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PubMed2004

Factors governing prepulse inhibition and prepulse facilitation of the acoustic startle response in mice.

The influence of prepulses on the acoustic startle response (ASR) was measured in three inbred mouse strains, C57BL/6J, 129/SvHsd, and AKR/OlaHsd, and one hybrid strain produced by crossing wild mice and NMRI mice. Prepulse inhibition (PPI), i.e. reduction of ASR by prepulses, was maximal when the interval between prepulses and startle stimuli was in the range of 37.5-100 ms. Prepulse facilitation (PPF), i.e. increase of ASR by prepulses, was maximal when the prepulse preceded the startle stimulus by 12.5 ms. PPI increased with increasing prepulse SPL, PPF first increased then decreased when prepulse SPL was increased. Percent PPI was independent from startle stimulus SPL. All strains showed a long-term increase of PPI when tested for several days; one strain (129) also showed an increase of PPF over days. The present results clearly show that PPI and PPF are independent processes, which add to yield the final response change. PPF and the observed long-term changes of PPI and PPF are stronger expressed in mice than have been observed in rats under similar conditions. Since there were significant differences between the strains of mice with respect to PPI and PPF, genetically different strains of mice are a promising tool to study these two processes.

Acoustic Stimulation↗
PubMed1994

Prepulse inhibition of the acoustic startle response of rats is reduced by 6-hydroxydopamine lesions of the medial prefrontal cortex.

Prepulse inhibition (PPI) of the acoustic startle response (ASR) is impaired by dopamine (DA) overactivity in the nucleus accumbens and anteromedial striatum. Since there is evidence that DA in the medial prefrontal cortex exerts an inhibitory control on striatal DA systems, it was investigated whether depletion of prefrontal DA reduces PPI. Rats were tested for PPI both before and after injections (2 x 1 microliter per side) of vehicle, a low (3.0 microgram/microliter) or a high (6.0 microgram/microliter) dose of 6-hydroxydopamine hydrobromide (6-OHDA) into the prefrontal cortex. Only the high dose of 6-OHDA, leading to an 87% depletion of prefrontal DA, impaired PPI. The ability of an acoustic prepulse (75 dB, 10 kHz) to reduce the response to a startle pulse (100 dB noise burst) was maintained in sham lesioned rats, but was significantly disturbed in rats lesioned with the high dose of 6-OHDA. The 6-OHDA treatment did not affect the ASR amplitude in the absence of a prepulse. The reduction of PPI in lesioned rats correlated with the extent of DA depletion. These results suggest that the DA innervation of the prefrontal cortex is involved in the modulation of the ASR and they provide further evidence for opposite actions of prefrontal and subcortical DA systems in the control of behaviour. The present findings are discussed with regard to the potential role of prefrontal DA in schizophrenia.

Acoustic Stimulation↗
PubMed2003

Auditory startle response in cervical dystonia.

The excitability of brainstem neurons is abnormally enhanced in patients with cervical dystonia (CD), but the extend of such abnormality is not known. We examined whether patients with CD showed abnormalities in the auditory startle response (ASR), a brainstem reflex elicited by an unexpected loud stimulus. Thirteen patients with CD were investigated 3 months after botulinum toxin treatment. Thirteen healthy volunteers served as controls. ASRs were elicited by binaural high-intensity auditory stimuli. Reflex electromyographic (EMG) activity was recorded simultaneously with surface electrodes bilaterally from masseter, orbicularis oculi, sternocleidomastoid, and biceps brachii muscles. We found that ASR onset latencies were similar for patients and controls. CD patients had significantly lower ASR probabilities than controls (P = 0.007). ASR area under the curve was significantly smaller in CD patients (P = 0.017). Similar to controls, patients showed a significant habituation of ASR (P < 0.001, each); however, CD patients showed a prolonged tonic or phasic EMG activity after the initial ASR that was not observed in controls. Normal latencies and recruitment pattern indicate a preserved organization of intrinsic neural pathways mediating ASR in CD. Reduced ASR probability and magnitude as well as prolonged EMG activity after the proper startle response corroborate and extend previous findings on brainstem dysfunction in CD.

Adult↗
PubMed2003

Alpha 4 beta 2* nicotinic acetylcholine receptors modulate the effects of ethanol and nicotine on the acoustic startle response.

BACKGROUND: Ethanol modulates the functional activity of alpha4beta2 neuronal nicotinic cholinergic receptors (nAChR) when measured in vitro, but the potential role of alpha4beta2 nAChRs in regulating behavioral effects of ethanol is unknown. Recently, Tritto et al. (Tritto T, Stitzel JA, Marks MJ, Romm E, Collins AC (2002) Variability in response to nicotine in the LSxSS RI strains: potential role of polymorphisms in alpha4 and alpha6 nicotinic receptor genes. Pharmacogenetics 12:197-208) reported that a polymorphism (A529T) in the alpha4 nAChR subunit gene is associated with variability in nicotine's effects on startle in the LSxSS recombinant inbred (RI) strains. Ethanol also alters the acoustic startle response. Thus, we evaluated the potential role of alpha4beta2 nAChRs in modulating ethanol's effects on acoustic startle. METHODS: The effects of ethanol on acoustic startle were determined in the LSxSS RI strains. In addition, the effects of ethanol and nicotine were also measured in alpha4 gain of function and beta2 null mutant mice. The beta2 mutants do not express the major variant of alpha4 nAChRs, alpha4beta2. RESULTS: An association between the alpha4 A529T polymorphism and ethanol's effects on startle was found in the LSxSS RI strains; those strains that express the A529 variant of alpha4 were more sensitive to ethanol-induced depression of startle. The alpha4 gain of function mutants were more sensitive to the effects of both nicotine and ethanol and the beta2 null mutants were less sensitive to both drugs. CONCLUSIONS: alpha4beta2-containing nAChRs may play important roles in modulating the effects of both ethanol and nicotine on the acoustic startle response. We suggest that nAChR subunit genes should be evaluated as potential contributors to both alcoholism and tobacco abuse.

Acoustic Stimulation↗
PubMed1999

Amphetamine dose dependently disrupts prepulse inhibition of the acoustic startle response in rats within a narrow time window.

Prepulse inhibition (PPI) of the acoustic startle response refers to the reduction in startle amplitude when a weak prepulse precedes a startle-inducing pulse. Prepulse inhibition has been shown to be disrupted by amphetamine at doses that also stimulate locomotor activity, and it has been suggested that the same neuroanatomical substrate, mesolimbic dopamine activation, mediates the effects of amphetamine on locomotor activity and PPI. Amphetamine stimulates locomotor activity and mesolimbic dopamine release over a 1- to 3-h period, whereas PPI is typically measured within the first 30 min following amphetamine treatment. The present study therefore determined whether delays in testing would alter the PPI-disruptive effect of amphetamine in male Wistar rats. Amphetamine dose dependently disrupted PPI when the test session occurred 10 min following amphetamine treatment and only when the prepulse intensity was 5-10 dB above background. Delays of 40 and 60 min post-amphetamine injection, however, resulted in a loss of the ability of amphetamine to disrupt PPI although locomotor activity was significantly stimulated by amphetamine at these time points. The data from the present study therefore do not readily fit with the notion that the effects of amphetamine on locomotion and PPI are mediated by the same substrate.

Acoustic Stimulation↗
PubMedDate not supplied

Validation of an auditory startle response system using chemicals or parametric modulation as positive controls.

Neurotoxicity regulatory guidelines mandate that automated test systems be validated using chemicals. However, in some cases, chemicals may not necessarily be needed to prove test system validity. To examine this issue, two independent experiments were conducted to validate an automated auditory startle response (ASR) system. In Experiment 1, we used adult (PND 63) and weanling (PND 22) Sprague-Dawley rats (10/sex/dose) to determine the effect of either d-amphetamine (4.0 or 8.0 mg/kg) or clonidine (0.4 or 0.8 mg/kg) on the ASR peak amplitude (ASR PA). The startle response of each rat to a short burst of white noise (120 dB SPL) was recorded over 50 consecutive trials. The ASR PA was significantly decreased (by clonidine) and increased (by d-amphetamine) compared to controls in PND 63 rats. In PND 22 rats, the response to clonidine was similar to adults, but d-amphetamine effects were not significant. Neither drug affected the rate of the decrease in ASR PA over time (habituation). In Experiment 2, PND 31 Sprague-Dawley rats (8/sex) were presented with 150 trials consisting of either white noise bursts of variable intensity (70-120 dB SPL in 10 dB increments, presented in random order) or null (0 dB SPL) trials. Statistically significant sex- and intensity-dependent differences were detected in the ASR PA. These results suggest that in some cases, parametric modulation may be an alternative to using chemicals for test system validation.

Acoustic Stimulation↗
PubMed2000

Effects of inescapable stress and treatment with pyridostigmine bromide on plasma butyrylcholinesterase and the acoustic startle response in rats.

Pyridostigmine bromide (PB) is a reversible, peripherally active inhibitor of acetylcholinesterase (AChE) activity, and is recommended by the military as a pretreatment against potential nerve gas exposure. Recent evidence suggests that exposure to inescapable stressors allows PB to cross the blood-brain barrier, and thereby affect central AChE activity in mice. Here, we evaluated the functional impact of a stress/PB treatment interaction on acoustic startle responding and plasma butyrylcholinesterase (BuChE) activity in male Sprague-Dawley rats. To model the treatment protocol used by the military, PB was delivered in the drinking water of rats for 7 consecutive days. The morning after the start of PB treatment, and for the next 6 days, half the rats were exposed to 1 h of supine restraint stress. We therefore employed a 2 x 2 (stress x PB treatment) between-groups design. Exposure to supine stress alone induced a persistent decrease in plasma BuChE activity. Further decreases in BuChE activity were not observed in rats exposed to supine restraint and PB treatment. Exposure to stress also induced an exaggerated startle response, evident on the last day of stress and 24 h after stressor cessation. Treatment with PB alone produced an exaggerated startle response over the same time period, albeit to a lesser degree. Although treatment with PB concurrent with stress did not produce further changes in either BuChE activity or acoustic startle responding, stress-induced alterations in drinking behavior (and thereby the dose of PB ingested) may have affected these results. Persistent stress-induced reductions in BuChE activity may increase the risk of adverse reactions to cholinomimetics.

Acoustic Stimulation↗
PubMed2002

Involvement of the human cerebellum in fear-conditioned potentiation of the acoustic startle response: a PET study.

Fear-conditioned potentiation of the startle response was used to study the role of the cerebellum in associative learning of non-specific aversive reactions in healthy human subjects using PET. Prior PET scanning initially neutral light stimuli were paired with painful electric shocks (fear-conditioning phase). Four PET-scans each were performed with presentation of acoustic startle stimuli (T), fear-conditioned light stimuli (L) or acoustic stimuli paired with light (LT, potentation phase). As a measure of fear-conditioning subtraction of condition T from LT revealed an increase of regional cerebellar blood flow (rCBF) in the left cerebellar hemisphere. Subtraction of condition L from LT, as a measure of fear-conditioned potentiation, revealed an increase of rCBF in the medial cerebellum. Different parts of the cerebellum appear to be involved in this form of motor associative learning.

Acoustic Stimulation↗
PubMed2002

Elevated plus maze behavior, auditory startle response, and shock sensitivity in predisease and in early stage autoimmune disease MRL/lpr mice.

Behaviors indicative of anxiety have been suggested to emerge with the onset of autoimmune disease in MRL/MpJ-Fas(lpr) (MRL/lpr) mice. This study extends the behavioral characterization of MRL/lpr and congenic MRL/MpJ+/+ (MRL/+) mice using the elevated plus maze (EPM), acoustic startle response, and foot-shock sensitivity tasks. In the elevated plus maze, predisease MRL/lpr mice exhibited less anxiety while MRL/lpr mice in the early stage of autoimmunity did not differ from age-matched control MRL/+ mice. MRL/lpr mice exhibited lower startle responses compared to MRL/+ mice. Similarly, predisease MRL/lpr mice were less reactive to various foot-shock levels than MRL/+ mice. Both the MRL/lpr and the MRL/+ strains exhibited startle habituation deficits, implicating the background MRL strain in the impairment in this process. These data do not support the hypothesis that increased anxiety is apparent with the emergence of autoimmune disease in MRL/lpr mice; however, anxiety may appear as the disease advances.

Acoustic Stimulation↗
PubMed1985

Age, sex and strain comparison of habituation of the startle response in the rat.

Habituation and sensitization of the acoustic startle response were studied in young (3 month) and aged (26 month) male and female Fischer 344 rats and in young (3 month) and aged (32 month) male Sprague Dawley rats. Tones were presented on 25 consecutive trials for a session, one session on each of four consecutive days. An air puff stimulus immediately preceded trial 20 on each day to test sensitization. All aged rats demonstrated greater short-term (within session) relative habituation than their younger counterparts. Across sessions, aged male rats of both strains habituated more quickly than younger males. Aged female rats habituated more slowly. Sensitization was more likely to occur in younger rats.

Acoustic Stimulation↗
PubMed1989

Long-term habituation and sensitization of the acoustic startle response in the normal adult human.

The development and independence of short-term and long-term habituation (and short-term sensitization) of the acoustic startle response to repetitive stimuli has been repeatedly demonstrated in the experimental animal. Although short-term habituation (and sensitization) of acoustic startle has been studied in humans, neither long-term habituation nor sensitization has been demonstrated. In this study, long-term habituation (response amplitude decrement) of the blink component of the acoustic startle response occurred in normal men across five consecutive daily sessions of repetitive acoustic stimulation. Long-term sensitization (onset latency shortening) developed after the third day. Both the long-term habituation and sensitization were independent of the day. Both the long-term habituation and sensitization were independent of the short-term habituation, which developed within each daily session.

Adolescent↗
PubMed2005

Unilateral electrical stimulation of the inferior colliculus of rats modifies the prepulse modulation of the startle response (PPI): effects of ketamine and diazepam.

The magnitude of an acoustic startle response can be reduced by a weak stimulus presented immediately before the startle-eliciting noise. This phenomenon has been termed prepulse inhibition of the startle reaction (PPI). Previous studies indicated that the primary neural pathways mediating PPI belong to the brain stem and that the inferior colliculus (IC) was crucial. Its destruction reduced PPI. Stimulations applied to brain areas may be as deleterious as lesions. Therefore, we looked for the possibility of a brain stimulation applied to the IC during a PPI test to reduce also PPI. Rats were implanted with chronic electrodes, their tips being aimed at the IC. They were located within or close to the inter-colliculus nucleus. A train of stimulations was applied and PPI was tested alternately during and between periods of stimulation. As the most common method used to attenuate PPI consists in administrating drugs, for example ketamine, we also tested the effect of this drug. Another drug was also tested, diazepam, since it alters the functioning of the IC without any known effect on PPI. This allowed a comparative analysis of the neurobiological and the pharmacological effects. It appeared that the stimulation decreased PPI quantitatively as much as ketamine (6 mg/kg) without an effect of the basic startle reaction. These effects did not interfere with each other. Diazepam (1 mg/kg) did not modify PPI, neither under stimulation nor per se. Only for a very high dose (4 mg/kg), a sedative and myo-relaxant one the basic startle and PPI were altered.

Acoustic Stimulation↗
PubMed1996

Auditory startle response is diminished in rats after recovery from perinatal copper deficiency.

Recovery from perinatal copper deficiency was studied in female and male Sprague Dawley rats for 6 mo. Month-old offspring reared by dams on copper-deficient treatment starting d 7 of pregnancy had up to 80% reductions in regional brain copper concentrations compared with offspring from copper-supplemented dams. Liver copper concentrations and plasma ceruloplasmin diamine oxidase activities of copper-deficient rats were restored to control levels within 1 mo of nutritional repletion with dietary copper. However, brain copper concentrations, with the exception of the hypothalamus and medulla, remain lower than in controls even after 5 mo of treatment. Rats were screened for startle responses and foot splay after 1, 3 and 5 mo of repletion. Diminished auditory startle was evident in rats of both sexes at all repletion times tested, whereas tactile startle and preimpulse inhibition of tactile startle were not influenced by prior copper deficiency, suggesting auditory sensory perception abnormalities. In a separate study, postweaning male rats deprived of dietary copper for 5 wk exhibited clear signs of copper deficiency but normal acoustic startle responses and foot splay. Long-term neurochemical and behavioral abnormalities persist in rats after perinatal copper deficiency.

Acoustic Stimulation↗
PubMed1998

The ventral pallidum mediates disruption of prepulse inhibition of the acoustic startle response induced by dopamine agonists, but not by NMDA antagonists.

Prepulse inhibition (PPI) of the acoustic startle response is observed when the startling noise pulse is preceded by a weak, non-startling stimulus. PPI has been considered as a measure for sensorimotor gating mechanisms. Disruption of PPI can be found in schizophrenic patients as well as after blockade of NMDA receptors or stimulation of dopamine receptors in rats. The neuronal circuitry which regulates PPI consists of cortico-limbic brain structures where the nucleus accumbens (NAC) plays a key role. The NAC exerts its modulating effects on PPI by way of a projection from the ventral pallidum (VP) to the pedunculopontine tegmental nucleus (PPTg). We recently postulated that the reduction of PPI by intra-NAC infusion of glycine-site NMDA antagonists is not mediated by the VP. We tested here this hypothesis in rats with excitotoxic lesions of the VP which were systemically treated with apomorphine or MK-801 or received intraNAC infusions of dopamine or the glycine-site NMDA antagonist 7-chlorokynurenic acid. Lesioned rats showed a marked deficit in PPI after MK-801 and 7-chlorokynurenate treatment but not after apomorphine or dopamine injection, in contrast to sham-lesioned controls showing deficits in PPI under all conditions. These data provide behavioral evidence for the existence of a pathway which does not include the VP for the mediation of sensorimotor gating deficits. We propose that a direct connection between the NAC and PPTg may be responsible for the effects of NMDA/glycine receptor blockade, whereas the VP is an indispensable relay for the disruptive effects on PPI exerted by the NAC dopamine system.

Acoustic Stimulation↗
PubMed1989

Mesencephalic reticular formation lesions made after habituation training abolish long-term habituation of the acoustic startle response in rats.

Lesions to the mesencephalic reticular formation (MRF) in rats severely attenuate the acquisition of long-term habituation of the startle response when the lesions are made prior to habituation training. The present experiments extend the finding of habituation deficits to animals with MRF damage made after the animals have habituated to an auditory stimulus. Following habituation training, some animals received lesions to the MRF. The startle amplitudes of these animals immediately changed from control levels to levels indistinguishable from those of animals that never habituated across days--animals with MRF lesions made prior to habituation training. The mechanism responsible for long-term habituation appears to be a progressive increase in activity within a long-term habituation pathway extrinsic to the reflex circuit for the startle response, but the synaptic mechanisms responsible for this change are unknown.

Acoustic Stimulation↗
PubMed1986

Fear conditioning, pre-pulse inhibition and drug modulation of a short latency startle response measured electromyographically from neck muscles in the rat.

The present study evaluated if startle measured electromyographically in the neck muscles (having a 5 msec latency) would exhibit behavioral and pharmacological plasticity known to alter startle measured in a stabilimeter device. A total of 15 rats were implanted with bilateral EMG electrodes in the dorsal neck muscles and subsequently exposed to a variety of manipulations known to affect the whole-body startle response. The peak-to-peak EMG response that occurred within 10 msec of startle stimulus onset displayed pre-pulse inhibition, enhancement by prior fear conditioning, inhibition by clonidine, and enhancement by strychnine. The data are discussed in terms of modulation of neural transmission along a primary startle-mediating pathway.

Animals↗
PubMed1985

Effects of 8-OH-DPAT, lisuride and some ergot-related compounds on the acoustic startle response in the rat.

Five ergot-related compounds were examined for their effects on the acoustic startle response in the rat. The startle amplitude and the startle latency were registered. 8-Hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT; 0.5-8 mg/kg) and lisuride (0.05-0.8 mg/kg) were found to enhance the startle amplitude, while the mainly DA receptor active ergot derivatives pergolide (0.2-0.8 mg/kg), bromocriptine (5-20 mg/kg) and LY 141865 (5-20 mg/kg) had no, or even the reverse, effect. All five compounds caused a prolongation of the startle latency. The increased startle amplitude caused by 8-OH-DPAT (2 mg/kg) and lisuride (0.2 mg/kg) was successfully antagonized by the 5-HT receptor antagonist methiothepin (0.1 mg/kg) but not by metergoline (1 mg/kg). 5-Hydroxy-L-tryptophan (L-5-HTP; 12.5-50 mg/kg), administered to pargyline- and benserazide-pretreated animals, was included for comparison. The serotonin precursor caused a marked increase in the startle amplitude and a shortening of the startle latency.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1976

Automated system for acquisition and reduction of startle response data.

A system specifically designed for the acquisition and reduction of startle data is described. It is able to (1) sample startle responses from 5 animals simultaneously during a specific time band after the eliciting stimulus; (2) convert the analogue startle amplitudes into 2-digit numbers; (3) print the digital results of each startle in each animal; (4) add up the startle amplitudes for each rat over a preset number of stimuli and print the totals; (5) print the interstimulus interval and (6) code for up to six diferent types of trials. A non-technical description and complete wiring diagrams are provided.

Animals↗