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PubMed2000

Startle responses to electric shocks: measurement of shock sensitivity and effects of morphine, buspirone and brain lesions.

The present study developed a new protocol to assess shock sensitivity in rats. Male Wistar rats were subjected to footshock stimuli ranging from 0 to 1.6 mA (0.1 s) in a startle apparatus and startle responses elicited by shocks were measured. Acoustic stimuli (95, 105, or 115 dB) were dispersed within the shock series serving as a control measurement of motor performance. Results indicated that the magnitude of shock startle responses significantly increased with the shock intensity in a linear trend. Morphine (8.0 mg/kg) and buspirone (1.0, 2.5, or 5.0 mg/kg), both of which possessing analgesic effects, depressed shock startle but had no such effect on acoustic startle. The effect of morphine was readily reversed by pretreatment of naloxone (1.0 mg/kg). To investigate the neural basis underlying this response, radio-frequency lesions of various structures implicated in processing of nociceptive or aversive information were undertaken. Lesions of the ventroposterior thalamic nucleus, insular cortex, or amygdala decreased startle reactivity to electric shocks but not to acoustic stimuli. Lesions of the anterior cingulate gyrus or medial prefrontal cortex, while altered the reactivity to acoustic stimuli, had no effect on the shock-elicited startle. These results suggested that the amplitude of startle in response to electric shocks provide a quantitative measurement of shock sensitivity within an extended range of stimulus intensities. Performing this response may engage the the central nociceptive pathway.

Animals↗
PubMed1985

Short-term and long-term habituation of the acoustic startle response in chronic decerebrate rats.

Chronic decerebrate rats, maintained in good condition for 31-84 postoperative days, showed significant within-session habituation of the acoustic startle response. However, they showed no habituation over days under conditions that produced significant response deficits in controls. The decerebrates' stimulus-provoked response deficits may have endured for up to 40 min between sessions, and they were apparently more than normally susceptible to stimulus-provoked sensitization. The data are consistent with intrinsic models which assume that the mechanisms for short-term habituation are intrinsic to the stimulus-response (S-R) pathway in the lower brain stem. On the other hand, relatively permanent long-term habituation of the acoustic startle response must be mediated by extrinsic mechanisms rostral to the S-R pathway which superimpose an inhibitory influence on that pathway.

Acoustic Stimulation↗
PubMed1983

Habituation of the acoustic startle response in rats after lesions in the mesencephalic reticular formation or in the inferior colliculus.

Extensive damage to the mesencephalic reticular formation (MRF) in rats altered long-term habituation of the acoustic startle response without disrupting short-term habituation. The MRF lesions did not alter initial startle amplitudes, but the animals with lesions were unable to attain as low a long-term asymptote of habituation as could control animals. Subsequent manipulation of stimulus intensity and interstimulus interval revealed no differences in short-term habituation between the two groups. Large lesions to the inferior colliculus (IC) did not disrupt long-term habituation of the acoustic startle response, but these animals were unable to suppress responding as much as controls to intense stimuli presented rapidly. The deficits in long-term habituation following MRF lesions suggested a disruption of an extrinsic, inhibitory mechanism of habituation. The deficits following IC lesions could be due either to a disruption of a short-term habituation mechanism or to an increase in response sensitization produced by the lesions.

Acoustic Stimulation↗
PubMed2000

Prepulse inhibition of the startle response in men with schizophrenia: effects of age of onset of illness, symptoms, and medication.

BACKGROUND: Prepulse inhibition of the startle reflex response refers to the ability of a weak prestimulus to transiently inhibit the response to a closely following strong sensory stimulus. This effect represents an operational index of sensorimotor gating and is found to be deficient in schizophrenia. Prepulse inhibition deficits in schizophrenia seem to be partially normalized by typical antipsychotics and more fully by some atypical antipsychotics. Early onset of schizophrenia, particularly in men, has been associated with abnormal brain maturation, profound neuropsychological deficits, and less responsiveness to antipsychotic medication. We evaluated the effects of the age of onset of illness, current positive and negative symptoms, and the type of medication (typical vs atypical) on prepulse inhibition of the startle response in schizophrenia. METHODS: Thirty-eight male schizophrenic patients and 20 healthy male controls underwent testing for prepulse inhibition of the acoustic startle response. RESULTS: Earlier onset of illness was associated with reduced prepulse inhibition, while adult onset of illness was not. No significant relationships occurred between current symptoms and prepulse inhibition. Patients given typical, but not atypical, antipsychotics exhibited less prepulse inhibition compared with healthy controls. CONCLUSION: Early onset of illness is associated with profound deficits in prepulse inhibition of the startle response in men with schizophrenia.

Acoustic Stimulation↗
PubMed1999

The adenosine A1 receptor agonist N6-cyclopentyladenosine blocks the disruptive effect of phencyclidine on prepulse inhibition of the acoustic startle response in the rat.

Systemic administration of the NMDA receptor antagonist phencyclidine (PCP; 4 mg/kg) produced a profound reduction in prepulse inhibition of the acoustic startle response in rats. Pre-treatment with the selective adenosine A1 receptor agonist N6-cyclopentyladenosine (CPA) blocked (0.5 mg/kg) or attenuated (0.1 and 0.2 mg/kg) the disruptive effect of PCP on prepulse inhibition. These findings suggest that adenosine may regulate the inhibitory effect of NMDA receptor blockade on prepulse inhibition, and raise the possibility that adenosine may be a potentially useful target for anti-psychotic medication. Further, 0.5 mg/kg CPA by itself was without effect on prepulse inhibition but did decrease startle amplitude, raising the possibility that adenosine, acting via A1 receptors, may be a component of the neurochemical substrate that modulates the acoustic startle response.

Acoustic Stimulation↗
PubMed1982

The effect of tail pinch on the acoustic startle response in rats.

A series of 3 experiments was carried out to evaluate the effect of tail pinch (TP) on the amplitude of the acoustic startle response (ASR) in rats. There is a consistent group of pharmacological findings which support the view that the amplitude of the ASR is facilitated by transmission in both dopaminergic and noradrenergic neural systems. It has recently been reported that TP increases cortical norepinephrine release and pars compacta unit activity. It might therefore be expected that TP would facilitate the amplitude of the ASR. This hypothesis was tested in the first experiment. Surprisingly, it was found that TP significantly depressed startle amplitude. In the second experiment if was found that this TP-induced depression in startle amplitude was reduced by damage to the nucleus accumbens and that the amount of reduction correlated with the extent of damage. In the third experiment the generality of the effect of TP on sensorimotor reactivity was evaluated by testing its effect on footshock threshold and airpuff-elicited startle response. TP also depressed responsiveness in these tests. These results are consistent with other observations that the nucleus accumbens plays a role in the modulation of sensorimotor reactivity.

Acoustic Stimulation↗
PubMed1990

Long-term habituation of the acoustic startle response: role of the cerebellar vermis.

The cerebellar vermis has been recognized as a key region of a circuit essential for long-term habituation of the acoustic startle response in rats. The removal of this neuronal structure before training prevents the build-up of this long-term behavioral change. Our data show that, when the same lesion is performed after training for long-term habituation, the learned behavior is not affected. These results indicate that the cerebellar vermis is essential for the acquisition, but not for the retention of long-term habituation of the startle response.

Acoustic Stimulation↗
PubMed1994

Social isolation in the rat produces developmentally specific deficits in prepulse inhibition of the acoustic startle response without disrupting latent inhibition.

A series of experiments examined the effects of 8 weeks of social isolation on spontaneous locomotor activity, prepulse inhibition (PPI) of the acoustic startle response, latent inhibition (LI) in a conditioned suppression paradigm, and basal and d-amphetamine stimulated dopamine (DA) release in the ventral striatum, as measured by in vivo microdialysis. Both isolation-reared animals (those isolated from the weaning age) and isolation-housed animals (those isolated as adults) were hyperactive when placed in a novel environment. Social isolation also led to deficits in PPI of the acoustic startle response that were specific to isolation-reared animals. Isolation rearing was without effect on the expression of LI but did lead to an enhanced response to systemic d-amphetamine in terms of striatal DA release. The data are discussed with respect to the involvement of ventral striatal DA mechanisms in the expression of PPI and LI, differences in the impact of social isolation in young and adult animals, and the utility of social isolation model as a nonlesion, nonpharmacologic means of perturbing ventral striatal DA function.

Acoustic Stimulation↗
PubMed1986

The influence of stimulus repetition on the acoustic startle response and on responses of inferior colliculus neurons of mice.

The acoustic startle response (ASR) and discharges of single units in the inferior colliculus (IC) were evaluated as a function of the repetition rate and trial (stimulus 1-10 at each rate) of intense noise bursts in mice. The amplitude of the ASR was inversely proportional to both rate and trial. The mean number of discharges for the sample population of units of the central nucleus (ICC) and the external nucleus (ICX) were also inversely proportional to stimulus rate. However, only ICX units were inversely proportional to trial (i.e. as was the ASR). When response properties of individual units were examined, a variety of profiles was observed with regard to rate and trial sensitivity: units were either not sensitive to stimulus rate, inversely sensitive, directly sensitive, or complexly sensitive. Superimposed on these rate classifications were trial sensitivity, with some units being insensitive to trial, directly sensitive, or inversely sensitive. The incidence of response types differed in some respects between ICC and ICX and these differences were, in general, consistent with the mean responses of the neuronal populations.

Acoustic Stimulation↗
PubMed1986

Central dopamine hyperactivity in rats mimics abnormal acoustic startle response in schizophrenics.

Schizophrenic patients show loss of the normal inhibition of the acoustic startle response (ASR) when the startle stimulus is preceded by a weak prepulse stimulus. In rats experimentally induced to have locally supersensitive dopamine receptors within forebrain dopamine terminal regions, we find a similar deficit in "prepulse inhibition" of the ASR. Our results suggest that there are intriguing parallels between the aberrant sensory gating of the ASR demonstrated by schizophrenics and that demonstrated by rats during stimulation of supersensitive brain dopamine receptors. Thus, prepulse inhibition of the ASR provides a useful paradigm for investigating the bridge between mesolimbic dopamine overactivity and the specific time-dependent information processing-sensory gating disturbances that have been identified in schizophrenic patients.

Acoustic Stimulation↗
PubMed2003

High illumination levels potentiate the acoustic startle response in preweanling rats.

Fear potentiation of the acoustic startle response (FPS) by aversive conditioned stimuli does not emerge in rats until Postnatal Day (P)23 (see P. S. Hunt & B. A. Campbell, 1997). However, the present study found that when presented with an unconditioned fear-eliciting stimulus, rats younger than P23 display FPS. Specifically, high illumination levels were found to enhance startle amplitudes in rats aged 18 and 25 days, but not 14 days. Furthermore, the light-enhanced startle observed in P18 rats was prevented by a systemic injection of the noradrenergic beta-receptor antagonist propranolol. These data suggest that conditioned and unconditioned FPS have different ontogenetic trajectories, and thereby provide support for the idea that learned and unlearned fear are subserved by dissociable neural systems.

Acoustic Stimulation↗
PubMed1981

Habituation of startle response, lick suppression, and exploratory behavior in rats with hippocampal lesions.

Rats with bilateral hippocampal lesions and controls with neocortical lesions were compared on the habituation of lick suppression and startle response. The animals with hippocampal lesions showed no consistent differences from controls on any measure within these two response systems. Importantly, the rats with hippocampal lesions showed significant retention of habituation over periods of 24 hr and 21 days. Experimental and control differences were not revealed when stimulation was presented on a 1-sec interstimulus interval. None of these results varied with the extent of the hippocampal lesions, which ranged from relatively small lesions restricted to the dorsal hippocampus to large lesions that damaged the hippocampus in its dorsal, posterior, and ventral aspects. In contrast to the startle response and lick suppression results, hippocampal lesions significantly disrupted Y-maze exploratory behavior, and the disruption was directly related to the extent of hippocampal damage. The data suggest that the hippocampus is not involved in any important way in the control of either short-term or long-term habituation of elicited, reflex-like behaviors but is importantly involved in the control of emitted, exploratory behaviors.

Animals↗
PubMed1996

The septohippocampal system is involved in prepulse inhibition of the acoustic startle response in rats.

Prepulse inhibition (PPI) of the acoustic startle response (ASR) can be used as an operational measure for brain mechanisms that prevent disruption of ongoing stimulus processing routines by other stimuli and that thereby avoid behavioral interference. Deficient PPI has been observed in schizophrenics; therefore, much interest has been devoted to the understanding of the neural basis of PPI. This study investigated the role of the septohippocampal system in the modulation of PPI in rats. Stimulation of the medial septum by injection of the glutamate agonist kainate led to a profound disturbance of PPI and reduced the ASR amplitude. The PPI deficit induced by intraseptal kainate was attenuated by systemic or intrahippocampal administration of the acetylcholine antagonist scopolamine. Lesions of the medial septum, made by the neurotoxin AMPA, did not affect PPI. The present data indicate that activation of the septohippocampal system reduces PPI of the ASR, suggesting its role in sensorimotor gating.

Animals↗
PubMed2001

Centrally administered corticotropin-releasing hormone and peripheral injections of strychnine hydrochloride potentiate the acoustic startle response in preweanling rats.

Attempts to condition fear potentiation of startle (FPS) in rats younger than 23 days of age have not been successful, regardless of the type of aversively conditioned stimulus used (P. S. Hunt, R. Richardson, & B. A. Campbell, 1994; R. Richardson, G. Paxinos, & J. Lee, 2000; R. Richardson & A. Vishney, 2000). In the present study, the authors report that peripheral injections of strychnine hydrochloride, a glycine receptor antagonist, and intracerebroventricular infusions of corticotropin releasing hormone (CRH) both potentiated the acoustic startle response (ASR) in 16-18-day-old rats. Because strychnine and CRH have distinct sites of activation in the primary startle pathway, it can be concluded that this pathway is functional and modifiable in rats younger than 23 days of age. This finding suggests that the failure to observe conditioned FPS in preweanling rats is due to an immaturity of the secondary fear circuit responsible for enhancing the ASR during a fear state.

Age Factors↗
PubMed1995

Glycine receptors in the caudal pontine reticular formation: are they important for the inhibition of the acoustic startle response?

The present paper sought to test the hypothesis that inhibitory glycine receptors (GlyRs) on giant neurons of the caudal pontine reticular formation (PnC) are involved in the inhibition of the acoustic startle response (ASR) in rats. First we provided evidence for the presence of the strychnine-sensitive inhibitory GlyR on PnC neurons by immunocytochemical labeling using an antibody against the alpha 1 subunit of the GlyR. We then measured the ASR as well as two ASR inhibiting phenomena, short-term habituation and prepulse inhibition, after microinjections of the glycine antagonist strychnine (0, 5 or 10 nmol) or the glycine agonist beta-alanine (0, 50 or 100 nmol) into the PnC. Neither strychnine nor beta-alanine had a measurable influence on any of the parameters of the ASR investigated (amplitude, short-term habituation, prepulse inhibition). In contrast, systemic injection of strychnine (1 mg/kg) markedly increased the ASR amplitude. The systemic administration of strychnine did not impair prepulse inhibition. The human 'startle disease' (hyperekplexia), an exaggerated startle response, is caused by a defect of the alpha 1 subunit of the inhibitory GlyR, but it is unclear at which site in the central nervous system this defect ultimately leads to the symptoms of hyperekplexia. Our data indicate that a blockade of the inhibitory GlyRs in the PnC does not affect the ASR of rats, suggesting that deficient GlyRs in the PnC might not be involved in the etiology of the human 'startle disease'. We conclude that the inhibitory GlyRs on PnC neurons are not necessary for the inhibition of the ASR and believe that they are involved in another behavioral context.

Animals↗
PubMed1977

Startle response and muscular fatigue effects upon fractionated hand grip reaction time.

The fractionation of a simple right-hand grip total reaction time (RT) into central and peripheral temporal components (premotor and motor time, respectively) helped to define the site of RT change following an auditory induced startle response and two fatiguing hand-grip exercise regiments for eight males and eight females. Following the startle response, mean values for RT significantly lengthened, due primarily to an increase in premotor time. In contrast, lengthened RT following both fatigue regimens (42% and 55% strength decrements) were due to substantial increases in the motor time component. These results suggest that although performance of tasks which demand a high degree of precision, accuracy, and fine motor control may be disrupted by the introduction of such stressors as an induced startle and local muscular fatigue, the neuromuscular mechanisms mediating performance disruption are dissimilar.

Journal Article↗
PubMed2005

Relation of sex and estrous phase to deficits in prepulse inhibition of the startle response induced by ecstasy (MDMA).

Sensorimotor gating is the ability of a weak sensory event to inhibit the motor response to an intense stimulus. Drugs that act as serotonin releasers, such as MDMA (3,4-methylenedioxymethamphetamine), impair sensorimotor gating, which is measured as a prepulse inhibition (PPI) of the acoustic startle response. The first objective of the present study was to compare the effect of different doses of MDMA on PPI and the acoustic startle response (ASR) in male and female Wistar rats. The second objective was to examine the effect of MDMA on PPI across the estrous cycle in female rats. MDMA was administered in doses of 2.5, 5 and 10 mg/kg s.c. 15 min before the start of the experiment. The controls received saline in equivalent volumes. MDMA dose-dependently decreased PPI in both the male and female rats and produced higher levels of ASR in the male rats compared to the females. In addition, we found that female rats in the diestrous and metestrous phases are more sensitive to MDMA and showed higher deficits in PPI than female rats in the proestrous and estrous phases. Our result showed that female rats in the proestrous and estrous phases were less sensitive to the disruption of PPI by MDMA.

Acoustic Stimulation↗
PubMed1997

The acoustic startle response in inbred Roman high- and low-avoidance rats.

To investigate the emotional reactions of two rat strains selectively bred for good and poor two-way avoidance acquisition (RHA/Verh and RLA/Verh), male animals of both strains were tested in an acoustic startle response test. They received 40 acoustic stimuli followed by 10 electric foot shocks and another 30 acoustic stimuli. RLA/Verh rats showed a significantly higher startle response compared to RHA/Verh animals, indicating a stronger emotional reaction to acoustic stimuli. In addition, the former showed a stronger response to foot shocks. Combined with earlier findings, we conclude that selection for two-way avoidance learning does not result in cognitive defects in the RLA/Verh strain but, rather, in stronger emotional reactions to fearful stimuli.

Acoustic Stimulation↗