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PubMed1997

Activation of a distinct arousal state immediately after spontaneous awakening from sleep.

In contrast to the many neural studies into the mechanisms of sleep onset and maintenance, few studies have focused specifically on awakening from sleep. However, the abrupt electrographic changes and large brief cardio-respiratory activation at awakening suggest that a distinct, transiently aroused, awake state may exist compared to later wakefulness. To test this hypothesis we utilized the acoustic startle reflex, a standard un-conditioned reflex elicited by a sudden loud noise. This reflex is modulated under specific conditions, one being a diminution of startle when a quieter pre-stimulus is presented immediately before the loud stimulus. This pre-pulse inhibition (PPI) is used as a measure of sensorimotor gating, with smaller PPI indicating less filtering of sensory inputs and increased responsiveness to external stimuli. Eight rats with electrodes for recording sleep-wake state were studied. An accelerometer measured startle responses. The startle reflex was elicited by 115 dB, 40 ms tones. PPI was produced by 74 dB, 20 ms tones preceding the 115 dB tone by 100 ms. Responses within 100 ms were measured. Stimuli were applied either 3-10 s after spontaneous awakenings, or in established wakefulness (> 30 s). Responses to the startle stimuli alone were similar in the different awake states (P = 0.821). However, PPI was smaller at awakening from non-REM sleep compared to established wakefulness (45.4 +/- 7.5% vs. 74.3 +/- 6.1%, P = 0.0002). PPI after awakening from REM sleep (52.8 +/- 17.9%) was not significantly different than established wakefulness (P = 0.297). Reduced PPI of the startle reflex at awakening from non-REM sleep supports the hypothesis that wakefulness immediately after spontaneous sleep episodes is neurophysiologically distinct from later wakefulness and associated with reduced gating of motor responses to sensory inputs. Spontaneous activation of this distinct, transiently aroused, state upon awakening may serve a protective function, preparing an animal to respond immediately to potentially threatening stimuli.

Acoustic Stimulation↗

PubMed1983

Hyperekplexia exacerbated by occlusion of posterior thalamic arteries.

A 65-year-old man with the onset of hyperekplexia at 37 years of age experienced resolution of the illness at the age of 45 years. Twenty years later after a posterior thalamoperforate artery occlusion that produced a "rubral tremor," severe hyperekplexia redeveloped. The patient's symptoms were controlled with clonazepam, except for brief periods. Interruption of the rubrothalamic pathways or neuronal aggregates at the level of the red nucleus seemed to disinhibit the startle reflex.

Acute Disease↗

PubMed2005

Vibroacoustic stimulation for fetal assessment in labour in the presence of a nonreassuring fetal heart rate trace.

BACKGROUND: Fetal vibroacoustic stimulation is a simple, non-invasive technique where a device is placed on the maternal abdomen over the region of the fetal head and sound is emitted at a predetermined level for several seconds. It is hypothesized that the resultant startle reflex in the fetus and subsequent fetal heart rate acceleration or transient tachycardia following vibroacoustic stimulation provide reassurance of fetal well-being. This technique has been proposed as a tool to assess fetal well-being in the presence of a non-reassuring cardiotocographic trace during the first and second stages of labour. OBJECTIVES: To evaluate the clinical effectiveness and safety of vibroacoustic stimulation in the assessment of fetal well-being during labour, compared with mock or no stimulation for women with a singleton pregnancy exhibiting a non-reassuring fetal heart rate pattern. SEARCH STRATEGY: We searched the Cochrane Pregnancy and Childbirth Group Trials Register (30 September 2004), the Cochrane Central Register of Controlled Trials (The Cochrane Library, Issue 1, 2004), MEDLINE (January 1966 to January 2005), EMBASE (January 1966 to January 2005) and reference lists of all retrieved articles. We sought unpublished trials and abstracts submitted to major international congresses and contacted expert informants. SELECTION CRITERIA: All published and unpublished randomised trials that compared maternal and fetal/neonatal/infant outcomes when vibroacoustic stimulation was used to evaluate fetal status in the presence of a non-reassuring cardiotocographic trace during labour, compared with mock or no stimulation. DATA COLLECTION AND ANALYSIS: Two independent review authors identified potential studies from the literature search and assessed them for methodological quality and appropriateness of inclusion, using a data extraction form. Attempts to contact study authors for additional information were unsuccessful. MAIN RESULTS: The search strategies yielded six studies for consideration of inclusion. However, none of these studies fulfilled the requirements for inclusion in this review. AUTHORS' CONCLUSIONS: There are currently no randomised controlled trials that address the safety and efficacy of vibroacoustic stimulation used to assess fetal well-being in labour in the presence of a non-reassuring cardiotocographic trace. Although vibroacoustic stimulation has been proposed as a simple, non-invasive tool for assessment of fetal well-being, there is insufficient evidence from randomised trials on which to base recommendations for use of vibroacoustic stimulation in the evaluation of fetal well-being in labour in the presence of a non-reassuring cardiotocographic trace.

Acoustic Stimulation↗

PubMed2003

Direct input from cochlear root neurons to pontine reticulospinal neurons in albino rat.

The cochlear root neurons (CRNs) are thought to mediate the auditory startle reflex (ASR) in the rat, which is widely used as a behavioral model for the investigation of the sensorimotor integration. CRNs project, among other targets, to the nucleus reticularis pontis caudalis (PnC), a major component of the ASR circuit, but little is known about the organization of this projection. Thus, we injected biotinylated dextran amine (BDA) in CRNs to study their projections with light and electron microscopy. Also, we performed double-labeling experiments, injecting BDA in the CRNs and subunit B of the cholera toxin or Fluorogold in the spinal cord to verify that CRNs project onto reticulospinal neurons. Electron microscopy of the labeled CRNs axons and terminals showed that even their most central and thinnest processes are myelinated. Most of the terminals are axodendritic, with multiple asymmetric synapses, and contain round vesicles (50 nm diameter). Double-labeling experiments demonstrated that CRN terminals are apposed to retrogradely labeled reticulospinal neurons in the contralateral nucleus reticularis PnC and bilaterally in the lateral paragigantocellular nucleus. Analyses of serial sections revealed that multiple CRNs synapse on single reticulospinal neurons in PnC, suggesting a convergence of auditory information. The morphometric features of these neurons classify them as giant neurons. This study confirms that CRNs project directly onto reticulospinal neurons and presents other anatomical features of the CRNs that contribute to a better understanding of the circuitry of the ASR in the rat.

Animals↗

PubMed1979

Development of the acoustic startle response in the rat: ontogenetic changes in the magnitude of inhibition by prepulse stimulation.

Three experiments examined the development of the acoustic startle reflex and its modification by a preliminary stimulus in the infant rat during the 2nd and 3rd postnatal weeks. The 1st experiment employed a white noise S1 (20 msec, 70 dB), the 2nd a cutaneous S1 (.5 msec, .5 mA and 1.0 mA shock), and the 3rd identical S1-S2 pairs (20 msec, 10 kHz, 110 dB tones). The results demonstrate a similar maturation of the prepulse modification pattern over days in the 3 experiments, evidenced mainly in the growth of inhibition. The findings indicate peripheral and central mechanisms that are maturing during the period of life under observation and that contribute to the developmental patterns of modification.

Acoustic Stimulation↗

PubMed1997

The acoustic startle response is normal in patients with multiple system atrophy.

We investigated the acoustic startle response in eight patients with MSA and compared the results with those from a group of age matched healthy subjects. Onset latency and amplitude of the responses obtained in the orbicularis oculi, masseter and sternocleidomastoid muscles were not different in patients and control subjects. We conclude that, in spite of the pathological derangement described in brainstem reticular nuclei in MSA, the neuronal circuits mediating the auditory startle reflex are functionally preserved.

Acoustic Stimulation↗

PubMed1977

Functional development in the Mauthner cell system of embryos and larvae of the zebra fish.

In the embryonic zebra fish as early as 40 hr after fertilization, the Mauthner cells (M-cells) initiate an escape response, elicited by tactile-vibrational stimulation. The initial part of this behavior is similar to the acoustic startle reflex seen during the larval stage which begins at 96 hr. The embryonic response is directional and is followed by a series of strong tail flexures which are more pronounced than those during swimming. In the embryo the M-cell fired at the beginning of the response and rarely fired again during subsequent contractions; in our experiments the M-cell did not mediate iterative movements of the tail. The M-cell system is probably involved in evoked hatching behavior, as the tactile response is sufficient to rupture the egg membrane and allow the animal to escape. The M-cell sometimes fired spontaneously, which suggests that it might function also in spontaneous hatching behavior which occurs in the absence of phasic stimulation. At 48 hr the M-cell has morphologically mature synapses on its soma and dendrites, but its cytoplasm is relatively undifferentiated; it has few oriented neurofilaments and no distinct axon hillock. During these stages the extracellular M-spike is longer in duration and smaller in amplitude than at later times when the cell is more mature morphologically. Our data suggest that long-term inhibitory control of the M-cell system begins to function at about the time of hatching. At this time the cell is morphologically mature and is richly supplied with synaptic endings over its soma and dendrites.

Action Potentials↗

PubMed1985

Evaluation of long-term consequences in behavioral and/or neural function following neonatal chlordecone exposure.

The effects of neonatal exposure of rats to chlordecone, during the major postnatal period of neuroendocrine differentiation were assessed after the animals matured to 90 days of age. On day 4 postpartum, pups received a s.c. injection of either DMSO vehicle or chlordecone (1 mg/pup) dissolved in DMSO. The neonatal exposure produced a significant sex-dependent alteration in adult body weight; chlordecone-exposed males were lighter than vehicle-exposed controls and chlordecone-exposed females were heavier than vehicle-exposed controls. Behavioral tests sensitive to neonatal chlordecone exposure during preweaning development--i.e., spectral analysis of movement, activity, and auditory startle responsiveness--gave no statistically significant evidence for residual effects of the early organochlorine treatment. When challenged with harmine, a known tremorogen with putative effects on olivocerebellar pathways, chlordecone-exposed males were less responsive than vehicle-exposed littermates in a spectral analysis of movement. The movement spectrum of chlordecone-exposed females was not differentially sensitive to the harmine challenge. However, subsequent evaluation of the auditory startle reflex indicated that harmine interacted with the neonatal treatment and sex of the animal; chlordecone-exposed males were less responsive and chlordecone-exposed females more responsive than same sex vehicle-exposed littermates. The responsiveness to a d-amphetamine challenge, expressed as a ratio of baseline activity in a pre- and post-test design, suggested the chlordecone-exposed males gave an exaggerated response to the drug challenge. Collectively, these findings suggest that the neonatal chlordecone exposure had a significant organizational effect on the development of behavioral and/or neural function. These findings also suggest the predictive utility of early behavioral tests; that is, long-term alterations were noted in each component of the toxicological syndrome previously identified during preweaning development.

Animals↗

PubMed2000

Infant vocalization, adult aggression, and fear behavior of an oxytocin null mutant mouse.

Previous studies have shown that oxytocin (OT)-deficient female mice produced by homologous recombination fail to lactate but exhibit normal parturition and reproductive behaviors. We examined the ultrasonic vocalizations of infant mice and the subsequent aggressive and fear behavior of adult male OT knockout (OT-KO) mice. Infant OT-KO mice were less vocal than wild-type (WT) control mice during separations from the mother and peers. Adult OT-KO males were generally more aggressive in isolation-induced and resident-intruder tests of aggression and less fearful in the plus maze and acoustic startle reflex tests than WT controls. Although the increase in tests of aggression was robust for OT-KO males from obligate litters (progeny of homozygous x homozygous crossings), the increase in aggression was reduced during tests for OT-KO males derived from nonobligate mating (progeny of heterozygous x heterozygous crossings), suggesting that the OT-KO genotype was not, by itself, responsible for the changes in adult behavior. We conclude that the absence of exposure to OT during development was associated with abnormalities in the development of emotional behavior.

Age Factors↗

PubMed1993

Intra-accumbens infusion of quinpirole impairs sensorimotor gating of acoustic startle in rats.

Prepulse inhibition (PPI) of the startle reflex is reduced by systemic administration of dopamine (DA) agonists. Since PPI is impaired in patients with schizophrenia, the DA agonist-induced disruption of PPI in rats may be a useful model for studying the pathophysiology of impaired sensorimotor gating in schizophrenia. In the present study, we replicated the observation that PPI is disrupted by systemic administration of the D2 agonist quinpirole, but not by the D1 agonist SKF 38393. PPI caused by weak [1-5 dB(A)] or more intense [10 dB(A)] prepulses was also disrupted by quinpirole infusion into the nucleus accumbens (NAC). The effects of intraaccumbens quinpirole on PPI were blocked by pretreatment with the D2 antagonist haloperidol. These results support the notion that the reduction of PPI after systemic administration of DA agonists is mediated via stimulation of NAC D2 receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1991

Carbachol infusion into the dentate gyrus disrupts sensorimotor gating of startle in the rat.

Prepulse inhibition (PPI) is the decrease in a startle response that occurs when the startling stimulus is preceded by a weaker stimulus or "prepulse". Schizophrenic patients exhibit abnormally low levels of PPI when the prepulse precedes the startle stimulus by less than 500 ms. A similar deficit in sensorimotor gating can be demonstrated in rats after stimulation of D2 dopamine (DA) receptors by systemic administration of DA agonists or by infusion of DA directly into the nucleus accumbens. We now demonstrate that carbachol infusion into the dentate gyrus of the hippocampal formation disrupts PPI in the rat. This disruption of sensorimotor gating occurs when the startling stimulus is either acoustic or tactile. Carbachol infusion into the neocortex has no effect on PPI. While pretreatment with the D2 DA receptor antagonist spiperone reverses the disruption of PPI caused by systemic administration of apomorphine, this pretreatment fails to reverse the disruption of PPI induced by carbachol infusion into the hippocampus. These results demonstrate that pharmacologic stimulation of the hippocampus disrupts sensorimotor gating in the rat by a mechanism distinct from that of DA agonists. Prepulse inhibition of the startle reflex is an animal model in which pharmacologic stimulation of the hippocampus mimics the deficits in sensorimotor gating observed in schizophrenic patients.

Acoustic Stimulation↗

PubMed1994

Seroquel (ICI 204,636) restores prepulse inhibition of acoustic startle in apomorphine-treated rats: Similarities to clozapine.

Seroquel (ICI 204,636) is a mixed D2/5HT2 antagonist with a preclinical profile suggestive of potential antipsychotic efficacy. We compared seroquel to clozapine in an animal model of sensorimotor gating deficits in shizophrenic patients. Like schizophrenic patients, rats treated with apomophrine (APO) exhibit deficits in prepulse inhibition (PPI) of acoustic startle. The ability of antipsychotics to restore PPI in APO-treated rats correlates (Rs = 0.991) with their clinical potency. Seroquel and clozapine both restore PPI in APO-treated rats. Seroquel's restoration of PPI in apomorphine-treated rats follows simple monotonic ascending dose-response properties, and is not accompanied by consistent changes in startle reflex amplitude. Seroquel's profile in this PPI model mimics that of other antipsychotics.

Acoustic Stimulation↗

PubMed2002

"Typical" but not "atypical" antipsychotic effects on startle gating deficits in prepubertal rats.

RATIONALE: Dopamine (DA) agonists and NMDA antagonists disrupt sensorimotor gating in rats, as measured by a loss of prepulse inhibition of the startle reflex. These effects are used in predictive models for antipsychotic efficacy: clinically "typical" and "atypical" antipsychotics restore PPI in adult rats treated with DA agonists such as apomorphine (APO), while clinically "atypical" antipsychotics restore PPI in rats treated with NMDA antagonists such as phencyclidine (PCP). We previously reported that the PPI disruptive effects of both APO and PCP are evident in 16- to 18-day-old rat pups, suggesting that the brain substrates for these effects are functional very early in development. OBJECTIVE: In the present study we assessed the developmental patterns of antipsychotic effects in these measures. METHODS: The PPI-disruptive effects of APO and PCP, and their antagonism by the typical antipsychotic haloperidol, and the atypical antipsychotic quetiapine, were assessed across development in Sprague-Dawley rats. RESULTS: Similar to the pattern seen in adults, both haloperidol and quetiapine opposed APO-induced PPI deficits in 16- to 19-day-old rat pups. However, the "atypical" antipsychotic quetiapine did not oppose PCP-induced PPI deficits in pups or prepubertal (45 day) adolescents, but did oppose these PCP effects in postpubertal rats. CONCLUSIONS: While brain substrates mediating the PPI-disruptive effects of DA agonists and NMDA antagonists are functional early in development, some physiological event associated with puberty is a necessary condition for the "atypical antipsychotic profile" in this predictive model.

Animals↗

PubMed2003

Heritable differences in the dopaminergic regulation of sensorimotor gating. I. Apomorphine effects on startle gating in albino and hooded outbred rat strains and their F1 and N2 progeny.

Sensorimotor gating, measured by prepulse inhibition (PPI) of the startle reflex, is reduced in schizophrenia patients and in rats treated with dopamine (DA) agonists. Strain and substrain differences in the sensitivity to the PPI-disruptive effects of DA agonists may provide insight into the basis for human population differences in sensorimotor gating. We have reported greater sensitivity to the PPI disruptive effects of the D(1)/D(2) agonist apomorphine in Harlan Sprague-Dawley (SDH) versus Long Evans (LEH) rats. In the present study, we assessed the generational pattern of this phenotypic difference across parental SDH and LEH strains under in- and cross-fostering conditions, offspring (F1) of an SDHxLEH cross, and subsequent offspring (N2) of an SDHxF1 cross. Apomorphine sensitivity followed a gradient across generations that suggested relatively simple additive effects of multiple genes. Cross fostering studies confirmed that SDH>LEH apomorphine sensitivity did not reflect post-natal maternal influences. Generational patterns of PPI apomorphine sensitivity were not associated with albino versus hooded phenotypes per se, but apomorphine sensitivity in hooded N2 rats was strongly related to body surface area of fur pigmentation. The association between pigmentation and PPI apomorphine sensitivity may provide an important clue to specific biochemical and genetic substrates responsible for population differences in the regulation of sensorimotor gating.

Acoustic Stimulation↗

PubMed2004

Effects of the beta-blocker propranolol on cued and contextual fear conditioning in humans.

RATIONALE: Beta-adrenergic receptors are involved in the consolidation of emotional memories. Yet, a number of studies using Pavlovian cued fear conditioning have been unable to demonstrate an effect of beta-adrenergic blockade on acquisition or retention of fear conditioning. Evidence for the involvement of beta-adrenergic receptors in emotional memories comes mostly from studies using fear inhibitory avoidance in rodents. It is possible that fear inhibitory avoidance is more akin to contextual conditioning than to cued fear conditioning, suggesting that context conditioning may be disrupted by beta-adrenergic blockade. OBJECTIVE: This study investigated the effects of the beta-adrenergic blocker propranolol on cued and contextual fear conditioning in humans. METHODS: Subjects were given either placebo (n=15) or 40 mg propranolol (n=15) prior to differential cued conditioning. A week later, they were tested for retention of context and cued fear conditioning using physiological (startle reflex and electrodermal activity) and subjective measures of emotional arousal. RESULTS: The results were consistent with the hypothesis. The skin conductance level (SCL) and the subjective measure of arousal suggested reduced emotional arousal upon returning to the conditioning context in the propranolol group, compared to the placebo group. The acquisition and retention of cued fear conditioning were not affected by propranolol. CONCLUSIONS: These results suggest that beta-adrenergic receptors are involved in contextual fear conditioning.

Adrenergic beta-Antagonists↗

PubMed2004

The CB receptor agonist WIN 55,212-2 fails to elicit disruption of prepulse inhibition of the startle in Sprague-Dawley rats.

RATIONALE: A growing evidentiary body indicates cannabinoid exposure is conducive to cognitive impairment and psychotic phenomena in vulnerable individuals. In this respect, recent studies have displayed controversial results on the ability of cannabinoids to elicit sensorimotor gating alterations and attentional filtering, whose disruption is a distinctive feature of psychosis. OBJECTIVES: The goal of this study was to investigate the effects of acute, subchronic, and chronic treatment with the synthetic CB receptor agonist WIN 55,212-2 (WIN) on prepulse inhibition (PPI) of the acoustic startle reflex (ASR), a powerful paradigm for evaluation of sensorimotor gating. METHODS: Different groups of adult Sprague-Dawley rats were treated with 0.5, 1, and 2 mg/kg WIN (i.p.) acutely, as well as for 7 days and 21 days. All animals underwent testing 40 min after the last treatment and their evaluation was compared with that of animals treated with vehicle. In a separate group, the effects of WIN withdrawal were also analyzed, 24 h after discontinuation of a 21-day treatment. RESULTS: No variation in PPI was detected in any of the test groups when compared with controls, whatever the dosage and the treatment. CONCLUSIONS: These findings suggest WIN does not impair sensorimotor gating in Sprague-Dawley rats and confirm clinical evidence according to which cannabis is an unlikely causative of psychosis among non-vulnerable individuals. Nonetheless, since in other studies the same compound was shown to induce PPI alterations in Wistar rats, our results are also suggestive that genetic differences might be critical for the development of cannabis-induced cognitive disorders.

Animals↗

PubMed2005

The effects of dopamine agonists on prepulse inhibition in healthy men depend on baseline PPI values.

RATIONALE AND OBJECTIVES: Dopamine (DA) agonists reliably disrupt prepulse inhibition (PPI) of the startle reflex in animals but less so in humans despite cross-species similarities in the neural regulation of PPI. This study examines whether individual variation in baseline PPI may account for the inconsistencies in DA agonist-induced PPI disruption in humans. METHODS: Baseline PPI measures were obtained from 32 healthy adult men. Subjects were subsequently tested in three sessions after ingestion of placebo or active drug in a balanced double-blind design. Seventeen subjects were given 0.05 and 0.1 mg of pergolide (a direct DA agonist) and 15 subjects were given 100 and 200 mg of amantadine (an indirect DA agonist). In each treatment group, subjects were assigned to "high" and "low" PPI subgroups based on the median split of their baseline PPI. RESULTS: Amantadine and pergolide disrupted PPI in high- but not in low-PPI subjects. In contrast, low-PPI subjects showed a trend towards PPI facilitation especially with pergolide. CONCLUSIONS: Our results suggest that baseline PPI is an important determinant of the effect of DA agonists on PPI.

Acoustic Stimulation↗

PubMed2005

Functional magnetic resonance imaging reveals similar brain activity changes in two different animal models of schizophrenia.

RATIONALE AND OBJECTIVES: In schizophrenia research, most of the functional imaging studies have been performed in psychotic patients, but little is known about brain areas involved in the expression of psychotic-like symptoms in animal models. The objective of this study was to visualize and compare brain activity abnormalities in a neurodevelopmental and a pharmacological animal model of schizophrenia. METHODS: Blood perfusion of specific brain areas, taken as indirect measure of brain activity, was investigated in adult rats following either neonatal ventral hippocampal lesion or acute administration of phencyclidine. Quantitative perfusion magnetic resonance imaging was performed on five frontal brain slices using the continuous arterial spin labeling technique. The mean perfusion was calculated in several brain structures, which were identified on anatomical images. RESULTS: Lesioned animals exhibiting deficits in prepulse inhibition of the startle reflex showed a significant blood perfusion increase in the nucleus accumbens, basolateral amygdala, ventral pallidum, entorhinal-piriform cortex, orbital prefrontal cortex, and in the bed nucleus of the stria terminalis, and a decrease of perfusion in the temporal cortex. Similar effects were seen following acute phencyclidine administration in naïve animals. CONCLUSION: Our data point out specific cortical and subcortical brain areas involved in the development of psychotic-like symptoms in two different animal models of schizophrenia. The observed brain activity abnormalities are reminiscent of classical neuroimaging findings described in schizophrenic patients.

Acoustic Stimulation↗