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PubMed2006

Metabotropic glutamate subtype 5 receptors modulate fear-conditioning induced enhancement of prepulse inhibition in rats.

Non-startling acoustic events presented shortly before an intense startling sound can inhibit the acoustic startle reflex. This phenomenon is called prepulse inhibition (PPI), and is widely used as a model of sensorimotor gating. The present study investigated whether PPI can be modulated by fear conditioning, whose acquisition can be blocked by the specific antagonist of metabotropic glutamate receptors subtype 5 (mGluR5), 2-methyl-6-(phenylethynyl)-pyridine (MPEP). The results show that a gap embedded in otherwise continuous noise sounds, which were delivered by two spatially separated loudspeakers, could inhibit the startle reflex induced by an intense sound that was presented 50 ms after the gap. The inhibitory effect depended on the duration of the gap, and was enhanced by fear conditioning that was introduced by temporally pairing the gap with footshock. Intraperitoneal injection of MPEP (0.5 or 5mg/kg) 30 min before fear conditioning blocked the enhancing effect of fear conditioning on PPI, but did not affect either the baseline startle magnitude or PPI if no fear conditioning was introduced. These results indicate that PPI is enhanced when the prepulse signifies an aversive event after fear conditioning. Also, mGlu5Rs play a role in preserving the fear-conditioning-induced enhancement of PPI.

Analysis of Variance↗

PubMed1983

Harmaline effects on the sensory-motor reactivity: modifications of the acoustic startle pattern.

The effects of harmaline, an indoleamine and a MAOI, were tested on the acoustic startle pattern. EMG measures of the startle reflex, the pinna reflex as well as the characters of the vertex evoked responses to brief intense tone bursts (60 msec, 110 dB, 8000 Hz) were simultaneously studied in 4 alert guinea-pigs. The basic experimental design was a 4 by 4 latin square, with the treatments being given at 2 day intervals. The four harmaline-HCl treatments were isotonic saline, 0.25, 5.0, and 10.0 mg/kg. Compared with saline baselines, all the doses resulted, throughout the 60 min session, in overall high significant depressions of the startle reflex, the pinna reflex and the initial wave of the acoustic evoked potential at the vertex. In contrast, harmaline had little or no influence on amplitude and latency of the late wave of the vertex response. The effects of harmaline on the general behavior of the guinea-pig are also reported. These results may support an involvement of serotonergic systems in the modulation of the sensory-motor reactivity at the brainstem level. Nevertheless, the probably more complex cortical processes involved in startle responsiveness do not appear univocally affected by the indoleamine drugs such as harmaline.

Acoustic Stimulation↗

PubMed1986

Differential effects of dopamine agonists on acoustically and electrically elicited startle responses: comparison to effects of strychnine.

This study sought to determine where drugs that are known to alter sensorimotor reactivity measured with the acoustic startle reflex ultimately act within the acoustic startle pathway. To do this, startle was elicited either acoustically or electrically within various nuclei believed to comprise the acoustic startle pathway. Direct infusion of serotonin into the subarachnoid space of the lumbar spinal cord increased acoustic startle and startle elicited electrically through the ventral cochlear nucleus (VCN) to a comparable degree. Subconvulsant doses of strychnine increased startle elicited acoustically or electrically through either the VCN or the nucleus reticularis pontis caudalis (RPC), pointing to a spinal locus of action of strychnine after systemic administration. In marked contrast, the dopamine agonists d-amphetamine and apomorphine consistently increased acoustic startle but actually depressed startle elicited electrically through the VCN or the RPC. These later results suggest that dopamine agonists increase sensorimotor reactivity measured with acoustic startle by acting on sensory rather than motor parts of the reflex arc.

Acoustic Stimulation↗

PubMed1975

Lead-stimulation effects of human cardiac orienting and blink reflexes.

Innocuous prestimulation can inhibit or facilitate a startle reflex in lower animals, depending on its lead time and on whether it is dircrete or continues throughout the lead interval. Similar effects of lead stimulation on the unconditioned blink reflex were found in human subjects, but human subjects also showed an effect not seen in lower animals. Under conditions of temporal and stimulus uncertainty, the presentation of discrete stimuli at lead times that have no effect in rats produced blink facilitation as well as pronounced cardiac decelerations during the lead interval in man. The article suggests that this effect might be mediated by an attentional process and that it could be dissociated from effects produced by a classical arousal mechanism.

Acoustic Stimulation↗

PubMed1996

Sensorimotor gating in rats is regulated by different dopamine-glutamate interactions in the nucleus accumbens core and shell subregions.

The amplitude of the acoustic startle reflex is normally reduced when the startling stimulus is preceded by a weak click or "prepulse'. Prepulse inhibition (PPI) of acoustic startle has been used as an operational measure of sensorimotor gating or inhibition, and is reduced in schizophrenia patients and in rats with central dopamine (DA) activation. The DA agonist-induced disruption of PPI in rats may thus offer a useful animal model to study impaired sensorimotor gating in schizophrenia. We have previously reported that DA-glutamate interactions in the nucleus accumbens (NAC) regulate PPI. The NAC has at least two major subregions-the core and shell-that have distinct anatomical and neurochemical properties. In this study, we compared changes in PPI after manipulations of DA-glutamate activity in these two NAC subregions. Consistent with previous findings, infusion of the non-NMDA agonist AMPA into the NAC core subregion significantly reduced PPI, and this effect was opposed by systemic administration of the D2 antagonist haloperidol. Also consistent with previous reports, infusion of the non-NMDA antagonist CNQX into the NAC core subregion did not alter PPI, but its co-infusion with D-amphetamine (AMPH) attenuated the AMPH-disruption of PPI. In contrast, while PPI was reduced after AMPA infusion into the NAC shell subregion, this effect of AMPA could not be blocked by pretreatment with haloperidol. Infusion of either AMPH or CNQX into the NAC shell subregion reduced PPI independently. The PPI-disruptive effects of intra-shell CNQX infusion were not blocked by haloperidol. The present results suggest striking differences between the NAC core and shell subregions in their neurochemical modulation of sensorimotor gating of acoustic startle in the rat.

Acoustic Stimulation↗

PubMed1996

Prepulse effects on magnitude estimation of startle-eliciting stimuli and startle responses.

The present studies investigated the relationship between prepulse effects on the modification of the brainstem startle reflex and magnitude estimates of startle-eliciting stimuli. In Experiment 1, startle eyeblink responses were elicited in 24 students, half of whom were instructed to estimate the loudness of the startle stimulus (actual intensities of 80, 90, and 100 dB) and half of whom were instructed to estimate the magnitude of their eyeblink. When weak acoustic prepulses preceded the startle-eliciting stimulus, eyeblink amplitude was inhibited, and estimates of response magnitude decreased, but estimates of startle stimulus magnitude decreased only when 100-dB startle stimuli were presented. In Experiment 2, the same startle stimuli were preceded on some trials by a vibrotactile prepulse to the hand. In conditions in which startle amplitude was inhibited, startle stimulus magnitude estimates were not affected. This suggests that the effect of acoustic prepulses on 100-dB startle stimuli in Experiment 1 may have been due to loudness assimilation, an effect independent of the prepulse inhibition of startle responding.

Acoustic Stimulation↗

PubMed2002

Affective imagery and the startle response: probing mechanisms of modulation during pleasant scenes, personal experiences, and discrete negative emotions.

Two experiments addressed the following issues concerning modulation of the acoustic startle reflex during emotional imagery: (1) Is startle inhibited or potentiated during imagery of pleasurable events? (2) Does startle modulation differ for personal versus standard imagery scenes? (3) Is startle modulated differently during anger versus fear? For standard scenes, startle was greater during aversive than pleasant imagery, with both exceeding neutral. Blink potentiation was greater during imagery of personal pleasant than nonpersonal pleasant scenes. Startle potentiation did not differ for anger versus fear material, but differences were found in self-report, corrugator EMG, and HR response. These results suggest that in addition to the emotional valence of imagined material, startle reactivity is influenced by the degree of engagement or active disengagement from the sensory environment. The findings also indicate that fear and anger are differentiable in terms of affective report, cardiac mobilization, and expressive behavior, but not at the primary motivational level at which reflex priming occurs.

Adolescent↗

PubMed1996

The site of sympathetic deficit in cluster headache.

The pattern of autonomic deficit in the face of cluster headache patients resembles the deficit in patients with a postganglionic sympathetic lesion from some other cause; however, the presence of abnormal cardiac rhythms and bilateral pupillary reflex deficit in some patients with cluster headache suggests that the lesion might compromise central sympathetic drive. To investigate this possibility, the vasomotor and sudomotor startle reflex was investigated in the hands of six cluster headache patients with ocular and thermoregulatory signs of postganglionic sympathetic deficit in the face; for comparison, responses were also investigated in 15 patients with a lesion in the cervical sympathetic pathway from some other cause. The startle reflex was intact in the hands of the six cluster headache patients, but was diminished ipsilaterally in patients with a central or preganglionic sympathetic lesion and also, surprisingly, in patients with a postganglionic lesion caused by an aneurysm of the internal carotid artery. Ocular sympathetic deficit was greater in patients with an aneurysm of the internal carotid artery than in cluster headache patients or in patients with a postganglionic sympathetic lesion from some other cause; the aneurysm may have compromised neurons with projections to the face and hand, or could have induced transsynaptic degeneration of preganglionic fibers supplying both regions. The findings indicate that central sympathetic drive is not impaired in cluster headache patients; thus, a peripheral lesion probably induces sympathetic deficit on the symptomatic side of the face.

Adult↗

PubMed1993

Men are more inhibited than women by weak prepulses.

The acoustic startle reflex is normally inhibited when the startling stimulus is preceded by a weak prepulse. We studied "prepulse inhibition" (PPI) to assess potential gender differences in this operational measure of sensorimotor gating. A review of data from our previously published studies in psychiatric patients and normal controls indicated that startle in women was less inhibited by weak prepulses than was startle in men, and that this gender difference narrowed when stronger prepulses were used to elicit maximal levels of PPI. Based on these observations, new subjects were selected for study using our established criteria to exclude individuals with psychiatric disorders, substance abuse, or serious neurologic or medical illness. Replicating our preliminary observation, women exhibited significantly less PPI than men, with the gender difference being most notable under conditions with weak prepulses. Potentially confounding variables, including electrode impedance, startle amplitude, habituation and latency did not differ between men and women. PPI was then measured in male and female rats, where no gender differences were noted. These findings identify significant gender differences in PPI in humans, and suggest that inhibitory "gating" processes are more robust in men than in women, when assessed using a sensitive range of inhibitory stimuli.

Acoustic Stimulation↗

PubMed2005

Enhanced prepulse inhibition of startle using salient prepulses in rats.

Prepulse inhibition (PPI) of the startle reflex occurs when a non-startling stimulus is presented shortly prior to the startling stimulus. PPI is an operational measure for sensorimotor gating. PPI in humans is enhanced by attention, but there is no evidence yet for attentional modulation of PPI in animals. We here combined PPI and conditioned inhibition paradigms in order to investigate attentional modulation of PPI in rats. PPI was assessed before and after training for conditioned inhibition of fear with the conditioned stimulus (auditory CS) and conditioned inhibitor (visual CI) as prepulses. The CI significantly enhanced PPI after training, whereas presentation of the CS had no effect on PPI. These data suggest attentional modulation of PPI in rats by biologically salient prestimuli. This new paradigm may be useful for examining attentional modulation of PPI in animals and to compare attentional modulation in humans and animals.

Acoustic Stimulation↗

PubMed2005

Influence of individual differences in Behavioral Inhibition System on the magnitude and time course of the fear-potentiated startle.

Previous research has shown that the startle reflex is potentiated during experimentally induced anxiety (fear-potentiated startle). In the present study, the magnitude and time course of the startle blink reflex were examined among 35 undergraduates scoring one standard deviation above (n = 14) or below (n = 21) the mean in a self-report measure of sensitivity to punishment (SP) in a paradigm involving the anticipation of electric shocks. Contrary to our predictions, SP did not relate to differences in the magnitude or in the time course of fear-potentiated startle. Our data do not support an association between this individual differences variable and the fear-potentiated startle.

Acoustic Stimulation↗

PubMed2004

Galvanic evoked vestibulospinal and vestibulocollic reflexes in stroke.

OBJECTIVE: Following stroke, the startle reflex, mediated via the reticulospinal tract, is often facilitated. Vestibulospinal reflexes are another bulbospinal reflex, abnormalities of which may contribute to impaired body posture and stance following stroke. We recorded galvanic evoked vestibulospinal and vestibulocollic reflexes to assess whether these showed similar changes to those for startle following stroke affecting the pons and above. METHODS: Twenty-four stroke subjects (aged 40-82) were studied in the vestibulospinal part of the study, 21 stroke subjects (aged 40-81 years) were studied in the vestibulocollic part, including 18 studied in both. Transmastoid galvanic (DC) current was used to stimulate the vestibular nerve. Vestibulocollic responses were recorded from the sternocleidomastoid muscles and vestibulospinal responses from over soleus in standing subjects. RESULTS: Vestibulocollic reflex amplitudes and latencies showed no significant differences between the two sides. Similarly short latency (SL) and medium latency (ML) vestibulospinal reflexes did not differ significantly in frequency, latency or amplitude between the affected and unaffected legs. CONCLUSIONS: Vestibular reflexes are not facilitated by stroke at or above the pontine level. The exaggeration of startle by stroke may be specific to this reflex.

Adult↗

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↗

PubMed2004

Effect of social isolation on stress-related behavioural and neuroendocrine state in the rat.

The present study investigated the effects of post-weaning social isolation (SI) on behavioural and neuroendocrine reactivity to stress of male and female rats. Innate aspects of fear and anxiety were assessed in the open field and elevated plus maze tests. Spontaneous startle reflex and conditioned fear response were further investigated. The neuroendocrine response of isolates was examined by measuring basal and stress release of ACTH and corticosterone and by evaluating the mRNA expression of mineralocorticoid (MR) and glucocorticoid (GR) receptors using in situ hybridization. Locomotor activity in the open field was not modified by chronic SI. In males, but not females, SI produced an anxiogenic profile in the elevated plus maze. Male isolates showed a trend towards increased startle reflex amplitude relative to socially-reared controls. Moreover, SI in males produced alterations of the HPA axis functioning as reflected by higher basal levels of ACTH, and enhanced release of ACTH and corticosterone following stress. In contrast, startle response or HPA axis functioning were not altered in female isolates. Social isolates from both genders showed reduced contextual fear-conditioning. Finally, the mRNA expression of MR and GR was not modified by SI. The results of the present study suggest that chronic SI increases emotional reactivity to stress and produces a hyperfunction of the HPA axis in adult rats, particularly in males.

Adrenocorticotropic Hormone↗

PubMed1996

Seroquel restores sensorimotor gating in phencyclidine-treated rats.

Phencylidine (PCP) is a psychotomimetic noncompetitive glutamate antagonist that has been used in studies of the neural substrates of psychosis. Both schizophrenic patients and PCP-treated rats exhibit reduced amounts of prepulse inhibition (PPI) of the startle reflex, which is the normal inhibition of startle that occurs when the starting noise is preceded 30 to 500 msec by a weak prepulse. The present study assessed the effects of seroquel (ICI 204,636), a mixed D2/5-hydroxytryptamine2 antagonist with a preclinical profile suggestive of potential antipsychotic efficacy, on the PCP-induced disruption of PPI. Clozapine, risperidone and haloperidol were also studied as comparison compounds. PCP (1.25 mg/kg) significantly reduced PPI, with prepulses that were 1 to 12 dB above background. Seroquel and clozapine significantly restored PPI in PCP-treated rats, whereas haloperidol and risperidone did not. Similar findings were obtained in studies using separate animals, a slightly lower dose of PCP (1.0 mg/kg) and a high dose of each of these antipsychotics. Separate studies verified that risperidone and haloperidol restored PPI in apomorphine-treated rats. In the present studies, seroquel exhibited a profile consistent with those exhibited by other "atypical" antipsychotics.

Animals↗

PubMed1999

Hyperekplexia phenotype due to compound heterozygosity for GLRA1 gene mutations.

Hyperekplexia (MIM 149400), or startle disease, is a neurological disorder characterized by generalized stiffness during the neonatal period, excessive startle reflexes, and generalized stiffness related to the startle response. Linkage analysis mapped a major gene for this disorder to chromosome 5q33-35. Subsequently, mutations in the GLRA1 gene, encoding the alpha1 subunit of the glycine receptor, were found in hyperekplexia families with an autosomal dominant or recessive inheritance pattern. In the present study, we describe the genetic analysis of the GLRA1 gene of a family consisting of 2 children with hyperekplexia, 2 nonaffected children, and their healthy nonconsanguineous parents. Although the pedigree suggested the presence of a recessive mutation, haplotype construction showed that the 2 affected children shared the same haplotype combination in which the maternal haplotype differed from the paternal haplotype, suggesting the presence of compound heterozygosity. Mutation analysis revealed different missense mutations on the two haplotypes, changing an arginine to a histidine at amino acid positions 252 and 392, respectively. It is interesting that the hyperekplexia phenotype was only seen in individuals compound heterozygous for the two mutations, whereas family members carrying either one of the two mutations had no clinical signs.

Chromosome Mapping↗

PubMed1998

Effect of lead acetate on neurobehavioral development of rats.

We investigated the effects of lead exposure during the pre- and postnatal period on the neurobehavioral development of female Wistar rats (70-75 days of age, 120-150 g) using a protocol of lead intoxication that does not affect weight gain. Wistar rats were submitted to lead acetate intoxication by giving their dams 1.0 mM lead acetate. Control dams received deionized water. Growth and neuromotor development were assessed by monitoring daily the following parameters in 20 litters: body weight, ear unfolding, incisor eruption, eye opening, righting, palmar grasp, negative geotaxis, cliff avoidance and startle reflex. Spontaneous alternation was assessed on postnatal day 17 using a T maze. The animals' ability to equilibrate on a breaker rim was measured on postnatal day 19. Lead intoxication was confirmed by measuring renal, hepatic and cerebral lead concentration in dams and litters. Lead treatment hastened the day of appearance of the following parameters: eye opening (control: 13.5 +/- 0.6, N = 88; lead: 12.9 +/- 0.6, N = 72; P < 0.05), startle reflex (control: 13.0 +/- 0.8, N = 88; lead: 12.0 +/- 0.7, N = 72; P < 0.05) and negative geotaxis. On the other hand, spontaneous alternation performance was hindered in lead-exposed animals (control: 37.6 +/- 19.7; lead: 57.5 +/- 28.3% of alternating animals; P < 0.05). These results suggest that lead exposure without concomitant undernutrition alters rat development, affecting specific subsets of motor skills.

Analysis of Variance↗

PubMed1998

5-HT1B receptor modulation of prepulse inhibition: recent findings in wild-type and 5-HT1B knockout mice.

Sensorimotor gating of the startle reflex occurs when the presentation of a weak "prepulse" 30-500 msec prior to a startling stimulus inhibits the reflex, and is called prepulse inhibition (PPI). The study of PPI has recently been extended to mice to take advantage of recent advances in molecular genetics, because several neuropsychiatric disorders including schizophrenia, obsessive compulsive disorder, and schizotypal personality disorder are characterized by PPI deficits. Studies in wild-type and 5-HT1B knockout mice suggest that activation of 5-HT1B receptors decreases PPI. The direct 5-HT1A/1B agonist RU24969 decreases PPI in wild-type but not 5-HT1B knockout mice. Likewise, the serotonin releasing compounds MDMA(+), MBDB(+/-), and alpha-ethyltryptamine (AET) have no effect on PPI in wild-type mice, but increase PPI in 5-HT1B knockout mice. As the direct 5-HT1A agonist 8-OH-DPAT increases PPI in mice, the unmasking of these effects may also contribute to the PPI-increasing effects of 5-HT releasers in 5-HT1B knockout mice.

Animals↗