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PubMed2006

Effects of prepulse intensity, duration, and bandwidth on perceived intensity of startling acoustic stimuli.

Intense abrupt stimuli can elicit a startle reflex; a weak "prepulse" 30-300 ms earlier can reduce both startle and perceived stimulus intensity. Prepulse inhibition (PPI) of startle, an operational measure of sensorimotor gating, is used to understand brain disorders characterized by gating deficits. Compared to startle, PPI of perceived stimulus intensity (PPIPSI) may provide information that is distinct, and easier to acquire and analyze. To develop this experimental measure, we examined PPIPSI under different stimulus conditions. Both PPI and PPIPSI exhibited a non-linear relationship to prepulse intensity, with prepulses 15 dB(A) above background causing maximal inhibition of both measures. A 50 ms broadband noise prepulse produced maximal PPI and PPIPSI, whereas 5 and 20 ms pure tone prepulses produced maximal PPIPSI and PPI, respectively. PPIPSI is a robust, parametrically sensitive and "low tech" measure of sensory gating that may become a valuable tool for understanding the biology of certain mental disorders.

Acoustic Stimulation↗
PubMed2002

Startle modulation before, during and after exposure to emotional stimuli.

Although affective modulation of the startle reflex is a highly replicable effect, the majority of studies have administered startle probes during exposure to affective stimuli. To examine more comprehensively the temporal course of startle potentiation, we assessed blink modulation before, during and immediately after exposure to positive, negative and neutral pictures. During each trial, cues about the affective content of pictures were presented, after which acoustic startle probes were delivered either before picture onset, during picture onset or immediately after picture offset. As expected, we observed a linear relation between picture valence and startle amplitude during picture viewing. Surprisingly, startle amplitude was larger while anticipating pleasant and unpleasant pictures relative to neutral pictures. No significant effects were observed during the offset phase. These results indicate that startle modulation is conditional upon temporal factors linked to stimulus onset and offset.

Adolescent↗
PubMed1986

Acquisition of acoustic startle shows a dose-response to serum free T4.

Methimazole, administered to rats in drinking water (0.1 and 0.05%) from embryonic day 17 to postnatal day 10, caused a dose-dependent decrease in serum Free T4 and an accompanying dose dependent delay in acquisition of acoustic startle reflex. In conjunction with other studies showing the specific dependence of acoustic startle development on thyroid hormone, this study suggests that the acoustic startle system may be a useful model for determining thyroid hormone requirements for normal neurologic development.

Animals↗
PubMed1995

Involvement of the central nucleus and basolateral complex of the amygdala in fear conditioning measured with fear-potentiated startle in rats trained concurrently with auditory and visual conditioned stimuli.

The goal of this work was to test the involvement of the central nucleus and basolateral complex of the amygdala in fear conditioning, using auditory and visual conditioned stimuli (CSs). The acoustic startle reflex in rats was used as the behavioral index of conditioning because startle is reliably enhanced in the presence of a conditioned stimulus (CS) previously paired with a footshock. Initially, differential conditioning procedures indicated reliable discrimination between a noise CS and a visual CS. Subsequently, the effects of amygdala lesions were evaluated when both modalities were paired with shocks in the same rats. Electrolytic or ibotenic acid lesions of the central nucleus of the amygdala blocked fear-potentiated startle to both auditory and visual CSs, consistent with the idea that the central nucleus serves as a response independent, final common relay for fear conditioning. Similarly, pre- or post-training electrolytic or NMDA-induced lesions of the basolateral complex of the amygdala, which damaged the lateral nucleus, and most of the basolateral nucleus, disrupted fear-potentiated startle to both CS modalities. This finding is consistent with the suggestion that, in fear conditioning, the basolateral complex of the amygdala serves as an obligatory relay of sensory information from subcortical and cortical sensory areas to the central nucleus of the amygdala.

Acoustic Stimulation↗
PubMed2006

The benzodiazepine alprazolam dissociates contextual fear from cued fear in humans as assessed by fear-potentiated startle.

BACKGROUND: The startle reflex is potentiated by aversive states. It has been proposed that phasic startle potentiation to a threat cue and sustained startle potentiation to contextual stimuli reflect distinct processes mediated by different brain structures. The present study tested the hypothesis that alprazolam would reduce the sustained startle potentiation to contextual threats but not the startle potentiation to a threat cue. METHODS: Sixteen healthy subjects received each of four treatments: placebo, .5 mg of alprazolam, 1 mg of alprazolam, and 50 mg of diphenhydramine (Benadryl) in a crossover design. Participants were exposed to three conditions, including one in which predictable aversive shocks were signaled by a cue, a second in which shocks were administered unpredictably, and a third condition in which no shocks were anticipated. Acoustic startle were delivered regularly across conditions. RESULTS: Phasic startle potentiation to the threat cue in the predictable condition was not affected by alprazolam. In contrast, the sustained increase in startle in the predictable and unpredictable conditions was reduced significantly by the high dose of alprazolam. CONCLUSIONS: Startle responses to an explicit threat cue and to an aversive context are psychopharmacologically distinct, suggesting that they may represent functionally dissociable aversive states.

Acoustic Stimulation↗
PubMed1994

Alphaxalone, a steroid anesthetic, inhibits the startle-enhancing effects of corticotropin releasing factor, but not strychnine.

Corticotropin releasing factor (CRF) is a 41 amino acid peptide implicated in the expression of stress- and fear-enhanced behaviors. CRF potentiates the amplitude of the startle reflex, and this effect is reversed by benzodiazepines (BDZ), suggesting that the startle-enhancing effects of CRF are modulated by changes in the GABA/BDZ receptor complex. In the present study, CRF-potentiated startle is inhibited by alphaxalone, a pregnane steroid anesthetic that is thought to act via the GABA/BDZ receptor complex. Alphaxalone (ALX) does not reduce CRF-potentiated startle by producing a generalized reduction in reactivity, since blockade of CRF-stimulated startle was not accompanied by an ALX-induced reduction in baseline startle amplitude and ALX does not reduce strychnine-potentiated startle. The effects of alphaxalone on CRF-potentiated startle may not be generalized to all CRF-stimulated behaviours, since alphaxalone failed to disrupt CRF-stimulated locomotor activity. CRF-potentiated startle is a useful assay for studying the effects of novel anxiolytic agents, and alphaxalone appears to be a steroid anesthetic with anxiolytic properties in this assay.

Anesthetics↗
PubMed1996

A primary acoustic startle pathway: obligatory role of cochlear root neurons and the nucleus reticularis pontis caudalis.

Davis et al. (1982) proposed a primary acoustic startle circuit in rats consisting of the auditory nerve, posteroventral cochlear nucleus, an area near the ventrolateral lemniscus (VLL), nucleus reticularis pontis caudalis (PnC), and spinal motoneurons. Using fiber-sparing lesions, the present study reevaluated these and other structures together with the role of neurons embedded in the auditory nerve [cochlear root neurons (CRNs)], recently hypothesized to be involved in acoustic startle. Small electrolytic lesions of the VLL of ventrolateral tegmental nucleus (VLTg) failed to eliminate startle. Large electrolytic lesions including the rostral ventral nucleus of the trapezoid body (rVNTB) and ventrolateral parts of PnC or lesions of the entire PnC blocked startle. However, small NMDA-induced lesions of the rVNTB failed to block startle, making it unlikely that the rVNTB itself is part of the startle pathway. In contrast, NMDA lesions of the full extension of the ventrolateral part of the PnC blocked startle completely, suggesting that the ventrolateral part of the PnC is critically involved. Bilateral kainic acid lesions of CRNs also blocked the startle reflex completely, providing the first direct evidence for an involvement of CRNs in startle. This blockade probably was not caused by damage to the auditory nerve, because the lesioned animals showed intact compound action potentials recorded from the ventral cochlear nucleus. Hence, a primary acoustic startle pathway may involve three synapses onto (1) CRNs, (2) neurons in PnC, and (3) spinal motoneurons.

Action Potentials↗
PubMed1995

Involvement of cyclic AMP at the level of the nucleus reticularis pontis caudalis in the acoustic startle response.

Rats were implanted with cannulas in the nucleus reticularis pontis caudalis (PnC), an obligatory part of the neural pathway that mediates the acoustic startle reflex. Following at least 1 week of recovery, rats were tested for acoustic startle amplitude before or after infusion of compounds known to alter the second messenger, adenosine cyclic 3', 5'-monophosphate (cAMP). Local infusion into the PnC of the cAMP analog, 8-bromo cAMP (0.125-1.0 micrograms), increased the amplitude of the acoustic startle response in a dose-dependent manner. In addition, local infusion of a phosphodiesterase inhibitor, rolipram (10 micrograms) or the water soluble adenylate cyclase activator, forskolin-DHA (2.5 micrograms), produced a significant enhancement of startle amplitude. These effects probably resulted from intracellular actions because cAMP itself, which does not readily penetrate lipid membranes, had no effect. Moreover, the effects seemed somewhat specific because the precursor of cAMP, ATP or 8-bromo cGMP, also failed to alter startle at doses where 8 bromo-cAMP did. The fact that a phosphodiesterase inhibitor elevated startle suggests that cAMP serves to tonically elevate startle at this level of the pathway. Hence, treatments that either increase (fear, sensitization) or decrease (habituation, pre-pulse inhibition) startle at the level of the PnC may do so via release of neurotransmitters either positively or negatively coupled to cAMP, which in turn may alter either sound evoked transmitter release, excitability of PnC neurons or both.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1982

Selective action of morphine on reflex expression to nociceptive stimulation in the rat: a contribution to the assessment of analgesia.

In two experiments startle reflexes to both loud noises and electric shocks were elicited in rats. The two stimuli were paired so that the inhibitory effect of each stimulus on the response to the other could be assessed. In the first study it was shown that morphine (0-16 mg/kg) had a selective and dose related depressive effect on the response to shock. The response to a leading tone and inhibition produced by the shock on the response to a following tone were minimally affected. In the second study, morphine (10 mg/kg) again depressed the reaction to shock but not to tone, and its effect was antagonized by naloxone (10 mg/kg). The selective effect on responses to shock, leaving responses to tone relatively unaffected, reveals that reflex depression should not be attributed to a loss in motor functions. Further, that morphine had little effect on reflex inhibition produced by the shock suggests that the nociceptive properties of shock were affected rather than simple sensory processes. It is proposed that the method described here is useful for assessing changes in nociception in laboratory animals, and for discriminating between nociceptive, afferent, and efferent processes.

Acoustic Stimulation↗
PubMed1999

Effects of prepulses and d-amphetamine on performance and event-related potential measures on an auditory discrimination task.

RATIONALE: Prepulse inhibition (PPI) of the startle reflex is a measure of sensorimotor gating, that is the processing of the startle stimulus (S2) is inhibited by the interfering processing of a closely preceding prepulse (S1). It has been demonstrated that PPI is disrupted in a variety of mental disorders and that several neurotransmitter systems, including dopamine, participate in the modulation of sensorimotor gating. Previous studies have also shown that a task-relevant S1 enhances PPI in healthy subjects but not in schizophrenic patients. These findings indicate an influence of attentional processes on sensorimotor gating and an impairment of this modulation in schizophrenia. OBJECTIVE: Assuming a dopamine-mediated suppression of S1 processing as a mechanism of resource management and selective attention, which might be impaired in certain mental disorders, the present study investigated the effects of the indirect dopaminergic agonist d-amphetamine on prepulse-altered S2 discrimination and event related potentials (ERPs). METHODS: Twelve healthy volunteers were tested in a double-blind, placebo-controlled experimental design. Here, S2 is the target in a difficult Go/NoGo auditory discrimination task. RESULTS: Confirming our previous results, S2 processing is "accentuated" by a weak acoustic prepulse in healthy subjects, thus leading to a lower rate of errors of omission but also to more false alarms (i.e. a liberal response bias). This performance change correlated with a prepulse-induced increase in the amplitude of the P3 ERP towards non-targets ("prepulse-induced non-target positivity"; PINTP). In addition, the results of the present study show that under prepulse conditions amphetamine disrupts "S2 accentuation" associated with a dose-related reduction of the P2 component of the S1 response and a plasma level related reduction of PINTP. CONCLUSIONS: These data suggest an involuntary attentional shift towards S1 processing with increasing dopamine-release similar to that observed in patients with schizophrenia or OCD. It is concluded that sensory gating alters selective attention via dopaminergic modulation.

Acoustic Stimulation↗
PubMed1995

Ventral pallidal GABA-A receptors regulate prepulse inhibition of acoustic startle.

Prepulse inhibition (PPI) of the acoustic startle reflex occurs when a weak auditory stimulus is presented 30-500 ms before the startling stimulus. Previous studies have shown that PPI is modulated by GABAergic projections from the ventral striatum to the ventral pallidum (VP). To evaluate the anatomical and pharmacological substrates of pallidal modulation of PPI, we measured PPI after intrapallidal infusion of GABA-B and GABA-A antagonists. Intrapallidal infusion of the GABA-B antagonist, 2-OH-saclofen (0.025-0.10 microgram), did not significantly alter PPI, startle amplitude or peak startle latency. Infusion of the GABA-A antagonist, picrotoxin (0.02-0.08 microgram), into the medial or central VP significantly reduced PPI; this effect appeared somewhat weaker after picrotoxin infusion into the lateral VP and was absent after infusion into the adjacent fundus striatum (FS). There was no significant effect of picrotoxin infusion into any of the VP sites or FS on startle amplitude or peak startle latency. Thus, ventral striato-pallidal GABAergic modulation of PPI appears to be mediated solely by GABA-A receptors and this modulatory substrate is predominantly distributed across the medial and central portions of the VP.

Acoustic Stimulation↗
PubMed2002

IL-2/15 receptor-beta gene deletion alters neurobehavioral performance.

The common IL-2/15 receptor-beta (IL-2/15Rbeta) is an essential signaling subunit that is shared exclusively by IL-2 and IL-15, and is enriched in the hippocampal formation and related limbic regions. We have previously shown that mice lacking IL-2 exhibit alterations in hippocampal-dependent learning, sensorimotor gating and accompanying reductions in hippocampal infrapyramidal mossy neuronal fiber length. Although the effects of exogenous IL-2 on various aspects of forebrain neuronal function are well documented, it is unclear whether IL-15 has neuromodulatory actions. Here we sought to test the hypothesis that the combined loss of the ability of IL-2 and IL-15 to signal through IL-2/15Rbeta in the brain would influence neurobehavioral performance, in particular spatial learning and memory performance. To test this hypothesis, we compared several different domains of behavior in mice that had one or both IL-2/15Rbeta gene alleles deleted. Compared with C57BL/6-IL-2/15Rbeta+/+ wild-type and C57BL/6-IL-2/15Rbeta+/- heterozygote littermates, C57BL/6-IL-2/15Rbeta-/- knockout mice exhibited a deficit in prepulse inhibition of the acoustic startle reflex (PPI). The IL-2/15Rbeta knockout mice also showed significant reductions in acoustic startle reactivity, and modest differences in behavior in the elevated plus-maze test indicative of reduced levels of fearfulness in response to novelty. The IL-2/15Rbeta knockout mice did not differ in locomotor activity in either the plus-maze or the Morris water-maze, and contrary to our working hypothesis, they did not differ in spatial learning or memory performance in the water-maze. Further studies are required to determine if these behavioral alterations may be attributable to factors such as the loss of the ability of IL-15 and/or IL-2 to modulate limbic neurons, autoimmunity or genetic factors associated with IL-2/15Rbeta gene deletion.

Acoustic Stimulation↗
PubMed1995

Prepulse inhibition in the rat is regulated by ventral and caudodorsal striato-pallidal circuitry.

It has been shown that the acoustic startle reflex is inhibited by weak auditory prepulses presented 30-500 ms prior to the startling stimulus and that this prepulse inhibition (PPI) is modulated by ventral striato-pallidal circuitry. However, dorsal striatal modulation of PPI has not been examined. Cell-specific lesions and intracerebral drug infusions were used to elucidate striatal modulation of PPI. Quinolinic acid lesions of the ventral and caudodorsal striatum significantly decreased PPI, whereas lesions of the rostrodorsal and middorsal striatum did not significantly alter PPI. Infusion of the GABA-A antagonist picrotoxin into the ventral and caudal dorsal pallidum also significantly reduced PPI, whereas rostral pallidal picrotoxin infusion had no significant effect. Thus, PPI in the rat seems to be modulated by both ventral and caudodorsal striato-pallidal circuitry, but not by rostrodorsal or middorsal striato-pallidal projections.

Acoustic Stimulation↗
PubMed2004

Menstrual cycle phase effects on prepulse inhibition of acoustic startle.

Prepulse inhibition (PPI) represents an attenuation of the startle reflex following the presentation of a weak prepulse at brief intervals prior to the startle eliciting pulse. It has been shown that increases in striatal dopamine levels decrease PPI; because dopamine release is sensitive to estrogen, it is likely that PPI varies across the menstrual cycle. Cross-sectional studies looking at estrogen effects suggest that this may be true. In this study, we compare effects of menstrual phase on PPI in a between-group design (men, follicular phase women, and luteal phase women) as well as a within-subjects design (women across the two phases). The study found a between-group as well as a within-subjects effect of phase on PPI. PPI in follicular phase women did not differ significantly from PPI in men. However, PPI was reduced in luteal women compared to follicular women. These data provide evidence that ovarian hormones affect sensorimotor gating.

Acoustic Stimulation↗
PubMed1999

Midazolam effects on prepulse inhibition of the acoustic blink reflex.

AIMS: The eye-blink response following sudden acoustic noise bursts is part of the startle reflex. The magnitude of the startle response can be attenuated by presentation of a weak stimulus before the 'startle-eliciting' stimulus (prepulse inhibition, PPI). PPI is a stable finding in awake humans but may be altered by anaesthetic drugs. We investigated whether the application of benzodiazepines altered the magnitude of PPI in healthy male volunteers. METHODS: In an open-label noncontrolled investigation, the effect of the benzodiazepine agonist midazolam on PPI was assessed in the absence and presence of the antagonist flumazenil. After an initial control period of 60 min three consecutive periods, each of 60 min, with progressively increasing concentrations of midazolam were studied (0. 02, 0.06, 0.14 mg kg-1 h-1 ). A final 60 min period during the administration of flumazenil (0.004 mg kg-1 h-1 ) and while the agonist was still present was also studied. Drug was administered intravenuously as a combination of bolus, 50% of total dose and continuous infusion over the 60 min period. Electromyographic (EMG) response of the right orbicularis oculi muscle was used to assess the startle response to noise bursts of 50 ms duration (95 dB(A)). Noise bursts were randomly preceded by nonstartling prepulses (800 Hz sinus, 50 ms duration, 65 dB(A), prepulse to noise interval 120 ms). The magnitude of PPI was calculated by dividing the EMG response to nonprepulsed stimuli by the response to prepulsed stimuli for each individual and period. Eleven subjects participated in the study, two of them were excluded from the statistical analysis because startle responses could not be reliably elicited (final sample size n=9). RESULTS: The magnitude of PPI was inversely related to the concentration of midazolam. This relationship was described by a sigmoidal Emax model, giving an Emax of 0.65+/-0.13, an ED50 of 33.9+/-10.9 ng ml-1 and gamma of 3.5+/-1.0. During infusion of flumazenil and in the presence of midazolam, the magnitude of PPI increased by 0.11 (95% CI, 0-0.22, P</=0.04), which is consistent with its mode of action as a benzodiazepine antagonist. CONCLUSIONS: In healthy male volunteers the magnitude of PPI varies according to agonism and antagonism of benzodiazepine receptors, suggesting that the assessment of PPI may be potentially useful to monitor the sedative effect of benzodiazepines in the clinical setting.

Acoustic Stimulation↗
PubMed1992

Hippocampal modulation of acoustic startle and prepulse inhibition in the rat.

Prepulse inhibition (PPI) is the normal reduction in a startle response that occurs when the startling stimulus is preceded by a weak lead stimulus ("prepulse"). Schizophrenic patients exhibit abnormally low levels of PPI; therefore, animal models of deficient PPI may provide information regarding neural dysfunctions underlying schizophrenia. We recently reported that infusion of the cholinergic agonist carbachol into the dentate gyrus (DG) disrupts PPI in the rat. We now report the effects of carbachol microinjected into CA1, the DG, or the ventral subiculum (VS) on acoustic startle and PPI. Carbachol infusion into CA1 or the DG depressed startle. Carbachol infusion decreased PPI with a regional rank-order potency CA1 > DG > VS. CA1 infusions more potently depressed the startle reflex. By contrast, DG infusions preferentially decreased PPI, while VS infusions decreased PPI without altering startle amplitude. Coinfusion with the muscarinic cholinergic antagonist atropine opposed the effects of carbachol. These results demonstrate the regional heterogeneity and pharmacological specificity of the hippocampal cholinergic modulation of acoustic startle and PPI and suggest that abnormalities within various regions of the hippocampal formation may contribute to deficient sensorimotor gating in schizophrenic patients.

Animals↗
PubMed1994

Baseline and fear-potentiated startle in panic disorder patients.

The present study investigated whether patients with panic disorder had an increase in the startle response and whether this effect, if present, was specific to anticipatory anxiety. The eyeblink component of the acoustic startle reflex was measured in a paradigm involving the anticipation of electric shocks (fear-potentiated startle) in 34 patients with panic disorder and 49 healthy controls. Startle was also recorded in the absence of specific threat at the beginning and at the end of the testing. The testing consisted of three phases: adaptation, fear-potentiated startle, and recovery. In the adaptation and recovery phases, startle stimuli were delivered in the absence of threat. In the fear-potentiated startle phase, startle stimuli were delivered in threat conditions, when subjects anticipated shocks, and in safe conditions that predicted the absence of shocks. Startle was larger in the younger patients (age < 40 years old) compared to the younger controls throughout the testing. The difference reached significance only during the fear-potentiated startle phase, however. Startle was nonsignificantly reduced in the older patients (age > or = 39 years old), compared to the older controls. The results are discussed in terms of the contextual effects of the experimental setting.

Adolescent↗