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PubMed2003

Acoustic startle responses and temperament in individuals who stutter.

Fourteen individuals who stutter and 14 individuals who do not stutter were presented with 10 bursts of white noise to assess the magnitude of their eyeblink responses as a measure of temperament. Both the magnitude of the eyeblink response to the initial noise burst and the mean of the 10 responses were significantly greater for the stuttering group. The Taylor-Johnson Temperament Analysis (R. M. Taylor & L P. Morrison, 1996) did not distinguish between the two groups, but informal follow-up statistics indicated that the Nervous subscale showed a significant group difference. Scores on this subscale were also significantly positively correlated with the magnitude of the startle response. A discriminant analysis demonstrated that although both the startle response and the nervous trait differentiated the two groups, the startle response measures were more powerful in making this differentiation.

Acoustic Stimulation↗

PubMed1992

Loss of the acoustic startle response following neurotoxic lesions of the caudal pontine reticular formation: possible role of giant neurons.

The effect of the excitotoxic N-methyl-D-aspartate agonist quinolinic acid in the caudal pontine reticular formation on the acoustic startle response was investigated in rats. Bilateral injections of 90 nmol of quinolinic acid led to large lesions in the reticular formation characterized by the loss of all neurons and a marked reduction or even abolition of the acoustic startle response; 18 nmol of quinolinic acid led to smaller lesions characterized by a selective loss of giant neurons within the caudal pontine reticular formation and a reduction of the startle amplitude. The partial correlation analysis revealed that the reduction of the amplitude of the acoustic startle response can be correlated with the loss of the giant neurons (r = 0.575; d.f. = 29; P less than 0.001) but not with the reduction of the number of all neurons (r = 0.207; d.f. = 29; P greater than 0.2) in the caudal pontine reticular formation. These findings were reconciled with electrophysiological and anatomical data indicating that the giant neurons in the caudal pontine reticular formation receive acoustic input and project to motoneurons of the spinal cord. It is concluded that the caudal pontine reticular formation is an important element of the startle pathway and that the giant reticulospinal neurons constitute an important part of the sensorimotor interface mediating this response.

Acoustic Stimulation↗

PubMed1984

The effects of clonidine, prazosin, and propranolol on short-term and long-term habituation of the acoustic startle response in rats.

The unique effect of clonidine in facilitating habituation of the acoustic startle response [10] was replicated. However, clonidine had no effect on between-session habituation, showing a pharmacological dissociation between short- and long-term habituation. Systematic manipulation of ISI showed clonidine's habituation-facilitating effect to be most striking with longer within-session ISIs where habituation was relatively weak in controls. Comparing clonidine's effect to that of two other hypotensive agents, prazosin and propranolol, showed that the habituation-facilitating effect was not due to blood pressure effects. Prazosin, an alpha 1-adrenergic blocker, facilitated short-term habituation, but significantly less so than did clonidine, an alpha 2-agonist. Propranolol, a beta-adrenergic blocker, had no effect on short-term habituation. Both prazosin and propranolol impaired long-term habituation, but propranolol did so without suppressing initial response levels. The data suggest that a synapse with both alpha-1- and alpha 2-adrenoceptors may be critically involved in habituation of the acoustic startle response. A beta-adrenergic involvement in long-term habituation is tentatively suggested.

Acoustic Stimulation↗

PubMed2000

Differential effects of cohort removal stress on the acoustic startle response of the Roman/Verh rat strains.

Male and female rats of the inbred Roman/Verh strains, which have been psychogenetically selected and bred for good (RHA-I/Verh) and extremely poor (RLA-I/Verh) two-way avoidance acquisition, were evaluated in an acoustic startle response test. One half of the rats of each strain and sex were previously subjected to 30 min of isolation by removal of their cage partners ("cohort removal"). During the testing session each animal received 40 acoustic stimuli at interstimulus intervals of 30 seconds. The hyperemotional RLA-I/Verh rats (especially the males) showed stronger acoustic startle responses than did their RHA-I/Verh counterparts. Startle amplitudes of the RLA-I/Verh males were further enhanced by the stress of 30 min isolation, whereas cohort removal did not significantly affect startle response amplitudes in RHA-I/Verh rats of either sex or in females of the RLA-I/Verh strain.

Acoustic Stimulation↗

PubMed2000

Temporal stability of the emotion-modulated startle response.

In the present study, we examined the stability of one measure of emotion, the emotion-modulated acoustic startle response, in an undergraduate sample. Using the acoustic startle paradigm on two different occasions, we measured stability of affective modulation of the startle response during and following the presentation of pictures selected to be of positive, negative, or neutral emotional valence. The two assessments were separated by 4 weeks. Two groups of subjects were compared: one group that viewed the same pictures at each assessment and a second group that viewed different pictures at the second assessment. We found that viewing different pictures at two assessments separated by 4 weeks yielded moderate stability of the emotion modulation of startle magnitude, whereas subjects who viewed the same pictures at both assessments showed poor stability. Furthermore, this difference was due to the stability of responses to high versus low arousal pictures, not to differences in valence.

Adolescent↗

PubMed2001

Effects of clonidine and diazepam on prepulse inhibition of the acoustic startle response and the N1/P2 auditory evoked potential in man.

Contraction of the orbicularis oculi muscle in response to a sudden loud sound (acoustic startle response) and the N1/P2 component of the auditory evoked potential are both attenuated when a brief low-intensity stimulus is presented 30-500 ms before the 'startle-eliciting' stimulus (prepulse inhibition). We examined the effects of two sedative/anxiolytic drugs, diazepam and clonidine, on prepulse inhibition of these two responses in healthy volunteers. Fifteen males (aged 18-35 years) participated in three sessions in which they received oral doses of placebo, diazepam 10 mg and clonidine 0.2 mg according to a balanced double-blind protocol. Thirty-minute simultaneous recordings of the electromyographic (EMG) responses of the orbicularis oculi muscle of the right eye and the vertex auditory evoked potentials took place 120 min after ingestion of clonidine and 60 min after ingestion of diazepam. Sound stimuli (1 kHz) were presented in 60 trials separated by variable intervals (mean 25 s): (i) 40-ms 115-dB ('pulse alone', 20 trials); (ii) 40-ms 85-dB (20 trials); (iii) 40-ms 85-dB, followed after 120 ms by 40-ms 115-dB ('prepulse/pulse', 20 trials). Mean amplitudes of the EMG response and the N1/P2 potential were derived from the pulse-alone trials and, in each case, percentage prepulse inhibition was calculated. The amplitude of the EMG response was significantly reduced both by diazepam and by clonidine; neither drug significantly altered prepulse inhibition of the EMG response. Diazepam, but not clonidine, significantly reduced the amplitude of the N1/P2 potential; neither drug significantly affected prepulse inhibition of the N1/P2 potential. Both drugs reduced self-rated alertness and anxiety, and systolic blood pressure; clonidine, but not diazepam reduced diastolic blood pressure and salivation. The results confirm previous findings that sedative drugs can suppress the startle response without affecting prepulse inhibition of this response, and provide new information on the effects of these drugs on the N1/P2 potential and its inhibition by prepulses.

Acoustic Stimulation↗

PubMed1986

Cardiovascular concomitants of tactile and acoustic startle responses in spontaneously hypertensive and normotensive rats.

In the present study we have simultaneously investigated cardiovascular and behavioral responses to repeated tactile and acoustic stimulation in adult, male, spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Blood pressure and heart rate responses were increased in SHR vs. WKY rats following both types of stimuli. The pressor responses, but not the tachycardic responses, habituated with repeated stimulation in both strains and with both stimulus modalities. The rates of habituation were not significantly different between the two strains. Magnitudes of the behavioral startle responses were significantly elevated in SHR vs. WKY rats with tactile, but not with acoustic stimulation. No significant differences were found between the two strains with respect to the latency, with which the startle responses occurred. These data indicate that SHR as compared to WKY rats respond to repeated stimulation with two different stimulus modalities (tactile and acoustic) with significantly increased pressor and tachycardic responses. This cardiovascular hyperreactivity is not due to different degrees of habituation between the two strains and can be observed even in the absence of significant differences in standard behavioral startle response measures.

Acoustic Stimulation↗

PubMed1983

Enhancement by the putative 5-HT receptor agonist 8-OH-2-(di-n-propylamino)tetralin of the acoustic startle response in the rat.

Two 2-(di-n-propylamino)tetralin (DPAT) compounds, 8-OH-DPAT and 5-OH-DPAT, with reported effects on central 5-HT and DA receptors respectively, were tested for their effects on the acoustic startle response in rats. 8-OH-DPAT was given in doses of 0.25-2.0 mg/kg IP and 5-OH-DPAT in doses of 1.0-8.0 mg/kg IP. Both compounds increased the startle response significantly in a dose-dependent manner, but 8-OH-DPAT appeared to be about 30 times as potent and to have a higher efficacy than 5-OH-DPAT. In addition, the effects on the startle response of L-5-HTP, 25-100 mg/kg IP, and L-dopa, 25-100 mg/kg IP, administration to animals pretreated with the inhibitor of aromatic L-amino acid decarboxylase, benserazide (25 mg/kg IP) were included for comparison. A small, but significant increase in the startle amplitude was found after the highest dose of L-5-HTP, whereas no effects were observed after L-dopa administration.

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

PubMed1998

Prepulse facilitation of auditory startle response in hamsters.

A visual prepulse was applied just before a burst of white noise with various lead intervals ranging from 50 to 400 ms in hamsters. After habituation each hamster received 120 trials of the auditory noise with or without the prepulse. Amplitude of startle response increased significantly at 100 ms and 200 ms (n = 10). This enhancement disappeared in blind controls (n = 6). The amplitude of startle response decreased during exploratory behavior, grooming, sniffing or other movements. However, the facilitatory effects of the visual prepulse were consistent, regardless of the animal's behavioral states, except sniffing. The authors conclude that visual prepulse task is useful for studying the ability to detect visual signals in hamsters, and that further study is necessary to elucidate the factors affecting the enhancement of startle response in hamsters.

Acoustic Stimulation↗

PubMed2006

Iron deficiency affects acoustic startle response and latency, but not prepulse inhibition in young adult rats.

Iron deficiency is associated with alterations in dopamine and serotonin transporters as well as changes in dopamine receptor (DR) density, monoamine concentrations, and in vivo extracellular contents of monoamines in terminal fields. Human infants with iron deficiency have both delayed maturation as well as lengthened central conduction times in auditory evoked potential studies. The current study utilizes the magnitude of the acoustic startle response (ASR), prepulse inhibition (PPI), and mean latency to maximum startle response (T(max)), to examine the functional integrity of response to environmental cues. Male and female rats consumed iron deficient (ID) or iron adequate (CN) diets from weaning until adulthood. ID rats of both sexes had 20-60% reductions in ASR when compared to CN rats but there was no effect on PPI. T(max) was significantly longer by 10-20% in females, but not males. Dopamine transporter density was significantly lower in putamen, nucleus accumbens, and olfactory tubercle in males, but not female rats while the serotonin transporter was significantly different from control animal density in five of 14 brain regions. Norepinephrine transporter density was lower in the locus ceruleus of ID male rats but was unaffected in ID female rats. Regression modeling of ASR with brain monoamine transporters and receptors showed hematocrit, norepinephrine transporter (NET) in dentate gyrus, and D1R in the nucleus accumbens account for nearly 49% of the variance in ASR. T(max) was not significantly associated with any of the independent variables. We conclude that iron deficiency affects the startle response, but not the inhibitory circuits involved in prepulse inhibition. Importantly, sex also strongly influenced these behavioral responses. Future studies, perhaps pharmacologic in nature, are necessary to ascertain whether iron deficiency modifies the contribution of monoaminergic systems to responses to environmental stimuli.

Acoustic Stimulation↗

PubMed1996

Habituation and sensitization of the acoustic startle response in rats: amplitude, threshold, and latency measures.

The amplitude of the acoustic startle response habituates to repetitive stimulation. The input and output of the startle system were measured to determine if the decrease in startle amplitude during repetitive stimulation is due to an increase in the startle threshold. Two experimental approaches were used in 35 Sprague-Dawley rats to probe the relationship between the input (the sound pressure level of the stimulus) and the behavioral output (startle amplitude). The results show that the minimum threshold for a response does not change during habituation; rather, the slope of the dependence of startle amplitude on stimulus level decreases. Because habituation does not influence startle threshold we propose that the site for habituation is located in the neural circuitry downstream from the site for startle threshold. Besides amplitude and threshold, as an additional parameter we measured startle latency. In general, the latency of the acoustic startle response is negatively correlated with the response amplitude. This correlation has been repeatedly shown, therefore one would expect a latency increase during the amplitude decrease caused by habituation. However, the latency of the startle reaction also decreased during the course of repetitive stimulation. According to the dual process theory of habituation, a stimulus has both a response-decreasing, i. e., habituating, as well as a response-increasing, i.e., sensitizing, influence on a behavior (Groves & Thompson, 1970). Our explanation of the present results is that startle amplitude is reduced following repetitive stimulation because it is mainly influenced by habituation; latency, however, is shortened because it is mainly influenced by sensitization.

Acoustic Stimulation↗

PubMed2004

Habituation of the acoustic and the tactile startle responses in mice: two independent sensory processes.

To test whether habituation is specific to the stimulus modality, the authors analyzed cross-habituation between the tactile startle response' (TSR) and the acoustic startle response (ASR). The acoustic artifacts of airpuffs used to elicit the TSR were reduced by using a silencer and were effectively masked by background noise of 90-100 dB sound-pressure level. ASR was elicited by 14-kHz tones. TSR and ASR habituated in DBA and BALB mice: both the TSR and ASR habituated to a greater extent in DBA mice than in BALB mice. In both strains, habituation of the TSR did not generalize to the ASR, and vice versa. From this, the authors concluded that habituation of startle is located in the sensory afferent branches of the pathway.

Acoustic Stimulation↗

PubMed2001

Influence of cigarette smoking on prepulse inhibition of the acoustic startle response in schizophrenia.

The prevalence of tobacco smoking is known to be higher in patients with schizophrenia than other psychiatric disorders and general population. These patients also show reduced prepulse inhibition (PPI) of the startle response. PPI refers to a reduction in response to a strong startling stimulus if preceded shortly by a stimulus of sub-threshold intensity. PPI is thought of as an objective index of sensorimotor gating. Nicotine administered subcutaneously or via cigarette smoking enhances PPI in healthy human beings. It also enhances PPI at low, but not high, doses in the rat. We examined the influence of smoking on PPI of the acoustic startle response in 46 male patients with chronic schizophrenia. In a naturalistic design, patients (n = 9) who smoked a cigarette less than 10 min prior to being tested on PPI were compared with other smoking (n = 23) and non-smoking patients (n = 14). We found that the group of patients who smoked a cigarette prior to being tested had significantly greater PPI than other two groups. These observations suggest a PPI-enhancing effect of cigarette smoking on PPI in patents with schizophrenia. Higher prevalence of cigarette smoking in schizophrenic patients may reflect an attempt to improve sensorimotor gating deficits. Copyright 2001 John Wiley & Sons, Ltd.

Journal Article↗

PubMed1994

Substance P is involved in the sensitization of the acoustic startle response by footshocks in rats.

The acoustic startle response (ASR) can be enhanced by administration of footshocks (sensitization). The neural mechanisms underlying this effect are largely unknown. A previous electrophysiological study (Kungel et al., Brain Res., 643 (1994) 29-39) has shown that the neuropeptide substance P (SP) increases the responsiveness to acoustic stimuli of neurons in the caudal pontine reticular nucleus (PnC). Since the PnC is an important part of the primary acoustic startle circuit, we hypothesized that SP is involved in the enhancement of the ASR by electric footshocks. We tested this hypothesis in different experiments by locally injecting SP and SP-antagonists into the PnC of freely moving rats. The present data show that SP (0.5 pmol-1 nmol) locally injected into the PnC dose-dependently increases the amplitude of the ASR in rats. This effect was antagonized by pretreatment with the SP-antagonist CP-96,345. Furthermore, we show that the sensitization of the ASR by 0.6 mA-footshocks can be blocked by local microinjections of the SP-antagonists CP-96,345 (5 pmol-10 nmol) or CP-99,994 (0.5 nmol-100 nmol) into the PnC. Possible pathways relevant for the sensitization of the ASR are discussed.

Animals↗

PubMed2005

The expression of prepulse inhibition of the acoustic startle reflex as a function of three pulse stimulus intensities, three prepulse stimulus intensities, and three levels of startle responsiveness in C57BL6/J mice.

Using the acoustic startle reflex, prepulse inhibition (PPI) is typically demonstrated by the interaction between two auditory stimuli presented in close temporal proximity. When a startle-eliciting pulse stimulus is shortly preceded by a weak prepulse stimulus, the reaction to the former is attenuated in comparison to when the pulse stimulus is presented alone. The present experiment evaluated the influence of different prepulse and pulse intensities upon the expression of PPI by additionally taking into account individual differences in startle reactivity. To this end, we subdivided a cohort of 102 mice into three subsets of equal size differing in startle responsiveness, and evaluated PPI using three levels of prepulse stimulus in combination with three intensities of pulse stimulus. Our results revealed additive as well as complex interactive effects amongst individual's reactivity, pulse intensity and prepulse intensity. At the same time, additional issues concerning the quantification of PPI are highlighted, especially when startle reactivity differs considerably between comparison groups. We concluded that the variation in pulse intensity represents a valuable addition to PPI assessment in general, and especially in genetically modified mice.

Acoustic Stimulation↗

PubMed2001

Effects of procyclidine on prepulse inhibition of the acoustic startle response in healthy human volunteers.

RATIONALE: Prepulse inhibition (PPI) of the startle response refers to an attenuation in response to a strong stimulus (pulse) if this is preceded shortly by a weak non-startling stimulus (prepulse). Patients with schizophrenia have repeatedly been found to show reduced PPI when compared to healthy people. Anticholinergic drugs are often used to control extrapyramidal symptoms induced by antipsychotic medication in schizophrenic patients. Antipsychotic medication, in particular with atypical drugs, has been shown to improve a range of cognitive functions and normalize PPI deficits in schizophrenia, whereas anticholinergic drugs disrupt cognitive functions in both normal and schizophrenic populations and also impair PPI in experimental animals. No previous study has investigated the effects of anticholinergic drugs on human PPI. OBJECTIVES: This study determined the effects of procyclidine, an anticholinergic drug, on PPI in healthy male volunteers, employing a double-blind placebo-controlled cross-over design. METHODS: Subjects underwent testing for PPI on two occasions: once after the oral administration of a placebo and once after the oral administration of procyclidine in two separate experiments. Experiment 1 examined the effects of 10 mg procyclidine, whereas experiment 2 examined the effects of 15 mg procyclidine. RESULTS: Procyclidine at a 10 mg dose, as compared to placebo, had no effect on PPI, but caused impairments at a 15 mg dose. In both experiments, procyclidine reduced response amplitude over the pulse-alone trials and heart rate 1-2 h post-administration. CONCLUSIONS: PPI of the human acoustic startle response is modulated by procyclidine. The use of anticholinergics needs to be considered in PPI studies in schizophrenia.

Acoustic Stimulation↗

PubMed1990

Effects of various direct or indirect dopamine agonists on the latency of the acoustic startle response in rats.

The effects of dopamine agonists were investigated on the latency of the acoustic startle response in male Wistar rats. Four indirect dopamine agonist were tested: GBR 12783 (5-20 mg/kg), BTCP (5-20 mg/kg), dexamphetamine (3-6 mg/kg) and L-DOPA 100 mg/kg associated with benserazide 25 mg/kg; they induced an increase in startle latency. Apomorphine at a dose (50 micrograms/kg) known to decrease dopaminergic transmissions, was ineffective on the startle response. On the contrary, at 0.6 or 2 mg/kg, apomorphine induced an increase in the startle latency. A similar effect was observed with bromocriptine at 10 mg/kg from the 10th min up to at least the 9th hour after treatment. The specific agonist of D2 receptors Ru 24926 (0.45 mg/kg) enhanced the startle latency as well as the specific agonist of D1 receptors SKF 38393 (10 mg/kg). The association of these drugs resulted in an apparent additivity of their individual effects. The effect of apomorphine (0.6 mg/kg) was only partially reduced by a high dose of the specific D2 antagonist amisulpride (80 mg/kg) and more clearly antagonized by the specific D1 antagonist SCH 23390 (50 micrograms/kg). It is concluded that D2 and D1 receptors contribute to the increase in startle latency elicited by direct or indirect dopamine agonists.

Acoustic Stimulation↗

PubMed2001

Neurobiological relationships between ambient lighting and the startle response to acoustic stress in humans.

A study was conducted to determine differences between psychophysiological responses to acoustic stress under different ambient lighting conditions. Typical cool-white indoor lighting was compared to full-spectrum lighting under dim and bright illumination levels. Full-spectrum lighting exhibits spectral characteristics that approximate those found in natural sunlight. The startle response was measured during three preliminary experiments using normal subjects. In the first experiment, one subject was evaluated. Electromyography (EMG) was used to measure eyeblink startle at the obicularis oculi muscle; heart rate (HR) was measured at the wrist; and galvanic skin conductance (GSC) was measured at the left index finger. There was a significant increase in galvanic skin conductance (GSC) and a decrease in heart rate. In the second experiment, GSC was used to measure the startle response under cool-white fluorescent lighting versus full-spectrum fluorescent lighting (n = 5 subjects) under both bright and dim lighting conditions. Higher arousal was detected measuring GSC under the cool-white lighting condition, and under the dim lighting condition using both types of lighting. In the third experiment, ten subjects were assessed for GSC startle response using both lighting types set at the dim brightness level. There was a strong trend indicating a higher GSC arousal under the dim cool-white lighting condition. Other studies support that a GABAergic inhibitory circuit is inhibited by darkness and that the spectral characteristics of cool-white lighting are more stressful to humans than full-spectrum lighting. These preliminary findings regarding stress and ambient lighting may be especially important in the neural development of children, and in those clinical populations that are particularly sensitive to environmental stress.

Acoustic Stimulation↗