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PubMed2000

Effects of caffeine on sensorimotor gating of the startle reflex in normal control subjects: impact of caffeine intake and withdrawal.

RATIONALE: Prepulse inhibition (PPI), a cross-species measure of sensorimotor gating, is impaired in certain neuropsychiatric disorders. This study was designed to assess caffeine effects on PPI in normal humans, as part of an effort to understand cross-species differences and similarities in the neurochemical regulation of PPI. METHODS: Startle was measured during a screening session; 7 days later, subjects were retested after placebo or caffeine (200 mg; double-blind design). Subjects were characterized as low versus high caffeine drinkers based on established scales (range 11-628 mg/day), and either maintained ad libitum caffeine intake (Ad lib study; n=18) or refrained from caffeine consumption for > or =15 h prior to testing (Withdrawal study; n=12). Autonomic and self-rating measures, acoustic and tactile startle, and unimodal and cross-modal PPI, were measured in divided sessions for 3 h post-treatment. RESULTS: There were significant effects of caffeine and/or caffeine withdrawal on several self-rating and autonomic measures, and on startle reflex habituation, but not on acoustic or tactile startle magnitude or PPI. Difference scores of startle data from screening versus test days revealed no group effects on startle magnitude, but PPI difference scores revealed that caffeine had opposite effects on low versus high caffeine drinkers (means=57 versus 258 mg/day) in the two withdrawal states. In the absence of withdrawal, caffeine reduced PPI in heavy caffeine drinkers; during withdrawal, caffeine increased PPI in heavy caffeine drinkers. The opposite pattern was evident in low caffeine drinkers. CONCLUSIONS: While a physiologically active dose of caffeine has no simple effects on PPI in normal humans, both withdrawal states and normal levels of caffeine consumption may be important factors in understanding this drug's effects on sensorimotor gating.

Adolescent↗

PubMed1990

Lesions producing REM sleep without atonia disinhibit the acoustic startle reflex without affecting prepulse inhibition.

This study determined whether the brainstem motor inhibition system that mediates muscle atonia during rapid eye movement (REM) sleep is involved in the elicitation and prepulse inhibition of the acoustic startle reflex. Electrolytic or neurotoxic (glutamate) lesions were made in the dorsolateral pontine tegmentum or the medial medulla, respectively, to produce the syndrome of REM sleep without atonia. Startle responses were released during REM sleep following the lesions. However, the amount of startle suppression produced by auditory prepulse after the lesion did not differ from that seen in intact controls. We conclude that REM sleep suppression of the acoustic startle responses is mediated by the system responsible for tonic motor inhibition, but auditory prepulse inhibition of the acoustic startle is not.

Animals↗

PubMed1990

Differential effects of apomorphine on prepulse inhibition of acoustic startle reflex in two rat strains.

Apomorphine disruption of prepulse inhibition (PPI) has been proposed as an animal model of sensorimotor gating deficits exhibited by schizophrenics. The effects of apomorphine on PPI of the acoustic startle reflex in male rats of Wistar and CD (Sprague-Dawley derived) strains were compared under identical test conditions. In Wistar rats, subcutaneous administration of 0.25-1.0 mg/kg apomorphine blocked PPI without affecting startle amplitude. In CD rats, apomorphine (0.3-3.0 mg/kg, SC) had no effect on PPI, but increased startle amplitude. Therefore, choice of rat strain is an important factor in the design of experiments studying apomorphine effects on PPI.

Acoustic Stimulation↗

PubMed1989

Sensitization of the startle reflex by footshock: blockade by lesions of the central nucleus of the amygdala or its efferent pathway to the brainstem.

Bilateral electrolytic lesions of the central, but not the lateral, nucleus of the amgydala blocked shock sensitization of startle (the increase in startle produced by presentation of ten 0.6-mA footshocks in rapid succession). Lesions of the central nucleus also decreased reactivity to shock (jumping and flinching) during shock presentation. However, this decrease in reactivity cannot account for the blockade of shock sensitization, because when a higher shock intensity (1.0 mA) was used, producing equivalent reactivity to that of controls at 0.6 mA, central nucleus lesions still blocked shock sensitization. Moreover, lesions of the caudal part of the ventral amygdalofugal pathway, which carries central nucleus efferents to the startle reflex pathway, also blocked shock sensitization. It is hypothesized that shock activates the central nucleus of the amygdala, which increases startle through modulation of the startle pathway. Activation of the amygdala by shock may be the unconditioned response relevant for fear conditioning.

Acoustic Stimulation↗

PubMed1992

Lesions of the central nucleus of the amygdala block the excitatory effects of septal ablation on the acoustic startle reflex.

Many studies have investigated the role of the septum and the amygdala in emotional behavior. While the literature is somewhat inconsistent, most studies suggest a role for the septal nuclei in the inhibition of fear and stress responses (at the behavioral, autonomic and hormonal levels) while the central nucleus of the amygdala is involved in the production of such responses. The present study examined the ability of lesions of the central nucleus of the amygdala to block the excitatory effects of complete septal ablation on the acoustic startle reflex. Septal ablation produced a significant increase in startle amplitude which was blocked by concomitant lesions of the central nucleus of the amygdala. These results suggest that the increase in startle amplitude resulting from septal damage might be due to a disinhibition of neuronal activity in the central nucleus of the amygdala, a structure known to mediate the increase in startle associated with conditioned and unconditioned fear, or from antagonistic interactions at other target sites which themselves modulate startle.

Acoustic Stimulation↗

PubMed2001

Reduced brain serotonin activity disrupts prepulse inhibition of the acoustic startle reflex. Effects of 5,7-dihydroxytryptamine and p-chlorophenylalanine.

These experiments examined the impact of extensive depletions of forebrain 5-hydroxytryptamine (5-HT; serotonin) levels on prepulse inhibition (PPI) of the acoustic startle reflex in rats. In Experiment 1, injection of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) into the dorsal and median raphe nuclei disrupted PPI. This deficit was observed beginning 2 days after lesioning and was still apparent 8 weeks later. Basal startle reactivity was not altered. The 5-HT(1A) receptor agonist 8-OH-DPAT (0.1 mg/kg) and the dopamine receptor agonist apomorphine (1mg/kg) also disrupted PPI; the effect of 8-OH-DPAT, but not apomorphine, was potentiated in 5-HT-depleted rats. Basal startle reactivity was enhanced by 8-OH-DPAT in sham-lesioned rats but not in 5,7-DHT-lesioned rats. In Experiment 2, a second method for depleting 5-HT was used. The tryptophan hydroxylase inhibitor p-chlorophenylalanine (PCPA) also disrupted PPI without altering basal startle reactivity. Again, 8-OH-DPAT disrupted PPI in control animals; this effect was not altered in PCPA-treated rats but the increase in basal startle reactivity induced by 8-OH-DPAT was not observed in PCPA-treated rats. Taken together with the results of previous experiments involving drugs that enhance 5-HT neurotransmission it appears that both increases and decreases in 5-HT activity disrupt PPI.

5,7-Dihydroxytryptamine↗

PubMed1992

Auditory startle reflex in post-traumatic stress disorder patients treated with clonazepam.

Manifestations of acute hyperarousal in the Post-Traumatic Stress Disorder (PTSD) have been assimilated with panic attacks. This study examines the auditory startle reflex in PTSD patients treated with clonazepam, a benzodiazepine with anti-panic properties. PTSD patients treated with clonazepam did not differ from drug-free PTSD patients in the magnitude and the habituation rate of their responses to an auditory startle, with both groups showing abnormally slow habituation. It is suggested that the mechanisms underlying phasic hyperarousal in PTSD might differ from those which have been implied in the genesis of panic attacks.

Adult↗

PubMed2001

[The startle reflex in schizophrenia research].

Abnormalities of attention and information processing are described as important features of schizophrenia. Theoretically, they may reflect deficiencies in central mechanisms of inhibition and selection. These deficiencies are believed to lead to cognitive fragmentation in patients with schizophrenia. Findings of an impaired prepulse-inhibition (PPI) and habituation of the startle reflex in patients with schizophrenia are thought to represent preattentive, i.e., automatic attention deficits. Other paradigms with attentional instructions help to detect and to quantify deficits in controlled attentional functions. The PPI of the auditory startle blink reflex-mediated primarily by brainstem structures--is regulated by cortico-striato-pallido-pontine influences and by neurotransmitters involved in the pathogenesis of schizophrenia. An animal model of PPI provides the possibility to test neurobiological hypotheses in schizophrenia and to screen substances for their potential antipsychotic properties. Because reduction of PPI also occurs in other neuropsychiatric disorders, further studies are required to develop new paradigms of startle modification with findings of higher specificity and probable diagnostic relevance in patients with schizophrenia.

Acoustic Stimulation↗

PubMed2005

Effects of background noise on the human startle reflex and prepulse inhibition.

Three experiments investigated whether background noise modified the startle blink reflex and prepulse inhibition (PPI). In Experiment 1 background noise was about 28 (ambient), 40, and 60 dB; in Experiments 2 and 3 background noise was ambient and 60 dB. Prepulses were 70-dB tones (Experiments 1 and 3) or a tactile stimulus (Experiment 2). Startle-eliciting stimuli were 94-dB noise (Experiments 1 and 2) or an airpuff to the face (Experiment 3). Prepulses were presented at stimulus onset asynchronies of 30, 60, 120, 240, and 2000 ms relative to the startle-eliciting stimulus. Background noise of 60 dB had no effect on control reflexes, whereas 40-dB background noise increased control reflexes. Background noise decreased PPI, but only when an acoustic stimulus was used as prepulse. In sum, the findings show that background noise reduces the signal-to-noise ratio of acoustic prepulses and decreases their modulatory effect on the startle reflex.

Acoustic Stimulation↗

PubMed2003

Altered affective modulation of the startle reflex in alcoholics with antisocial personality disorder.

BACKGROUND: Individual differences in neural circuitry that regulate emotional reactivity may be associated with alcoholism and antisocial personality disorder (ASPD), a common comorbid condition. The emotion-modulated startle reflex was used to investigate emotional reactivity among alcohol-dependent (AD) men with and without ASPD. METHODS: Sixty-two men were tested: (1) AD (n = 24), (2) AD-ASPD (n = 17), and (3) non-AD, non-ASPD controls (n = 21). Participants completed self-report instruments and clinical interviews and had eye-blink electromyograms measured in response to acoustic startle probes while viewing color photographs rated as affectively pleasant, neutral, and unpleasant. RESULTS: Startle blink magnitudes were larger during unpleasant as compared with pleasant slides for control and AD groups, resulting in significant linear trend effects (p < 0.001) and nonsignificant quadratic trend effects. In contrast, AD-ASPD did not show a significant difference in blink magnitude during unpleasant and pleasant slides and did not show a significant linear valence trend or quadratic trend effect (p > 0.6). Subjective valence and arousal ratings of the photographs were similar across groups. CONCLUSIONS: Adult male alcoholics with ASPD have abnormal emotional responsiveness to both pleasant and unpleasant stimuli relative to alcoholics without ASPD and to controls.

Acoustic Stimulation↗

PubMed2002

Differing effects of the cannabinoid agonist, CP 55,940, in an alcohol or Tween 80 solvent, on prepulse inhibition of the acoustic startle reflex in the rat.

It has been suggested that cannabinoid agonists increase dopamine (DA) transmission in the mesolimbic dopamine system. However, evidence for such an effect is inconsistent. Prepulse inhibition (PPI) of the acoustic startle reflex is a behavioural paradigm that is modulated by an increase of mesolimbic dopamine. This study sought to ascertain whether or not a cannabinoid agonist, CP 55,940, mimicked the effects of amphetamine (a drug which increases dopamine release) on PPI. The first experiment measured the PPI of 16 male Wistar rats injected (i.p.) with different doses of CP 55,940 in a Latin-square design. A second experiment replicated the effects of the first experiment in a between-subjects design, and also examined the effects of using a 5% alcohol solution as a solvent for cannabinoid agonists, in comparison to the more inert detergent, Tween 80. In both experiments, CP 55,940 in Tween 80 significantly reduced basal activity, increased startle onset latencies and increased PPI, effects opposite to those of amphetamine. These results suggest that the net behavioural effects of cannabinoids are opposite to those of amphetamine. In addition, it was found that 1 ml/kg of a 5% alcohol solution has significant behavioural effects on its own, and reverses the effects of CP 55,940 on PPI.

Acoustic Stimulation↗

PubMed1997

Effect of acute subcutaneous nicotine on prepulse inhibition of the acoustic startle reflex in healthy male non-smokers.

In a double-blind placebo-controlled trial, the effects of two doses (6 micrograms/kg, 12 micrograms/kg) of acute SC nicotine were investigated on prepulse inhibition (PPI) of the acoustic startle reflex in healthy non-smoker male volunteers. Each subject received three injections [placebo (saline), 6 micrograms/kg nicotine, 12 micrograms/kg nicotine] on separate occasions, 2 weeks apart. No influence of either 6 micrograms/kg or 12 micrograms/kg nicotine was observed for the amplitude and habituation of the startle response over pulse-alone stimuli, relative to the saline-treated condition. Percent of PPI (expressed as percent reduction of non-prepulse trials) was significantly greater, but PPI as measured by absolute difference scores was not significantly different, when subjects were given the 12 micrograms/kg dose of nicotine than saline. There was an increase in percent of PPI from saline through low to high doses of nicotine, but PPI observed under the low dose did not differ significantly from either the high dose or placebo. These results provide some support for previous findings showing an enhancement in PPI by cigarette smoking in overnight smoking-deprived smokers and by acutely administered nicotine in experimental animals. The findings indicate that previously observed effects of smoking on percent of PPI in smoking-deprived subjects were not attributable to the restoration of a deficit induced by smoking withdrawal, but represent a direct pharmacological action of nicotine.

Adult↗

PubMed1994

Nicotine modulates effects of stress on acoustic startle reflexes in rats: dependence on dose, stressor and initial reactivity.

Cigarette smokers report that one reason for smoking is that smoking helps them cope with stress, but there is conflicting evidence as to whether nicotine reduces physiological and behavioral responses to stress. The acoustic startle reflex amplitude, pre-pulse inhibition, and habituation of the reflex provide quantifiable measures of behavioral reactivity that may be sensitive to stress-induced changes that are altered by nicotine. In the present experiment, rats classified as high and low reactors according to baseline startle amplitudes were administered nicotine (6 or 12 mg/kg/day) or saline by osmotic minipump for 11 days. On day 11, animals were acutely stressed by restraint or observation of restraint of conspecifics prior to startle measurement. Nicotine and stress each independently increased acoustic startle amplitude and amount of pre-pulse inhibition, but in combination, the effect of restraint stress and 12 mg/kg nicotine were indistinguishable from saline-treated, non-stressed controls. In contrast, the 6 mg/kg nicotine dose enhanced effects of both restraint and observation stressors on startle amplitude and pre-pulse inhibition. Animals classified as highly reactive prior to treatment were more responsive to nicotine, stress, and the combination, suggesting that initial reactivity is an important determinant of drug and stress effects. Results indicate that nicotine can both reduce and enhance stress effects on reflex amplitude and pre-pulse inhibition depending upon nicotine dose, stressor, and individual differences in reactivity.

Acoustic Stimulation↗

PubMed2006

Effects of age-related hearing loss on startle reflex and prepulse inhibition in mice on pure and mixed C57BL and 129 genetic background.

The present study examined the developmental course of the age-related hearing loss and its consequences on the expression of acoustic startle reflex (ASR) and prepulse inhibition (PPI) generated by white-noise bursts in 129S2/SvPas (129) and C57BL/6J (C57) mouse strains and their F(1) hybrids. Auditory brainstem responses (ABR), ASR and PPI were assessed at various time points: 6, 28, 41 and 94 weeks. Both parental strains showed marked ABR threshold shifts with age, with C57 mice having the most pronounced deficits. By contrast, the hybrids displayed only minor hearing loss with age. The time courses of ASR and PPI varied considerably between the mouse strains. From 6 to 41 weeks of age, ASR and PPI elicited by weak stimuli (70-90dB) increased in C57 mice, whereas the startle responses to intense stimuli (95-120dB) declined progressively. In 129 and hybrid mice, PPI levels remained relatively stable during the first year, but a progressive increase of ASR was observed in the hybrids for intense stimuli (95-120dB). When animals reached 94 weeks of age, marked deterioration of ASR was observed in all strains, while deficits in PPI were only seen in 129 and C57 mice. These findings show that the time course and the severity of the hearing loss vary considerably between 129, C57 strains and their hybrids, thus suggesting a marked heterogeneity in the genetic mechanisms underlying deafness in mice. They also demonstrate that the age-related hearing loss may have complex consequences on auditory behavioral performances depending of the severity of the deficits, the genetic background as well as the stimuli parameters.

Acoustic Stimulation↗

PubMed2001

The differential effects of prenatal stress in rats on the acoustic startle reflex under baseline conditions and in response to anxiogenic drugs.

RATIONALE: The prenatal stress syndrome (PS) is characterized by exaggerated behavioral and physiological responses to stressful stimuli and anxiogenic agents. OBJECTIVES: To characterize the behavioral effects of PS on the acoustic startle reflex (ASR) and to determine the possible role of PS-induced alterations in noradrenergic control of ASR by determining the effects of the alpha2-adrenoceptor antagonists, yohimbine, idazoxan, and RS79948-197. METHODS: PS was induced by exposing pregnant dams to a mild stressor of handling and saline injection (0.1 ml, s.c.) from gestational days 14 to 21. Control dams were left undisturbed throughout pregnancy. Using adult male offspring, all ASR studies consisted of either a 30- or 60-min testing period containing 60 or 120 acoustic startle stimuli trials (95 dB, 50 ms noise burst) at a fixed intertrial interval of 30 s after a 5-min acclimation period. For drug studies, a 3-day repeated measures design was implemented. RESULTS: With the exception of the response to the first startle stimulus on the first day of testing, there were no significant differences in baseline ASR between control and PS offspring. Low doses of yohimbine, idazoxan, and RS79948-197 were anxiogenic in the ASR test in both control and PS offspring. PS offspring were less responsive to higher doses of yohimbine (5 mg/kg) and idazoxan (8 mg/kg) but did not differ from control in their responses to any dose of RS79948-197. CONCLUSIONS: Anxiogenic effects of yohimbine, idazoxan, and RS79978-197, likely mediated via alpha2-adrenoceptor blockade, are similar in control and PS rats. Differences between control and PS rats occurred in the response to higher doses of yohimbine and idazoxan. Non-specific effects of these drugs, such as actions at 5HT1A receptors, may cause their behavioral profile to be altered by PS, and to differ from the highly selective RS79948-197.

Adrenergic alpha-Antagonists↗

PubMed1997

Mitochondrial toxin 3-nitropropionic acid produces startle reflex abnormalities and striatal damage in rats that model some features of Huntington's disease.

Systemic administration of the mitochondrial toxin 3-nitropropionic acid (3NP) to rats produces striatal lesions that mimic some aspects of pathology in Huntington's disease (HD). To evaluate whether 3NP-induced lesions cause sensorimotor gating deficits observed in HD, we measured prepulse inhibition (PPI) of the acoustic startle reflex after systemic administration of 3NP (10, 15, or 20 mg/kg) to 5-month-old rats. PPI, the reduction of startle magnitude by a weak auditory prestimulus, is significantly reduced in patients with HD. Two daily injections of 3NP produced gross histologic evidence of striatal lesions in some rats and significantly reduced PPI. Striatal lesions also significantly disrupted amphetamine-induced stereotypy, another index of dorsal striatal function. 3NP thus reproduces a specific objective and quantifiable gating deficit found in patients with HD.

Animals↗

PubMed1998

Repeated testing of prepulse inhibition and habituation of the startle reflex: a study in healthy human controls.

The aim of this study was to examine the effect of repeated testing on prepulse inhibition (PPI) and habituation of the startle reflex. Fifteen healthy control subjects (eight males, mean age 30 years; seven females, mean age 29 years) were tested on three occasions across the same day separated by a minimum of 2 h. An acoustic probe of 40-msec bursts of 116 dB(A) white noise over a continuous background noise of 70 dB(A) was presented binaurally through headphones and the eye-blink component of the startle response was measured taking electromyographic recordings from the right orbicularis oculi. The test session was identical at each time point and consisted of two blocks of 12 randomly mixed trials of four pulse-alone, four 60-msec prepulse and four 120-msec prepulse trials enclosed by two blocks each of six pulse-alone trials. There was huge variation in individual response magnitude that was independent of subsequent PPI in both women and men. Women showed greater PPI in the second half of sessions with the 120-msec prepulse only; but PPI was not altered significantly in either group between sessions across the day. In general, there was good test-retest reliability of PPI especially within trial type. Normal reflex habituation occurred across sessions and this effect was preserved in sessions across the day. Latency of response was significantly reduced in a session by the 60-msec trial type compared to the 120-msec trial type, as previously reported. Our results suggest that measures of PPI and habituation of the startle response are appropriate and reliable for a within-subject, test-retest design.

Acoustic Stimulation↗

PubMed2003

The startle reflex in schizophrenia: habituation and personality correlates.

Schizophrenia has long been associated with abnormal patterns of arousal that are thought to reflect disturbances in the reticular-activating system of the brain. Psychophysiological investigations of sensory responsivity have repeatedly demonstrated reduced reactivity and habituation to moderately intense stimuli in patients with schizophrenia. While not traditionally used as a measure of physiological arousal, the startle reflex represents an alternative method for studying reactivity and habituation in schizophrenia. This study examined eye blink responsivity to a repeatedly presented intense acoustic startle probe in men with chronic schizophrenia and healthy normal controls. Subjects' personality profiles were also measured, as increased reactivity and arousal have been traditionally implicated as a physiological component to the personality trait of neuroticism. Results indicated that schizophrenic subjects did demonstrate significantly reduced rates of habituation to the acoustic startle probe and higher scores on measures of neuroticism in comparison to normal controls. However, no correlation between habituation rate and neuroticism emerged. These studies replicate previous findings of habituation in schizophrenia and provide further evidence for sensory reactivity disturbances in schizophrenia. The relationship of these findings to cognitive disturbances in schizophrenia is considered and directions for future research are discussed.

Acoustic Stimulation↗