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PubMed1997

The acoustic startle response in rats--circuits mediating evocation, inhibition and potentiation.

This review describes the neuronal mechanisms underlying the mediation and modulation of the acoustic startle response (ASR) in rats. The combination of anatomical, physiological and behavioral methods has identified pathways which mediate and modulate the ASR. The ASR is mediated by a relatively simple, oligosynaptic pathway located in the lower brainstem which activates spinal and cranial motor neurons. An important element of the pathway which mediates the ASR is the caudal nucleus of the pontine reticular formation (PnC). Interestingly, this nucleus is also the target of input from various brain nuclei which are involved in the modulation (e.g. fear-potentiation, sensitization, habituation, prepulse inhibition and pleasure-attenuation) of the ASR. Hence, the PnC can be described as a sensorimotor interface, where the transition of sensory input into the motor output can be directly influenced by excitatory or inhibitory afferents. On the basis of these facts we conclude that the ASR may be a valuable model for the study of general principles of sensorimotor-motivational information processing at the behavioral and neurophysiological level in mammals.

Acoustic Stimulation↗
PubMed2005

Sensorimotor gating and habituation of the startle response in schizophrenic patients randomly treated with amisulpride or olanzapine.

BACKGROUND: Schizophrenic patients exhibit impairments in prepulse inhibition (PPI) and habituation of the acoustic startle response (ASR). Recent studies suggested that PPI deficits and habituation deficits are normalized after antipsychotic treatment. Despite clear evidence of gating and habituation mechanisms in animal models, it is still unknown which neurotransmitter systems are involved in schizophrenic patients. Thus, we compared the effects of a combined 5-HT2A/D2 and a pure D2/D3 antagonist on PPI and habituation of ASR in patients with schizophrenia. METHODS: The ASR was measured in 37 acute schizophrenic patients who were randomized and double-blinded as to treatment with amisulpride or olanzapine. Patients were assessed during the first week and after four and eight weeks of treatment. Twenty healthy matched control subjects were examined likewise. RESULTS: Schizophrenic patients showed a significant PPI deficit and significantly decreased startle amplitude at baseline. The gating deficit disappeared after antipsychotic treatment in both treatment groups. Amisulpride sensitized the startle amplitude, whereas startle amplitude was not changed by olanzapine. After correcting for startle amplitude, patients did not show a habituation deficit; however, amisulpride accelerated habituation, whereas olanzapine had no effect. CONCLUSIONS: Our findings suggest that the PPI-restoring effect of antipsychotics is probably attributed to a dopamine D2 receptor blockade.

Acoustic Stimulation↗
PubMed1986

The role of spinal cord cyclic AMP in the acoustic startle response in rats.

Drugs thought to increase intracellular levels of cAMP were infused intrathecally into the subarachnoid space of the lumbar spinal cord, and the effects on the acoustic startle response in rats were measured. Intrathecal infusions of the cAMP analogs dibutyryl cAMP or 8-bromo cAMP (12.5-100 micrograms) produced marked, dose-dependent increases in startle amplitude compared to the infusion of artificial cerebrospinal fluid (CSF). Local infusions of dibutyryl cAMP at more rostral levels of the spinal cord or brain failed to mimic the excitatory effect seen following lumbar intrathecal infusion. No excitation of startle was seen following intrathecal infusion of cAMP itself, ATP, 5'-AMP, or dibutyryl cGMP. A weak excitation of startle was seen following intrathecal, but not intraventricular, infusion of the water-soluble adenylate cyclase activator forskolin 7-deacetyl-7-O-hemisuccinic acid (forskolin-DHA; 5.0-100 micrograms, in artificial CSF), whereas forskolin itself [0.01-200 micrograms, in dimethyl sulfoxide (DMSO)] was without consistent effect. Finally, intrathecal infusion of the selective phosphodiesterase inhibitor Rolipram (12.5-200 micrograms) produced a marked excitation of startle similar in magnitude to the effects produced by cAMP analogs. The excitatory effects of intrathecally infused dibutyryl cAMP, 8-bromo cAMP, forskolin-DHA, or Rolipram support a functional link between spinal cord cAMP and the acoustic startle reflex. Possible sites of cAMP action on startle are discussed.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1996

Prenatal cocaine exposure affects the acoustic startle response in adult rat.

This study investigated whether prenatal exposure to cocaine alters reflux excitability in adulthood. Pregnant rats received 30 or 60 mg/kg/day cocaine HCl i.g. during gestational days 8-22. Vehicle-treated control rats were pair-fed/watered to rats receiving 60 mg/kg cocaine. A non-treated control group was also maintained. At parturition, litters from all four groups were surrogate fostered and then weaned at 21 days of age. In adulthood, rats were tested in an acoustic startle response (ASR) apparatus for 120 trials using a 116 dB signal on 2 consecutive days. On Day 2, subjects received a single injection of d-amphetamine sulfate s.c. (1.0 mg/kg) just prior to testing. ASR amplitude and latency were recorded. For average amplitude, significant effects for prenatal treatment were observed. Cocaine-exposed female rats demonstrated decreased ASR amplitude compared to offspring of pair-fed controls during both the initial test Session and following amphetamine administration as well. Overall, amphetamine increased startle. For latency, there were no significant treatment effects or effects of amphetamine administration. However, preplanned comparisons indicated that prenatal cocaine exposure interacted with trial block. Therefore, these data indicate that prenatal cocaine decreased startle amplitude in adults, primarily in females, and that startle-elicited amphetamine responses were dampened as well. The effects on latency indicate that amphetamine does not alter reaction times in prenatal cocaine exposed rats while it does in controls.

Animals↗
PubMed2002

Effects of ovariectomy and estradiol on acoustic startle responses in rats.

Long-term (3 months) ovariectomized (OVX) rats were used to model hormone withdrawal as occurring in menopause. We previously reported alterations in brain dopamine (DA), GABA and serotonin receptors following ovariectomy in this model. To assess the functional effect of these biochemical changes, we compared rats that were intact, OVX and OVX-treated with 17beta-estradiol (E(2); OVX+E(2)) for 2 weeks on measures of their acoustic startle responses (ASR) and prepulse inhibition (PPI) of acoustic startle. The effects of a mixed D(1)/D(2) dopaminergic agonist, apomorphine (APO; 0.25, 0.5 and 0.75 mg/kg sc) were tested on ASR and PPI of acoustic startle. Without APO, all groups of rats showed no difference in baseline ASR or PPI of acoustic startle. Following administration of APO (0.25, 0.5 and 0.75 mg/kg), ASR was significantly increased in OVX rats compared to intact rats and this was corrected with E(2) treatment. In all groups of animals, APO decreased PPI of acoustic startle. APO disrupted PPI to a lesser extent in OVX animals with or without E(2) treatment compared to intact rats. However, when group differences in APO-induced ASR were statistically controlled for, there were no longer any differences in APO disruption of PPI among the three treatment groups. These results indicate that long-term ovariectomy has persistent effects on the modulation of ASR, and these effects can be at least partly corrected with E(2) replacement therapy.

Acoustic Stimulation↗
PubMed1989

Startle responses measured in muscles innervated by facial and trigeminal nerves show common modulation.

Electromyographic (EMG) potentials of several head muscles were recorded simultaneously in freely moving rats with chronically implanted electrodes. The startle responses of m. temporalis, m. levator auris, and m. levator labii superior were compared. All muscles showed a parallel decrease in latency and an increase in response elicitability and amplitude with an increase in stimulus intensity. A significant latency difference of about 1 ms existed between m. levator auris and m. temporalis. The shortest latency of the EMG response in m. levator auris was 5.5 ms (110 dB SPL). A common fluctuation in response amplitude and latency was found in simultaneous recordings of muscles innervated by the facial and trigeminal nerve, respectively. This shows a common modulatory input to the startle pathway to the cranial motor nuclei.

Animals↗
PubMed2002

Difference in anxiety and sensitization of the acoustic startle response between the two inbred mouse strains BALB/cAN and DBA/2N.

The inbred mouse strain BALB has been proposed to be an animal model for pathological anxiety. BALB exhibits a stronger acoustic startle response (ASR) than the 'less emotional' inbred strain DBA. Four experiments were conducted to determine whether this strong ASR is due to a higher anxiety level and/or to greater sensitization in BALB than in DBA, with the following results: (1) The ASR to the very first startle stimulus was found to be much stronger in BALB than in DBA, and freezing behavior evoked by startle stimuli was more pronounced in BALB than in DBA. These findings indicate a higher level of anxiety in this strain. (2) ASR amplitudes of BALB initially rose much higher during consecutive startle stimuli and remained at a high level much longer than in DBA. Thereafter, ASR amplitude dropped more slowly and to a lesser degree than in DBA. Startle amplitudes decreased similarly in both strains (strong exponential decrease) only when a low sound pressure level (SPL) was used which elicited approximately the same low ASR in both strains. These results can only be explained by increased sensitization in BALB. (3) The slope of the i/o-function, which represents the relation between sensory input and motor output, was steeper in BALB than in DBA. As it has been shown recently, sensitization increases the slope of the startle i/o-function indicating increased sensitization in BALB. It is discussed, however, whether anxiety also contributes to this effect. (4) Footshocks increased the ASR much less in BALB than in DBA, again showing increased sensitization in BALB. Both a higher level of anxiety and greater sensitization therefore determined the greater strength of the ASR in BALB than in DBA.

Acoustic Stimulation↗
PubMed1976

Long-term retention of the habituation of lick suppression and startle response produced by a single auditory stimulus.

Response decrement produced by a single, 2-sec, 98 dB, auditory stimulus in rats was retained without detectable loss for intervals ranging from approximately 30 sec to 30 days. Response decrements produced by stimulation over these intervals reached an apparent asymptote after 2 or 3 stimulus presentations. These response decrements were unambiguously associated with stimulus presentation for the lick suppression measure, but nonspecific decremental effects may have contributed to the startle response decrements. After these long-term decrements had reached asymptote, 300 stimulus presentations with 1-sec interstimulus intervals produced further response decrements, but these decrements recovered completely within 24 hr., responsiveness returning to the previously established long-term asymptote. The data show that unreinforced stimulus presentations can produce both relatively permanent response decrements and apparently independent short-term decrements. The data also suggest that long-term retention may be more generally characteristic of habituation than is usually assumed.

Acoustic Stimulation↗
PubMedDate not supplied

The effects of perinatal AZT exposure on the acoustic startle response in adult rats.

AZT (azidothymidine, zidovudine, ZDV) has become the standard medication to prevent the transmission of the human immunodeficiency virus from mother to fetus. The present study was designed to assess the acoustic startle response (ASR) in adult rats that had been perinatally exposed to AZT. Each litter was randomly assigned to a treatment group: nontreated, AZT 0, 50, 100 or 150 mg/kg. Once daily gastric intubation began prenatally between gestational day (G) 19 and 22 and then continued postnatally between postnatal day (PND) 2 and 20. Between PND75 and PND80, animals were tested for habituation to the acoustic stimuli and prepulse inhibition following a challenge of either saline or 1.0 mg/kg amphetamine (AMP) intraperitoneally. Amphetamine increased ASR and startle latencies throughout the session. The AZT100 dose increased ASR habituation. AZT treatment did not affect prepulse inhibition. Females treated with AZT150 continued to show high ASRs at the end of the startle session. AZT-treated animals showed a dose-dependent increase in peak latency, suggesting a possible abnormal conduction velocity. These effects are independent of handling and intubation effects. Therefore, perinatal AZT treatment results in long-term changes within the primary acoustic startle pathway.

Acoustic Stimulation↗
PubMed2006

The tactile-stimulated startle response of tadpoles: acceleration performance and its relationship to the anatomy of wood frog (Rana sylvatica), bullfrog (Rana catesbeiana), and American toad (Bufo americanus) tadpoles.

I described the tactile-stimulated startle response (TSR) of wood frog (Rana sylvatica), bullfrog (Rana catesbeiana), and American toad (Bufo americanus) tadpoles. One purpose was to rank species in terms of maximum acceleration performance. Also, I tested whether anatomical indicators of performance potential were predictive of realized performance. TSRs were elicited in a laboratory setting, filmed at 250 Hz, and digitally analyzed. TSRs began with two, initial body curls during which tadpoles showed a broad spectrum of movement patterns. TSR performance was quantified by maximum linear acceleration and maximum rotational acceleration of the head/body, both of which tended to occur immediately upon initiation of motion (< 0.012 sec into the response). Bullfrog tadpoles had higher maximum acceleration than the other species, but other interspecific differences were not significant. The species' rank order for the anatomical indicator of linear acceleration potential was bullfrog > wood frog > American toad. The species' rank order for the anatomical indicator of rotational acceleration potential was bullfrog > wood frog = American toad. Thus, the anatomical indicators roughly predicted the rank order of interspecific average performance. However, the anatomical indicators did not correlate with individual tadpole performance. Variability in behavioral patterns may obscure the connection between anatomy and performance. This is seen in the current lack of intraspecific correlation between a morphological indicator of acceleration capacity and acceleration performance.

Animals↗
PubMed2001

Effects of psychostimulant withdrawal on latent inhibition of conditioned active avoidance and prepulse inhibition of the acoustic startle response.

RATIONALE: Chronic intermittent administration of amphetamine and cocaine can precipitate psychotic episodes in humans and produce persistent behavioral changes (i.e. increased locomotion, stereotypy) in the rat. The psychostimulant sensitization model of psychosis holds that the repeated administration of drugs such as amphetamine and cocaine induces long-lasting neuroadaptations and behavioral outcomes in animals that parallel aspects of the schizophrenic condition. OBJECTIVES: In the present study, we attempted to validate this model further by examining the effects of short-term withdrawal from repeated administration of cocaine and amphetamine on performance in two animal behavioral models of cognitive deficits found in schizophrenia: latent inhibition and prepulse inhibition. Reductions in both of these behavioral phenomena have been reported in schizophrenic patients and in acutely amphetamine-treated rats. METHODS: Animals were tested after 4 days of withdrawal from 5 days of daily systemic 20 mg/kg cocaine or 1.5 mg/kg amphetamine injections for either latent inhibition of two-way active avoidance acquisition or prepulse inhibition of an acoustic startle response. RESULTS: Our results indicate that, rather than reducing the expression of these behaviors, withdrawal from either cocaine or amphetamine enhanced the expression of latent inhibition of the active avoidance response while having no effect on prepulse inhibition of acoustic startle. CONCLUSIONS: These data indicate that although the sensitized response to amphetamine and cocaine administration may model some aspects of schizophrenic psychosis, behaviors exhibited by sensitized animals in the absence of an acute drug challenge are not consistent with models of the positive symptoms of schizophrenia.

Acoustic Stimulation↗
PubMed1994

Clozapine's effects on phencyclidine-induced disruption of prepulse inhibition of the acoustic startle response.

The reduction in magnitude of the startle reflex in response to a loud noise produced by prior presentation of a stimulus of lower intensity is known as prepulse inhibition (PPI). PPI may be disrupted by a variety of drugs, most notably by dopaminergic agonists such as apomorphine and by phencyclidine (PCP), and related noncompetitive N-methyl-D-aspartate (NMDA) antagonists. Apomorphine-induced disruption of PPI is antagonized by both typical and atypical neuroleptics. The present study examined the effects of the atypical neuroleptic, clozapine, alone and in combination with PCP, on PPI in rats. The results of previous studies suggest that disruption of PPI by PCP and similar drugs is not sensitive to antagonism by typical neuroleptics such as haloperidol. The results of the present study show that clozapine's effect on PCP-induced disruption of PPI is also limited. The failure of clinically effective antipsychotics of diverse chemical classes to block the effects of PCP on PPI of acoustic startle suggest that the effects of PCP in this procedure may represent a model of attentional deficits observed in treatment-resistant schizophrenia.

Acoustic Stimulation↗
PubMed2005

Neural cell adhesion molecule-null mice are not deficient in prepulse inhibition of the startle response.

Mice constitutively deficient in the neural cell adhesion molecule have morphological changes in the brain, which are hallmarks of schizophrenia. Schizophrenic patients are impaired in sensorimotor processing indicated by a deficit in prepulse inhibition of the acoustic startle response. Here we tested whether prepulse inhibition and prepulse facilitation are changed in neural cell adhesion molecule-deficient mice compared with their wild-type littermates. Neither prepulse inhibition nor prepulse facilitation (which occurred only at the lowest prepulse intensity used and was weak) was altered. This result is discussed in the light of the 'two-hit' hypothesis of schizophrenia, suggesting that in neural cell adhesion molecule-deficient mice, a prepulse inhibition deficit may become apparent only after treatment with a 'second hit' (such as increased stress).

Acoustic Stimulation↗
PubMedDate not supplied

An increase in startle response in rats administered oxytocin.

Twenty-four male albino Wistar rats were allocated to four groups and given either 23.2, 11.6 or 5.8 IU OXT/kg or vehicle (0.9% saline). A significant increase in startle response was observed in the 11.6 and 5.8 IU OXT/kg groups when compared to vehicle. Our results further support the suggestion that OXT is a "stress hormone" by implicating this peptide with increased emotionality/reactivity during a stressful experience.

11-Hydroxycorticosteroids↗
PubMed1988

The effects of type I and II pyrethroids on motor activity and the acoustic startle response in the rat.

Recent data have demonstrated that the in vivo effects of low dosages of two pyrethroids, cismethrin and deltamethrin, can be differentiated. Two behavioral tests, locomotor activity and the acoustic startle response (ASR), were utilized to separate the behavioral actions of Type I and II pyrethroids using permethrin, RU11679, cypermethrin, RU26607, fenvalerate, cyfluthrin, flucythrinate, fluvalinate and p,p'-DDT. Dosage-effect functions for all compounds were determined for both figure-eight-maze activity and the ASR in the rat. All compounds were administered po in 1 ml/kg corn oil 1.5-3 hr prior to testing. All compounds produced dosage-dependent decreases in locomotor activity. The Type I compounds, permethrin and RU11679, along with p,p'-DDT, increased amplitude and had no effect on latency to onset of the ASR. In contrast, the Type II pyrethroids, cypermethrin, cyfluthrin, and flucythrinate, decreased amplitude and increased the latency to onset of the ASR. Fenvalerate increased the amplitude, had no effect on latency, but unlike the other compounds tested, increased ASR sensitization. Fluvalinate had no effect on any measure of the ASR. These data provide further evidence of the differences between the in vivo effects of low dosages of Type I and II pyrethroids, and extend the findings of our previous work to other representatives of the two classes of pyrethroids.

Acoustic Stimulation↗
PubMed1999

Interaction between acoustic and electric sensitization of the acoustic startle response in rats.

Sensitization is the general increase of responsiveness observed after aversive stimulation. Usually footshocks are used as aversive stimuli. According to the 'Dual Process Theory' by Groves and Thompson. Psychol. Rev. 1970;77:419-450, not only additional aversive stimuli but also the response-eliciting stimuli themselves have a sensitizing effect, the degree of sensitization depending upon the stimulus intensity. We tested this suggestion in the footshock sensitization paradigm of the acoustic startle response (ASR): (1) High SPL (sound pressure level) acoustic stimuli (119 dB SPL) presented instead of footshocks also elicited strong sensitization. (2) While footshocks presented after startle stimuli with low SPL (95 dB) were able to produce a strong further sensitization of the ASR, footshocks presented after startle stimuli with high SPL (110 dB) only caused a minor sensitization of the ASR. (3) Diazepam (3 mg/kg i.p.) decreased ASR to high SPL (115 dB) stimuli. In this case footshocks elicited significant sensitization of the ASR despite intense startle stimuli. The present results support the 'Dual Process Theory'. Furthermore we could show that acoustic and footshock sensitization interact. We therefore suggest that both, acoustic and footshock sensitization, are mediated partly via the same neural circuitry.

Acoustic Stimulation↗
PubMed2001

The acoustic startle response as an effective model for elucidating the effect of genes on the neural mechanism of behavior in mice.

One current approach in investigating the neural basis of behavior is to use mutant mice with specific genetic alterations which affect neural functions. We are convinced that this approach is only effective if a behavioral model with sufficiently known underlying neuronal mechanisms is used. We present a model system which is well-suited for the above approach. Because the neural basis is known in great detail, in the startle system behavioral results can be very well interpreted. This is demonstrated here by using footshock sensitization of the acoustic startle response (ASR) as an example. Sensitization is elicited by aversive stimuli such as electric footshocks and causes an increase in ASR amplitude. The present experiment showed that this ASR increase is not due to a drop in the startle threshold but to increased gain in the response to suprathreshold stimuli. This makes it possible to draw conclusions about the neuronal site of the startle threshold in the startle pathway and the synapse at which the gain shift during sensitization occurs. The possibility of interpreting behavioral output on a well known neural basis (as demonstrated here) makes the ASR a promising model system for investigating (neuro-) genetic influences of behavior.

Amygdala↗
PubMed1987

Pertussis toxin or 8-bromo-cAMP block inhibition of the acoustic startle response by the alpha 2-adrenergic agonist ST-91.

Stimulation of supraspinal alpha 2-adrenergic receptors by intraventricular infusion of the alpha 2-adrenergic agonist ST-91 depresses a simple vertebrate behavior, the acoustic startle response. Intraventricular pretreatment with pertussis toxin, an agent known to inactivate the inhibitory guanine nucleotide binding protein (Gi) which can inhibit adenylate cyclase, completely prevented the depressant behavioral effect of ST-91. In contrast, pertussis toxin did not alter the depressant effect of intraventricular infusion of the 5-HT 1B agonist 1-m-chlorophenylpiperazine (mCPP). Intraventricular infusion of the cyclic adenosine monophosphate (cAMP) analog 8-bromo-cAMP also reversed the depressant effect of ST-91 without altering the effect of mCPP. These data suggest that inhibition of adenylate cyclase may be involved in the effect of activation of central alpha 2-adrenergic receptors.

8-Bromo Cyclic Adenosine Monophosphate↗