response in hooded rats.

The acoustic startle response (ASR) depends on stimulus parameters such as duration, intensity and particularly on the stimulus rise time. The aim of our study was to determine to what extent the ASR parameters are affected by the spectral characteristics of the stimulus. Therefore, in this experiment the amplitude and the latency of the acoustic startle reflex were assessed for a fixed pulse duration and for a variety of stimulus frequencies ranging between 3 and 23 kHz. The ASRs were studied in 11 adult hooded rats exposed to 2-ms (120 dB SPL) tone pulses of different frequencies presented in random order, with or without 70 dB white noise background. Statistical analysis of the data revealed significant differences between ASR amplitudes for different frequencies. In our experimental situation the rats responded more readily to a low frequency stimulus. The startle amplitude decreased with tonal frequencies and distinguishable difference were seen for 3, 7, and 10 kHz pulses. However, such differences were not readily observed for higher frequencies i.e. 15, 20, 23 kHz. The same pattern of differences was observed when the acoustic stimulus was presented with the white noise background. The observed differences may be attributed, firstly, to a spectral characteristic of the stimulus and thus to an audibility in rats and secondly to a behavioral meaning of a stimulus of a different frequency.

Acoustic Stimulation↗
PubMed2004

Habituation of an odorant-induced startle response in Drosophila.

Habituation is a fundamental form of behavioral plasticity that permits organisms to ignore inconsequential stimuli. Here we describe the habituation of a locomotor response to ethanol and other odorants in Drosophila, measured by an automated high-throughput locomotor tracking system. Flies exhibit an immediate and transient startle response upon exposure to a novel odor. Surgical removal of the antennae, the fly's major olfactory organs, abolishes this startle response. With repeated discrete exposures to ethanol vapor, the startle response habituates. Habituation is reversible by a mechanical stimulus and is not due to the accumulation of ethanol in the organism, nor to non-specific mechanisms. Ablation or inactivation of the mushroom bodies, central brain structures involved in olfactory and courtship conditioning, results in decreased olfactory habituation. In addition, olfactory habituation to ethanol generalizes to odorants that activate separate olfactory receptors. Finally, habituation is impaired in rutabaga, an adenylyl cyclase mutant isolated based on a defect in olfactory associative learning. These data demonstrate that olfactory habituation operates, at least in part, through central mechanisms. This novel model of olfactory habituation in freely moving Drosophila provides a scalable method for studying the molecular and neural bases of this simple and ubiquitous form of learning.

Adenylyl Cyclases↗
PubMed1996

Lesions of the amygdala do not affect the enhancement of the acoustic startle response by background noise.

The acoustic startle response (ASR) is enhanced in the presence of loud background noise. We examined whether or not this increase of response strength is mediated by the amygdala, which is known to be involved in various phenomena of enhancement of the ASR. To achieve this aim, we tested whether or not amygdaloid lesions with the excitotoxin N-methyl-D-aspartate (NMDA) would abolish the enhancement of the ASR by background noise in 13 Wistar rats. Loss of foot-shock sensitization in these rats, as well as histological evaluation, proved the successful destruction of the amygdala. However, the enhancement by background noise of the ASR, which was observed in sham-operated controls, was not affected in amygdala-lesioned rats. Therefore, we conclude that the background noise facilitation does not involve emotional components that are mediated by the amygdala. On the basis of these findings, we differentiate between the startle-enhancing effect of background noise and the amygdala-mediated effect of foot shocks on the ASR.

Acoustic Stimulation↗
PubMed1992

Daily rhythmicity of the rat acoustic startle response.

We have measured the acoustic startle response (ASR) amplitude and latency in rats housed in a 12:12 light:dark (LD) cycle. The response amplitudes to eliciting stimuli (ES) of 110 dB or 120 dB (white noise) were significantly higher (nearly two-fold) during D than during L. Similar, but nonsignificant, trends were also observed at ES intensities of 90 dB or 100 dB. While some significant LD ASR latency differences were observed, we cannot ascribe them to the photoperiodic phase at this time. These findings conclusively demonstrate that the mammalian ASR amplitude exhibits daily rhythmicity.

Acoustic Stimulation↗
PubMed2001

Fos-like immunohistochemical identification of neurons active during the startle response of the rainbow trout.

Activity-dependent Fos-like expression was investigated immunohistochemically in rainbow trout (Oncorhynchus mykiss) that had performed vibratory-evoked startle responses. We found significantly higher numbers of Fos-like-immunoreactive neurons in the reticular formation, in the octavolateral area, and in several cranial nerve motor nuclei in the brain and in the motor column of the spinal cord of startled fish than in control fish. In one fish, in which stimulation did not evoke startle responses, substantial numbers of positive cells occurred in the brain, primarily in the magnocellular octavolateral nucleus. We observed Fos-like-immunoreactive neurons in cell groups that are known to participate in the startle response (e.g., the Mauthner cell) as well as in cell groups that have been proposed but until now not shown to be involved.

Animals↗
PubMedDate not supplied

Intraventricular insulin suppresses the acoustic startle response in rats.

We and others have previously reported that the hormone insulin alters brain noradrenergic function at the synaptic and molecular levels. In the present study, we examined the in vivo effect of insulin (administered chronically via osmotic minipumps at a dose of 5 mU/day into the third cerebral ventricle) on the acoustic startle response. Rats receiving chronic intraventricular insulin had a significantly reduced startle response relative to vehicle-treated controls (i.e., 47 +/- 21% of baseline control startle response). Because our previous findings suggest that on an acute basis, insulin may enhance endogenous noradrenergic activity by inhibiting norepinephrine reuptake, we speculate here that the chronic effect of insulin is similar to that of the noradrenergic reuptake blocker, desipramine, which has been reported to decrease baseline startle performance.

Acoustic Stimulation↗
PubMed1993

Auditory startle response in blind subjects.

Blindness is often associated with hypervigilance and arousal. The auditory startle response has been suggested as a measure of arousal. This study evaluated the auditory startle response of 10 blind individuals and 10 sighted controls who were exposed to a series of 15 1000-Hz, 95-db, 0-rise-time pure-tone stimuli, administered to both ears. The subjects' heart-rate, skin-conductance, and orbicularis-oculi-electromyogram responses to the tones were measured. Blind subjects did not differ from controls in the magnitude and in the habituation-rate of their responses. Results were interpreted as showing that blind persons' capacity for discriminative learning and for regulation of arousal is unimpaired. Task-related anxiety of blind persons should be differentiated from stimulus-related anxiety.

Acoustic Stimulation↗