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PubMed1996

Midlatency auditory evoked potentials and the startle response in the rat.

The P13 midlatency auditory evoked potential in the rat is (i) sleep state dependent, (ii) undergoes rapid habituation and (iii) is blocked by the cholinergic antagonist scopolamine. As such, the P13 potential in the rat shows the same characteristics as the P1 (or P50) potential in the human. These potentials are thought to be mediated, at least in part, by the cholinergic arm of the reticular activating system. Previous studies have linked the reticular activating system with the startle response. The present study was undertaken to explore this relationship by simultaneously recording the P13 potential and the electromyographically recorded startle response using stimuli designed to elicit each response. Simultaneous recordings from the vertex and neck musculature following auditory click stimuli showed that: (i) the mean threshold of the P13 potential was 69.3 +/- 1.9 dB, while that for the startle response was 87.9 +/- 6.4 dB; (ii) the P13 potential was present during waking and paradoxical sleep, but absent during slow-wave sleep, while the startle response was present reliably only during waking; (iii) both responses habituated in response to paired stimuli, but the startle response was more habituated than the P13 potential; and (iv) both responses were facilitated by trains of stimuli in a similar manner. Recordings carried out from the auditory cortex verified that the primary cortical response had properties different from the P13 potential; i.e. it was present during all sleep-wake states, had a lower threshold and did not habituate rapidly. Finally, different patterns of startle responses were detected in the neck muscles. In every case, the P13 potential occurred during the middle, inhibitory phase of the startle response. These results suggest that the P13 potential and the startle response share response features, but the P13 potential appears to be more sensitive to auditory stimulation and to sleep-wake states. The startle response may be modulating descending systems by priming the spinal cord to respond in a "fight vs flight" fashion. On the other hand, the P13 response may be modulating ascending systems by triggering thalamocortical activity and resetting descending systems to allow novel motor strategies.

Animals↗
PubMed2000

Moxonidine, a selective imidazoline-1 receptor agonist, suppresses the effects of ethanol withdrawal on the acoustic startle response in rats.

BACKGROUND: There is a need for improved treatments for ethanol withdrawal in humans. Previously, ethanol withdrawal has been shown to enhance the acoustic startle response in rats. Because many ethanol withdrawal symptoms are caused by autonomic hyperactivity, we examined the effects of two antihypertensives, the imidazoline(I)(1) agonist moxonidine and the alpha(2)-adrenergic partial agonist clonidine, on the ethanol-withdrawal-enhanced acoustic startle response in rats. d-amphetamine-enhanced startle served as a positive control. METHODS: Male, Long-Evans rats were made ethanol-dependent through unlimited access to liquid diet containing 6.7% v/v ethanol for 10 days. The concentration of ethanol was reduced to 3.3% v/v on the 11th day. On the 12th day, the rats received control diet. The acoustic startle response was tested 24 hours following the withdrawal of ethanol. Control rats were maintained on control liquid diet throughout the experiment. RESULTS: As has been shown previously, withdrawal from the chronic ingestion of ethanol significantly enhanced the acoustic startle response. Pretreatment with moxonidine (0.01, 0.1, and 1.0 mg/kg, subcutaneously), but not clonidine (0.3, 1.0, and 3.0 mg/kg, subcutaneously), significantly attenuated the ethanol withdrawal-induced elevation of the acoustic startle response. Moxonidine did not suppress the elevation in the startle response caused by d-amphetamine. CONCLUSIONS: These results indicate that I(1) receptors can play an important role in ethanol withdrawal and that moxonidine may be useful for the treatment of ethanol withdrawal in humans.

Animals↗
PubMed1977

The Mauthner-initiated startle response in teleost fish.

1. A characteristic behaviour, the 'Mauthner-initiated startle response', was recorded and quantitatively analysed with high-speed cinematography (200 frames/sec) after vibrational stimulation in 11 of 13 teleost species which possess Mauthner cells. 2. The latency of the response is 5-10 msec. This behaviour has: (a) an initial phase, the 'fast-body-bend', lasting about 20 msec and consisting of a stereotyped displacement of the head and tail to one side and (b), a second phase, the 'return-flip', consisting of a non-stereotyped flip of the tail to the opposite side. 3. Within 100 msec after the start of the Mauthner-initiated startle response, most fish were displaced 0-5-1-5 body lengths from their initial position. The variability of the animal's location after 100 msec suggests that the behaviour is adaptively non-predictable; 4. In goldfish, the Mauthner-initiated startle response could also be elicited by visual stimulation. 5. We conclude that the fast-body-bend is the direct result of activation of one Mauthner cell and its spinal motor neurone pool. 6. In four species we described examples of apparently non-Mauthner initiated startle responses.

Animals↗
PubMed1989

Influence of long-term sensitization on long-term habituation of the acoustic startle response in rats: central gray lesions, preexposure, and extinction.

The relation between long-term decrements of the acoustic startle response in rats and the development of freezing behavior during habituation training was examined. Freezing behavior developed over the initial trials of habituation training, and the rate of long-term response decrements was found to be inversely related to the development of freezing. Manipulations (neurological or behavioral) that either reduced the level of freezing or retarded its development promoted startle response decrements. In Experiment 1, rats receiving electrolytic lesions of the ventrolateral periaqueductal gray demonstrated both accelerated long-term startle response decrements and retarded development of freezing behavior. In Experiment 2, preexposure to the startle apparatus (i.e., latent inhibition) accelerated long-term startle decrements and inhibited development of freezing. In Experiment 3, exposure to the startle apparatus following initial habituation training (i.e., extinction) reduced both freezing behavior and startle response amplitudes. The results are discussed in terms of the influence of Pavlovian fear conditioning on long-term habituation of the acoustic startle response.

Animals↗
PubMed1998

Comparison of fast startle responses between two elongate bony fish with an anguilliform type of locomotion and the implications for the underlying neuronal basis of escape behavior.

A comparative anatomical and behavioral approach was used to elucidate the role of medullary networks associated with Mauthner cells (M-cells) in determining the type of fast startle responses of elongate bony fish with an anguilliform type of locomotion. The M-cell initiates fast startle responses in goldfish and is thought to initiate such responses in other fish as well [Wilson, 1959; Eaton et al., 1977; Currie and Carlsen, 1987; Currie, 1991]. Goldfish M-cells have a specialized structure, termed an axon cap, that surrounds their axon hillock-initial segment region and is critical for the control of M-cell excitability. The M-cell axon cap is present in some elongate fish such as the African lungfish (Protopterus, Lepidosireniformes) and absent in others such as the American eel (Anguilla, Anguilliformes). The lungfish startle response is characterized by a rotation of the head and upper trunk, similar to the initial phase of the goldfish (Carassius, Cypriniformes) startle response. The American eel, on the other hand, displays a withdrawal-type startle response. We hypothesize that the withdrawal-type startle response of the American eel results from the absence of inhibitory networks associated with the M-cell axon cap. The correlation of the absence of an axon cap and a withdrawal-type startle response may be a general feature of all Anguilliformes and elongate ray-finned fish with an anguilliform type of locomotion.

Anguilla↗
PubMed2005

Startle response in inpatients with borderline personality disorder vs. healthy controls.

Startle response is found to be enhanced in conditions that are accompanied by intense emotions, high levels of anxiety in particular. We assessed the autonomous and behavioral component of the startle reflex in a sample of 28 unmedicated inpatients with borderline personality disorder (BPD) compared to 28 controls. Amplitudes of electrodermal and startle response as well as habituation were measured in response to 15 bursts of white noise (100-db, 40-ms). We assessed prepulse inhibition to study gating capacities in BPD, with each prepulse (70-db, 30-msec) delivered 100 ms before the startling tone. In contrast to our hypothesis, our study revealed neither enhanced amplitudes of autonomic and electromyographic startle responses nor differences in habituation compared to healthy controls. In addition, no deficit in prepulse inhibition was found in BPD. In summary, our data indicate normal response to unconditioned threatening stimuli as well as normal gating capacities in BPD.

Acoustic Stimulation↗
PubMed2005

Characterization of the effects of corticotropin-releasing factor on prepulse inhibition of the acoustic startle response in Brown Norway and Wistar-Kyoto rats.

Sensori-motor gating, as assessed by prepulse inhibition of the startle response is diminished in patients with schizophrenia. We have previously shown that inbred Brown Norway (BN) rats display significantly less prepulse inhibition of the acoustic startle response than inbred Wistar-Kyoto (WKY) rats, and that prepulse inhibition is decreased by central administration of the neuropeptide, corticotropin-releasing factor (CRF) in both strains. The present study was conducted to establish whether peripheral administration of CRF alters prepulse inhibition, whether a low, threshold dose for decreasing prepulse inhibition is the same in the two rat strains, and whether central administration of a CRF receptor antagonist enhances prepulse inhibition in the BN strain. CRF-induced behavioral activation was also examined to determine whether the two rat strains are differentially sensitive to a behavioral effect of CRF that does not involve the startle response. In each experiment, BN rats showed significantly less prepulse inhibition than WKY rats. Subcutaneous administration of CRF had no affect on startle amplitude or prepulse inhibition of the startle response in either rat strain. In BN, but not in WKY rats, low-dose CRF (0.3 microg) decreased prepulse inhibition. However, doses of CRF that did not alter prepulse inhibition in the WKY strain, did result in behavioral activation. No dose of CRF tested affected baseline startle amplitude. Central administration of the CRF receptor antagonist, astressin had no effect on prepulse inhibition or startle amplitude in either rat strain. Central administration of the CRF receptor antagonist, D-Phe CRF (12-41) had no effect on prepulse inhibition in WKY rats, resulted in a only a small, non-significant increase in prepulse inhibition in BN rats, while it decreased startle amplitude. The results suggest that CRF reduces prepulse inhibition of the acoustic startle response independently of effects on the pituitary-adrenal axis, and that endogenous CRF has at most, a minor role in the low prepulse inhibition found in BN rats.

Acoustic Stimulation↗
PubMed1997

Effects of clonidine and diazepam on the acoustic startle response and on its inhibition by 'prepulses' in man.

This experiment examined the effects of two sedative/anxiolytic drugs, diazepam and clonidine, on the eyeblink component of the acoustic startle response in healthy volunteers. Twelve males (18-30 years), screened for normal hearing thresholds, participated in three sessions in which they received oral doses of placebo, diazepam 10mg and clonidine 200 microg according to a balanced double-blind protocol. Thirty-minute electromyographic recordings from the orbicularis oculi muscle of the right eye were carried out 120 min after ingestion of clonidine and 60 min after ingestion of diazepam. Subjects received 36 40-msec sound pulses (115 dB), separated by variable intervals (mean 25 sec); in 24 of the trials the pulse was preceded by a 40-msec prepulse (75 dB in 12 trials and 85 dB in 12 trials; prepulse-pulse interval, 120 msec). The amplitude of the startle response was significantly reduced both by diazepam (mean+/-SEM: -43.9+/-7.4%) and by clonidine (-75.7+/-4.7%). Under the placebo condition, the 75 and 85dB prepulses inhibited the startle response by 38.6+/-6.5 and 70.3+/-2.9%, respectively. Neither drug significantly altered the degree of prepulse inhibition. Both drugs reduced self-rated alertness; clonidine reduced systolic blood pressure and salivation. The results confirm the suppressant effect of clonidine on the startle response and show a qualitatively similar effect of diazepam; the results also demonstrate the insensitivity of prepulse inhibition of the startle response to doses of sedative drugs that are sufficient to attenuate the startle response itself.

Acoustic Stimulation↗
PubMed2001

Footshock-induced sensitization of the acoustic startle response in two strains of mice.

It has been shown before that unconditioned footshocks can augment the acoustic startle response in rats. In the present study, male mice of two strains, C57Bl/6N and BALB/c, were compared with regard to footshock-induced sensitization of the acoustic startle response. Presentation of footshocks did not affect the acoustic startle response in C57Bl/6N mice, while in contrast, footshock-induced sensitization was apparent in the BALB/c strain. Shocked C57Bl/6N mice, but not BALB/c mice, displayed robust conditioning to the startle context when re-tested the next day. These findings indicate that mice may exhibit footshock-induced sensitization of the acoustic startle response, but that the effects of footshocks on the acoustic startle are strain- and time-dependent.

Acoustic Stimulation↗
PubMed1996

Fear-potentiated startle response is remarkably similar in two laboratories.

The fear-potentiated startle response paradigm is used to investigate anxiolytic properties of drugs. The first objective of the present study was to further investigate the predictive validity of this paradigm. The anxiolytics chlordiazepoxide (2.5-10 mg/ kg IP) and oxazepam (1-10 mg/kg PO) and the putative anxiolytic flesinoxan (1-10 mg/kg PO) decreased startle potentiation dose-dependently, indicating an anxiolytic effect. The antidepressant fluvoxamine (5-20 mg/kg PO) did not affect startle potentiation. Ideally, anxiolytic drugs attenuate startle potentiation without affecting control startle levels, although some studies report altered control startle amplitudes. The second objective was to investigate whether different effects on control startle amplitudes are related to different startle devices. Therefore, the drugs were tested in two laboratories. Results showed no significant differences between laboratories, indicating that equipment is not a critical factor in the drug-induced alteration of control startle levels. In an additional experiment, it was shown that flesinoxan (10 mg/kg PO) did not affect strychnine-induced startle potentiation, supporting the idea that the attenuating effect of flesinoxan on the fear-potentiated startle response is due to its anxiolytic properties. Thus, the fear-potentiated startle response paradigm appears a valid and reliable model for anxiolytic properties of drugs.

Animals↗
PubMed1996

Increased startle responses in mice carrying mutations of glycine receptor subunit genes.

An exaggerated startle response caused by mutations of the alpha 1 subunit gene of the inhibitory glycine receptor (GLRA1) is the key symptom of human hyperekplexia or startle disease. The recessive mouse mutant spasmodic (spd) carries a missense mutation in the corresponding murine Glra1 gene which reduces the affinity of agonists for the mutant receptor. This mutant has been regarded as an animal model with which to investigate the molecular basis of hyperekplexia and related motor disorders. The recessive mouse mutant spastic (spa) carries an insertional mutation in the glycine receptor beta subunit gene (Glrb) that results in aberrant splicing and, consequently, in a reduced number of functionally intact receptors. The resulting phenotype is similar to that of spasmodic. This study measured the acoustic startle response of spasmodic and spastic mice under different stimulus conditions, in order to test for sensorimotor processing deficits in these animals. Both mutants show increased startle responses to acoustic stimuli of different intensities compared with wild-type animals.

Acoustic Stimulation↗
PubMed2000

Effects of pentagastrin and the cold pressor test on the acoustic startle response and pupillary function in man.

Pentagastrin, a cholecystokinin2 (CCK2) receptor agonist, evokes autonomic and subjective features of anxiety in healthy volunteers. The present experiments examined the effects of pentagastrin on two responses with known sensitivity to another anxiogenic procedure (threat of electric shock): the acoustic startle response and the pupillary light reflex. The effects of pentagastrin were compared with those of the cold pressor test, a procedure known to elicit sympathetic activation. Twelve healthy males (18-35 years) participated in two experiments each consisting of two sessions in which they received (1) pentagastrin (0.3 microg/kg, i.v.) and a control infusion (saline), and (2) cold pressor test (90 s hand immersion at 4 degrees C) and a control immersion (37 degrees C), using a balanced single-blind protocol. Electromyographic responses of the orbicularis oculi to 40 ms, 1 kHz, 115 dB tones ('startle responses') [Experiment 1], and miotic responses to 200 ms, 0.43 mW/cm2 light pulses [Experiment 2] were recorded before, during and after the infusions and hand immersions. Heart rate, blood pressure and subjective feelings were also recorded. The amplitude of the startle response was not significantly affected by pentagastrin, but was reduced during the cold pressor test. Resting pupil diameter increased during both pentagastrin infusion and the cold pressor test, but neither procedure altered the amplitude of the light reflex. Tachycardia, increased blood pressure and subjective anxiety were induced by both pentagastrin and the cold pressor test. The cardiovascular and mydriatic effects of pentagastrin and the cold pressor test are consistent with the known ability of these treatments to induce sympathetic activation. The anxiety induced by these treatments, unlike anxiety induced by threat of electric shock, was not accompanied by potentiation of the startle response or reduction of the miotic response. The results indicate that different anxiogenic procedures do not have equivalent effects on these reflexes.

Adolescent↗
PubMed1998

Persistently exaggerated startle responses in rats treated with pyridostigmine bromide.

Troops in the Persian Gulf War have registered complaints consistent with CNS dysfunction that emerged after returning from the Gulf. A common experience among Persian Gulf War veterans was exposure to pyridostigmine bromide (PB) for prophylaxis against nerve gas exposure. To determine whether PB causes emergent CNS dysfunction, Wistar-Kyoto (WKY) and Sprague-Dawley (SD) rats were given PB for 7 consecutive days in their drinking water. The WKY, but not the SD, rats exhibited a delayed-onset, persistently exaggerated startle response. The WKY rats exhibited exaggerated startle responses that appeared 15 days after the end of PB treatment and were still evident 22 days after the end of treatment. Both the duration and the magnitude of the exaggerated startle responses were related to the dosage of PB. The PB-treated rats exhibited normal short-term and long-term habituation. However, exaggerated startle responses were related to the development of enhanced short-term sensitization. Treating the rats for a second time, 7 weeks after the end of the first PB treatment, induced an exaggerated startle response that appeared sooner and dissipated faster than was evident after the first PB treatment. Inasmuch as the WKY rat has inherently low butyrylcholinesterase activity, a scavenger for PB, these results suggest that prophylactic PB may influence CNS function in individuals with low butyrylcholinesterase activity. Elaboration of the factors that mediate enhanced sensitization in the WKY rat may provide insight into some of the complaints registered by veterans of the Persian Gulf War.

Animals↗
PubMed2006

Fmrp is required for the establishment of the startle response during the critical period of auditory development.

Fragile X syndrome, the most common form of inherited mental retardation, is caused by the absence of the FMR-1 gene product FMRP. In addition to the hallmark cognitive defect, other symptoms are also apparent including hyperactivity, seizures and sensory abnormalities including a characteristic increase in sensitivity to auditory, tactile, visual, and olfactory stimuli. Fragile X is a developmental disorder with the first symptoms apparent in the first year of life but little is known about the role of FMRP in developmental processes. The sensory hyperreactivity of fragile X can be reproduced in fmr-1 knockout (KO) mice evident as abnormal audiogenic startle response and increased audiogenic seizure susceptibility. Here, we studied the onset and emergence of the startle deficit in fmr-1 KO mice during development. The startle response was first detectable at the end of the 2nd postnatal week in wild-type mice. The amplitude of startle response showed a substantial increase until the 4th postnatal week followed by a further but moderate increase up to adulthood. Expression of the fmr1 gene was detectable in the startle circuit before the onset and throughout the development of the startle response. Although the onset and amplitude of the startle response were not altered in fmr1 KO mice until the 3rd-4th postnatal week, beyond this age it failed to develop further resulting in an overall response deficit in adult KO mice. This indicates that although Fmrp is dispensable at the initial steps of startle response development, it is necessary for the full development of the response.

Acoustic Stimulation↗
PubMed2001

Prepulse inhibition of the acoustic startle response in cocaine-withdrawn rats.

Prepulse inhibition (PPI) of startle is a sensorimotor gating task in which a low-intensity acoustic stimulus presented prior to a high-intensity, startle-eliciting stimulus can attenuate the acoustic startle response (ASR). Previous studies on startle reactivity in cocaine-withdrawn rats have found minimal changes; the present study extends this work to the gating of ASR. In Experiment 1, rats were injected daily with either saline or cocaine (30 mg/kg i.p.) for 2 weeks. ASR and PPI were measured prior to, and at 3- and 14-day withdrawal from, the chronic treatment. No effect of cocaine treatment was found on either measure. In Experiment 2, treatment was extended to 8 weeks, and an earlier withdrawal time point (1 day) was added. Rats treated with cocaine for 8 weeks exhibited lower startle reactivity during withdrawal compared with saline-treated controls. PPI did not differ between treatment groups. Thus, extended chronic treatment with cocaine rendered significant effects on startle responsivity. Further, this finding mirrors the blunted ASR exhibited in chronic cocaine users [Neuropsychopharmacology 22 (2000) 89.].

Acoustic Stimulation↗
PubMed2005

Affective dysregulation and dissociative experience in female patients with borderline personality disorder: a startle response study.

Affective dysregulation and dissociation are currently discussed as core features of borderline personality disorder (BPD). Affective dysregulation is hypothesized to be correlated with increased amygdala functioning and dissociation is linked to inhibited processing on the amygdala and dampened autonomic output, according to the corticolimbic disconnection model of dissociation from Sierra and Berrios [Biological Psychiatry 44 (1998) 898]. We assessed startle response, which is mainly mediated by the amygdala, to investigate the relationship between affective dysregulation and dissociation. We hypothesized that patients with BPD would reveal enhanced responses to startling tones, but that these would be lessened by the presence of state dissociative experiences. 21 unmedicated female patients with BPD and 21 healthy female controls listened to 15 startling tones (95-dB, 500-ms, 1000-Hz) while heart rate, skin conductance and orbicularis oculi electromyogram responses were measured. Covariance analysis showed that the BPD group had a significantly higher startle response in the electromyogram as compared to controls. Furthermore, present-state dissociative experiences significantly influenced the startle response. Patients with low dissociative experiences revealed enhanced startle responses whereas patients with high dissociative experiences showed reduced responses. Our data support affective dysregulation in BPD as well as the corticolimbic disconnection model of dissociation, at least for EMG. Furthermore, it highlights the importance of assessing present-state dissociation in basic research as well as psychotherapy.

Adult↗
PubMed2002

Effects of corticotropin-releasing factor on prepulse inhibition of the acoustic startle response in two rat strains.

RATIONALE: Prepulse inhibition (PPI) of the acoustic startle response is altered by manipulations that affect brain monoamine neurotransmission. Corticotropin-releasing factor (CRF), a neurotransmitter that is released during stress, and CRF receptors are expressed in areas of the brain which contribute to PPI, and central administration of CRF changes extracellular concentrations of the monoamines. Therefore, CRF is in a position to alter PPI, either by causing the release of other neurotransmitters, or by direct effects at CRF receptors. OBJECTIVES: The present experiments were conducted to test the hypothesis that intracerebroventricular (ICV) administration of CRF would decrease PPI in rats. Additionally, these experiments were used to examine whether CRF results in differential changes in PPI in rat strains that show high and low basal PPI, and whether CRF-induced grooming behavior and increased startle amplitude are also strain-dependent. METHODS: Male Wistar-Kyoto (WKY) rats inbred in our colony in La Jolla, WKY rats obtained from Charles River, and Brown Norway (BN) rats from Harlan, Sprague-Dawley were tested for grooming behavior, PPI and startle amplitude following ICV infusion of either CRF (1.0-3.0 microg) or saline. RESULTS: CRF significantly decreased PPI in both BN rats, which show relatively little PPI in the basal condition and, in WKY rats. The amplitude of the acoustic startle response was increased in WKY rats only and, only by the 3.0 microg dose of CRF. CRF increased grooming behavior in the La Jolla colony WKY and BN rats. However, within the time frame during which the rats were being observed, CRF failed to significantly increase grooming in Charles River WKY rats. CONCLUSIONS: CRF diminished PPI of the acoustic startle response in rats that show high (WKY) and low (BN) basal PPI. This effect does not appear to be dependant on CRF-induced changes in startle amplitude. The results suggest the possibility that stress-induced exacerbation of symptoms in schizophrenia, which is characterized by deficient PPI, may be CRF-dependent.

Acoustic Stimulation↗
PubMed2000

Changes in the magnitude of the eyeblink startle response during habituation of sexual arousal.

Modulation of the startle response was used to examine emotional processing of sexual stimulation across trials within a session. Eyeblink startle was elicited by a probe (burst of intense white noise) presented intermittently while men were viewing an erotic film segment. Repeated display of the film segment resulted in a progressive decrease in sexual arousal. Habituation of sexual arousal was accompanied by a reduction over trials in the extent the men felt absorbed when viewing the erotic stimulus and by an increase over trials in the magnitude of the eyeblink startle response. Replacing the familiar stimulus by a novel erotic stimulus increased in sexual arousal and absorption and reduced startle (novelty effect), while dishabituation was evident for all three response measures when the familiar stimulus was reintroduced. This pattern of results indicates that with repeated presentation an erotic stimulus is experienced not only as less sexually arousing but also as less appetitive and absorbing. The question of whether habituation of sexual arousal is mediated by changes in attentional and affective processing over trials is discussed, as are clinical contexts in which eyeblink startle can be used in studying aspects of sexual functioning.

Adolescent↗