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PubMedDate not supplied

Neonatal methamphetamine-induced long-term acoustic startle facilitation in rats as a function of prepulse stimulus intensity.

Neonatal exposure to methamphetamine (MA) has previously been shown to induce acoustic startle facilitation when the animals were tested as adults. The present experiment sought to replicate and extend this effect using a lower dose of MA and to determine if the effect varied as a function of prepulse stimulus intensity. Sprague-Dawley CD rat offspring were culled on the day after birth to eight (preferentially retaining females). On days 1-10, progeny were injected SC with either 20 mg/kg of d-MA twice per day (doses spaced at least 8 h apart) or distilled water. On postnatal day 50, offspring were administered 51 acoustic startle trials followed by 36 prepulse trials. Prepulse intensities were 0, 70, 75, 80, 85, or 90 dB. MA progeny showed augmented startle response amplitudes on both paradigms but the effect was most pronounced on the prepulse trials. Prepulse intensity interacted with MA treatment in that significant facilitation in the MA animals occurred on 0 and 70 dB prepulse trials but was only a trend (p < 0.10) on 75, 80, 85, and 90 dB trials. This implies that the effect of MA is most likely upon the basic startle reflex and not upon inhibitory pathways that modify startle reactivity.

Acoustic Stimulation↗

PubMed1991

Tolerance to the analgesic, but not discriminative stimulus effects of morphine after brief social defeat in rats.

One of the most prominent consequences of defeat in a social confrontation is a long-lasting tolerance-like insensitivity to the analgesic effects of opiates, even when only small short-lived changes in nociception are detectable during the acute social stress. The present experiments examined (1) which kinds of social experiences lead to morphine tolerance, (2) whether or not the morphine tolerance in defeat-experienced rats extends from the analgesic effects to the discriminative stimulus and rate-decreasing effects of morphine, and (3) how long morphine tolerance lasts after a defeat experience. After five brief social confrontations including attack and threat by a resident rat leading to submission or defeat of the intruder, the latter exhibits marked tolerance to the analgesic effects of morphine, but not to the discriminative stimulus or behaviorally suppressive effects. Changes in social housing did not alter morphine's behavioral effects. Tolerance to the analgesic morphine effects was detected for 2 months after the defeat experience, whereas the discriminative stimulus and rate-decreasing effects were closely similar to those before defeat. This pattern was seen in animals for whom discriminative stimulus training with morphine was suspended after defeat as well as in those for whom it continued. In additional defeated and non-defeated animals, morphine's effects on the acoustic startle reflex was assessed. In contrast to the tail flick reflex to a noxious heat stimulus, the acoustic startle response remained unaffected by defeat experience or by morphine (up to 30 mg/kg). The long-lasting and large degree of tolerance after brief social defeat experiences appears to be limited to the analgesic effects of morphine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗

PubMed2002

A direct assessment of the role of state and trait negative emotion in aggressive behavior.

Affective priming of aggression was examined in groups low and high in trait negative emotionality (NEM) using a Buss aggression paradigm. Negative affect was induced by exposure to aversive air blasts during some intervals (threat) and not others (safe). Phasic negative affect was assessed using startle reflex potentiation, and tonic distress was indexed by startle sensitization. Participants delivered shocks faster during threat versus safe intervals, indicating that phasic distress primed aggression. Following initial exposure to air blasts, high NEM participants showed enhanced tonic distress and delivered persistently more intense shocks than low NEM participants. These findings indicate that sustained negative affect biases high stress-reactive individuals toward more intense acts of aggression, with phasic distress affecting the rapidity of aggressive response.

Adult↗

PubMed1994

Diazepam withdrawal: effects of diazepam and gepirone on acoustic startle-induced 22 kHz ultrasonic vocalizations.

It has proven difficult to demonstrate and study the "anxiogenic" quality of drug withdrawal states in animals. Ultrasonic vocalizations (USV) in response to acoustic startle stimuli have shown promise as a measure of affect and may represent "distress" responses during diazepam withdrawal. Three experiments evaluated the association between USV and "distress" by comparing the effects of diazepam as a prototypic benzodiazepine agonist and the putative anxiolytic gepirone with affinity for 5-hydroxytryptamine (5-HT1A) receptors in naive and diazepam-withdrawn subjects. Adult male Long-Evans rats were exposed to acoustic startle sessions consisting of nine 105 dB and nine 115 dB stimuli. USV at 20-30 kHz were readily emitted during startle and often commenced after the third or fourth stimulus presentation. Acutely, intraperitoneal (IP) administration of diazepam (0.1-3 mg/kg) and gepirone (0.1-1 mg/kg) decreased USV dose-dependently without affecting the startle reflex; gepirone also decreased tail flick latency. Startle-induced USV were also sensitive to the "anxiogenic" effects of withdrawal from diazepam exposure (0, 2.5, 5, 10 mg/kg b.i.d. IP x 5 days). Twenty-four hours after the last diazepam injection, rats were hyperreactive to startle stimuli and doubled their rate of USV over vehicle-treated controls. Gepirone (0.1-1 mg/kg IP), but not diazepam (3-20 mg/kg IP) antagonized the increased rate of USV in rats withdrawn from 10 mg/kg b.i.d. diazepam. Diazepam (2.5-10 mg/kg IP) antagonized the increased rate of USV in rats withdrawn from 2.5 mg/kg b.i.d. diazepam.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗

PubMed1999

Effects of nicotine and stress on startle amplitude and sensory gating depend on rat strain and sex.

We recently reported that 14 days of nicotine administration (12 mg/kg/day) reduced acoustic startle reflex amplitude and impaired prepulse inhibition (PPI) of startle in male and female Long-Evans rats. These findings contrasted with reports of nicotine-induced enhancement of startle and PPI in Sprague-Dawley (a different strain) male rats. The present experiment administered 0, 6, or 12 mg/kg/day nicotine via osmotic minipump for 14 days to 120 Sprague-Dawley rats (male and female) and to 120 Long-Evans rats (male and female) and examined ASR and PPI. Half of the subjects also were stressed by immobilization once each day to examine nicotine-stress interactions. Nicotine enhanced ASR and PPI responses of Sprague-Dawley rats but impaired these responses in Long-Evans rats, regardless of sex. Effects of stress were complex and depended on strain, sex, and drug dose. These findings indicate that effects of nicotine on measures of reactivity (ASR) and sensory gating (PPI) depend on genotype and that nicotine stress interactions depend on genotype, sex, and nicotine dosage.

Animals↗

PubMed1988

Hyperbaric effects on sensorimotor reactivity studied with acoustic startle in the rat.

In three experiments, startle responses to brief intense tone-bursts (30 msec, 110 dB, 6000 Hz) and single pulse (0.1 msec) stimulation of the cochlear nucleus and the nucleus reticularis pontis caudalis are studied under high pressures of heliox (from 0 bar to 50 bars) in the rat. For each rat (N = 12), mean amplitude and latency changes in startle responses (nuchal electromyography and whole-body accelerometry) are compared at normobaric pressure and during compression, at a speed of 100 bar/H. The results indicate that high pressures decrease (50% of control size) tone evoked startle by acting on the peripheral auditory organ, probably through middle and/or inner ear barotrauma. The large increases in electrically-elicited startle (250% of control size) from the cochlear and reticular nuclei, under hyperbaric conditions, suggest that high pressures affect sensorimotor reactivity by excitatory action on synaptic transmission in the relays of the acoustic startle reflex arc at the lower brainstem and spinal levels. Startle latencies remain unaffected by the heliox high pressures studied here.

Acoustic Stimulation↗

PubMed1978

Involvement of norepinephrine in startle arousal after acute and chronic d-amphetamine administration.

Treatment with d-amphetamine produced a dose-dependent increase in startle amplitude in response to a buzzer. This increase appeared to be a reflection of a sensitization effect, i.e., enhanced responsivity as a function of repeated stimulus presentations. Treatment with alpha-methyl-p-tyrosine, which reduced whole brain concentrations of dopamine (DA) and norepinephrine (NE), or treatment with FLA-63, which reduced only NE, antagonized the effects of d-amphetamine on the startle reflex, suggesting a role of NE in this behavior. Startle amplitude was also reduced following chronic d-amphetamine treatment. The effect of d-amphetamine on startle was found to be independent of changes in drug-induced locomotor excitation. The data of the present investigation, together with earlier reports, suggests that tolerance occurs to those behaviors that involve a noradrenergic component.

Animals↗

PubMed1991

Efferent pathway of the amygdala involved in conditioned fear as measured with the fear-potentiated startle paradigm.

Fear-potentiated startle in the rat is a measure of conditioned fear that is blocked by lesions of the central nucleus of the amygdala. In a companion study, Rosen, Hitchcock, Sananes, Miserendino, and Davis (1991) demonstrated a direct anatomical projection from the central nucleus to the brainstem startle reflex circuit. In the present study, fear-potentiated startle was blocked by lesions that interrupted this pathway at 3 different levels or by a crossed lesion that interrupted the pathway at its source on one side and at a more caudal level on the other side. Although synaptic relays have not been ruled out entirely, the data suggest that the direct projection from the central nucleus of the amygdala to the startle circuit mediates the expression of fear-potentiated startle. These findings are consistent with the literature indicating that efferent projections from the central nucleus to various brainstem structures are involved in the expression of several conditioned fear responses.

Amygdala↗

PubMed2006

Processing of emotional adjectives: Evidence from startle EMG and ERPs.

Affective startle modulation in the electromyographic (EMG), auditory startle evoked potentials, and visually evoked potentials (VEPs) were assessed while subjects evaluated pleasant, unpleasant, and neutral adjectives. Acoustic startle probes were presented at random time points 2.5-4.0 s after word onset. The visual P2 and P3 potentials were generally larger during processing of emotional than of neutral adjectives. In contrast, the late positive component was enhanced and was correlated with larger EMG startle responses and auditory startle evoked potential P3 amplitudes for pleasant words only. During internal cognitive activity, the startle reflex represents a measure of "processing interrupt." Thus the startle tone interrupted processing of particularly pleasant adjectives and caused re-alerting to environmental stimuli. Specific effects for pleasant material may arise from a "positivity offset," favoring responses to pleasant material at lower arousal levels.

Acoustic Stimulation↗

PubMed1980

5-Methoxy-N,N-dimethyltryptamine: spinal cord and brainstem mediation of excitatory effects on acoustic startle.

The effects of different doses (0.03, 0.06, 0.12, 0.25, 1.0, 2.0, 4.0, and 8.0 mg/kg body weight) of 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) were tested on the acoustic startle reflex in rats. Beginning at 0.12 mg/kg, 5-MeODMT increased startle monotonically up to the highest dose used. 5-MeODMT still increased startle in acutely decerebrate rats or when infused directly onto the spinal cord. The excitatory effects of a high systemic dose of 5-MeODMT were completely blocked by cinanserin, cyproheptadine, and propranolol, but not by parachlorophenylalanine, alpha-methyl-p-tyrosine, haloperidol, sotalol, or phenoxybenzamine. The results were discussed in terms of a new theory, which suggests that stimulation of serotonin receptors in the spinal cord enhance startle whereas serotonin receptors in the forebrain inhibit startle.

Acoustic Stimulation↗

PubMed1991

Opiate-dopamine interactions in the neural substrates of acoustic startle gating in the rat.

1. The acoustic startle reflex (ASR) was measured in adult male Dawley rats using startling acoustic stimuli presented either alone or 60-500 msec after a weak acoustic prepulse. 2. The inhibition of the ASR by the prepulse, termed "prepulse inhibition" (PPI), was blocked in animals treated either with the indirect dopamine (DA) agonist d-amphetamine (AMPH) or with the direct DA receptor agonist apomorphine (APO). 3. Pretreatment with the opiate receptor antagonist naloxone (NAL) prevented the AMPH-induced loss of PPI, but did not diminish the APO-induced loss of PPI. 4. The opiate heroin had no significant effect on PPI. 5. Dopaminergic mechanisms that modulate PPI in the rat may be regulated by opiate systems that act presynaptic to the DA receptor; brain opiate receptors may not have direct effects on startle gating independent of this opiate-DA interaction.

Animals↗

PubMed1989

Neural systems involved in fear-potentiated startle.

The acoustic startle reflex offers a number of advantages for analyzing the neural bases of behavior. Startle apparently is mediated by excitatory amino acids at several of the synapses that comprise the short-latency startle pathway. The reflex is modulated by a variety of neurotransmitters at both the spinal and the supraspinal levels. In addition to showing habituation and sensitization, startle is increased in the presence of a fear stimulus. This may result from activation of the central nucleus of the amygdala which projects directly tot he acoustic startle pathway. A major challenge for future studies will be to determine what neurotransmitters, which are known to modulate startle, are involved in habituation, sensitization, and fear conditioning and to begin to analyze these processes at a cellular level.

Amygdala↗

PubMed2003

Elevated startle during withdrawal from acute morphine: a model of opiate withdrawal and anxiety.

RATIONALE: An elevated startle response has been observed in humans and animals during withdrawal from multiple substances of abuse, a phenomenon thought to reflect the anxiogenic effects of withdrawal. Although anxiety is a common symptom of opiate withdrawal, few studies have examined the effects of morphine withdrawal on acoustic startle. OBJECTIVE: To develop a procedure for assessing opiate dependence through measurement of the startle reflex in rats. METHODS: The effects of opiate withdrawal on startle were evaluated using both spontaneous and naloxone-precipitated withdrawal from an acute dose of morphine. The ability of the treatment drugs clonidine and chlordiazepoxide to block withdrawal-induced increases in startle was also tested. RESULTS: Spontaneous withdrawal from an injection of morphine sulfate produced a significant increase in acoustic startle 2 h (3.2 mg/kg) or 4 h (10 mg/kg) after drug administration. Morphine withdrawal (10 mg/kg morphine sulfate) precipitated by the opiate antagonist naloxone (2.5 mg/kg) also produced a significant increase in startle magnitude. This elevation of startle was blocked by both clonidine (35 microg/kg) and chlordiazepoxide (10 mg/kg). CONCLUSIONS: These data demonstrate that both spontaneous and precipitated withdrawal from an acutely administered opiate produce anxiety-like effects on acoustic startle. This paradigm may be useful in the study of anxiety and the early mechanisms of drug dependence.

Acoustic Stimulation↗

PubMed1992

Reflex modification in psychosis-prone young adults.

The present study examined modification of the startle reflex in psychosis-prone and normal control subjects, using a continuous pure tone prestimulus (S1) and an intense white noise startle stimulus (S2). Reflex modification conditions consisted of stimulus pairs with onset asynchronies of 60, 120, and 2000 ms with a startle-alone condition as control. Startle was indexed by the eyeblink, which was measured by vertical electro-oculography. Subjects were identified as psychosis-prone by their high scores on the Perceptual Aberration or the Physical Anhedonia scales. Group differences in blink magnitude inhibition were observed between perceptual aberration and control subjects during short stimulus onset asynchronies, with perceptual aberrators showing significantly less inhibition than controls at 120 ms. No differences were evident between anhedonic and control subjects at the two short onset asynchronies nor were there any significant between-group differences when the interval between stimuli was long (2000 ms). These results suggest that subjects with perceptual aberrations may share with schizophrenics and other schizophrenia-spectrum subjects an underdeveloped mechanism which in normal subjects is presumed to operate during preattentive processing and functions to protect sensory information from the interfering effects of subsequent stimuli.

Acoustic Stimulation↗

PubMed2006

Prepulse inhibition of acoustic startle response in mild cognitive impairment and mild dementia of Alzheimer type.

Amnestic mild cognitive impairment (MCI) describes the condition of memory-impaired individuals who otherwise function well and do not meet the clinical criteria for dementia. Such individuals are considered to represent a transitional stage between normal aging and dementia of Alzheimer type (DAT). Neurobiologic changes in amnestic MCI, and their significance for psychophysiologic function, are poorly understood. In this study, the authors compared acoustic prepulse inhibition (PPI) between subjects with amnestic MCI and mild DAT to characterize sensorimotor gating. The acoustic startle reflex, which the authors measured using an accelerometer and electromyogram, involves whole-body movement and eye blink in response to a sudden loud noise (115 dB). PPI is inhibition of this reflex by a softer noise (prepulse; 85 dB) preceding the startle stimulus by 30 ms. PPI was examined in 30 controls, 20 subjects with amnestic MCI, and 20 subjects with mild DAT. Neither amnestic MCI nor mild DAT affected startle movement amplitude. Subjects with amnestic MCI showed significantly enhanced PPI (gating facilitation), while subjects with mild DAT exhibited significantly less PPI than controls (gating deficit). This pattern of PPI changes suggests that neuropathologic changes in the limbic cortex, mainly the entorhinal cortex, at the earliest stage of DAT might be responsible for PPI abnormalities via disturbed regulation of the limbic cortico-striato-pallido-pontine circuitry. Startle PPI changes could be used as a biologic marker for amnestic MCI and mild DAT.

Acoustic Stimulation↗

PubMed2004

Affective modulation of the startle response in depression: influence of the severity of depression, anhedonia, and anxiety.

BACKGROUND: The amplitude of the startle reflex response is known to be influenced by the concomitant presentation of affect-toned material--if it is positive affect-toned, the reflex is inhibited, and if it is negative affect-toned, the reflex is augmented. Abundant evidence demonstrates the utility of the affect-startle paradigm as a significant tool for measuring both positive and negative emotions. We applied this paradigm to study emotional reactivity in depression, particularly in relation to symptoms of depression, anhedonia, and anxiety. METHODS: Depressed patients (22) and controls (22) were shown a series of film clips, consisting of two clips with positive valence, two with negative valence, and two with relatively neutral valence. The startle response was measured in reaction to the acoustic startle-eliciting stimuli presented three times binaurally during each clip. RESULTS: Highly depressed and anhedonic patients, relative to controls, showed a reduced mood (self-ratings) and a lack of startle modulation in response to affective film clips whereas patients relatively low on depression/anhedonia displayed a reduced mood only with pleasant clips and a normal pattern of affective startle modulation. Anhedonia and depression were highly positively correlated but neither correlated with anxiety. Anxious patients displayed larger reflexes across all clips and showed a reduced mood modulation with pleasant, but not unpleasant, clips. LIMITATIONS: The large majority of patients was medicated with antidepressants which may have influenced the results. CONCLUSIONS. Reactivity to pleasant stimuli is diminished in patients suffering from low levels of depression and/or anhedonia, but reactivity even to unpleasant stimuli seems compromised at high levels of depression and/or anhedonia. Anxiety is associated with hyperstartle responding.

Adult↗

PubMed1997

Activation of amygdala cholecystokininB receptors potentiates the acoustic startle response in the rat.

The acoustic startle reflex is a sensitive index of "anxiety" and "fear." Potentiation of startle by conditioned and unconditioned fear stimuli appears to be mediated by the amygdala. CholecystokininB (CCKB) agonists increase "anxiety" in laboratory animals and induce "panic" in humans. Here, we investigate the role CCKB receptor-mediated mechanisms in the amygdala in the potentiation of startle. First, intra-amygdala infusions of the CCKB receptor agonist pentagastrin (0, 0.01, 0.1, 1, and 10 nM) produced a dose-related potentiation of acoustic startle responses. At the highest dose, startle amplitudes were increased up to 90% above preinfusion baseline levels. Second, similar infusions of pentagastrin had no effect on locomotor activity over the same time course, showing that increases in startle responsivity after infusions of pentagastrin are not attributable to nonspecific changes in motor activity. Third, infusions of similar doses of pentagastrin into the striatum or nucleus accumbens did not potentiate startle responses. Fourth, pretreatment with the CCKB receptor antagonist L-365,260 (0.1 mg/kg, i.p.) attenuated the potentiation of startle produced by intra-amygdala infusions of pentagastrin. Finally, intra-amygdala infusion of the CCKB receptor-selective antagonist PD-135158 (10 micro;g) blocked the potentiation of startle produced by i.c.v. infusions of pentagastrin, suggesting that i.c.v. infusions of pentagastrin potentiate startle responses via activation of amygdala CCKB receptors. These results show that amygdala CCKB receptor-mediated mechanisms are involved in the potentiation of acoustic startle responses.

Acoustic Stimulation↗

PubMed1993

Parameters affecting gap detection in the rat.

The present research used a startle amplitude reduction paradigm to investigate the ability of the rat's auditory system to track rapidly changing acoustic transients. Specifically examined was the ability of brief gaps in otherwise continuous noise to reduce the amplitude of a subsequently elicited acoustic startle reflex. The duration of the gap, time between gap offset and startle elicitation (the interstimulus interval or ISI), and rise-fall characteristics of the gap were systematically varied. Consistent with previous research, gaps reliably reduced startle amplitude. Gaps 2 msec long were reliably detected, and a 50-msec ISI resulted in the greatest amplitude reduction. Gaps presented at short ISIs produced amplitude reduction that followed a different time course than did gaps presented at longer ISIs. These results may reflect differences in the length of time available for the processing of the stimulus and may involve two different processes.

Acoustic Stimulation↗