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At least 19 recordsLinked to original sources
PubMed2002

Tactile, acoustic and vestibular systems sum to elicit the startle reflex.

The startle reflex is elicited by intense tactile, acoustic or vestibular stimuli. Fast mechanoreceptors in each modality can respond to skin or head displacement. In each modality, stimulation of cranial nerves or primary sensory nuclei evokes startle-like responses. The most sensitive sites in rats are found in the ventral spinal trigeminal pathway, corresponding to inputs from the dorsal face. Cross-modal summation is stronger than intramodal temporal summation, suggesting that the convergence of acoustic, vestibular and tactile information is important for eliciting startle. This summation declines sharply if the cross-modal stimuli are not synchronous. Head impact stimuli activate trigeminal, acoustic and vestibular systems together, suggesting that the startle response protects the body from impact stimuli. In each primary sensory nucleus, large, second-order neurons project to pontine reticular formation giant neurons critical for the acoustic startle reflex. In vestibular nucleus sites, startle-like responses appear to be mediated mainly via the vestibulospinal tract, not the reticulospinal tract. Summation between vestibulospinal and reticulospinal pathways mediating startle is proposed to occur in the ventral spinal cord.

Acoustic Stimulation↗
PubMed1991

The hyperekplexias and their relationship to the normal startle reflex.

The startle response to unexpected auditory and somaesthetic stimulation was studied in 8 patients with hereditary or symptomatic hyperekplexia. It was abnormal in its resistance to habituation and in its exaggerated motor response. Both noise and taps to the face and head elicited a normal early blink response, separate from the subsequent true startle reflex. The earliest reflex EMG activity recorded after the blink was in sternocleidomastoid. EMG activity in masseter, and trunk and limb muscles followed later. This pattern of muscle recruitment suggests a brainstem origin for the abnormal startle responses. In addition, the abnormal startle responses exhibited disproportionately long latencies to the intrinsic hand and foot muscles and relatively slow recruitment of caudal muscles. The pattern of muscle recruitment was similar between patients, irrespective of the absolute latency of the response, and regardless of whether stimulation was auditory or somaesthetic. This suggests that auditory and somaesthetic afferents converge on a common brainstem efferent system, and that this system forms the final common pathway for abnormal startle responses of differing latency. The characteristics of this efferent system differ from those previously described in brainstem reticular reflex myoclonus, but are similar to those described in the normal auditory startle reflex in man. This suggests that the abnormal startle response in hyperekplexia, and the normal startle reflex represent pathological and physiological activity in the same brainstem efferent system.

Acoustic Stimulation↗
PubMed1993

Attention and schizophrenia: impaired modulation of the startle reflex.

The startle reflex (SR) elicited by abrupt stimuli can be modified by attention to nonstartling stimuli that shortly precede the startle-eliciting stimulus. The present study of 15 recent-onset, relatively asymptomatic schizophrenic outpatients and 14 demographically matched normal control subjects demonstrated that attentional modulation of SR is impaired in schizophrenic patients. Specifically, the control group exhibited greater startle eye-blink modification following to-be-attended prestimuli than following to-be-ignored prestimuli, whereas the patients failed to show the attentional modulation effect. These results suggest traitlike attentional deficits in schizophrenia because the patients were relatively asymptomatic. The measurement of attentional modulation of SR may provide a nonverbal, reflexive, state-independent marker of the vulnerability to schizophrenia.

Adult↗
PubMed2001

Contributions of the vestibular nucleus and vestibulospinal tract to the startle reflex.

The startle reflex is elicited by strong and sudden acoustic, vestibular or trigeminal stimuli. The caudal pontine reticular nucleus, which mediates acoustic startle via the reticulospinal tract, receives further anatomical connections from vestibular and trigeminal nuclei, and can be activated by vestibular and tactile stimuli, suggesting that this pontine reticular structure could mediate vestibular and trigeminal startle. The vestibular nucleus, however, also projects to the spinal cord directly via the vestibulospinal tracts, and therefore may mediate vestibular startle via additional faster routes without a synaptic relay in the hindbrain. In the present study, the timing properties of the vestibular efferent pathways mediating startle-like responses were examined in rats using electrical stimulation techniques. Transient single- or twin-pulse electrical stimulation of the vestibular nucleus evoked bilateral, startle-like responses with short refractory periods. In chloral hydrate-anesthetized rats, hindlimb electromyogram latencies recorded from the anterior biceps femoris muscle were shorter than those for stimulation of the trigeminal nucleus, and similar to those for stimulation of the caudal pontine reticular nucleus or ventromedial medulla. In awake rats, combining vestibular nucleus stimulation with either acoustic stimulation or trigeminal nucleus stimulation enhanced the whole-body startle-like responses and led to strong cross-modal summation without collision effects. In both chloral hydrate-anesthetized and awake rats, combining vestibular nucleus stimulation with ventromedial medulla stimulation produced a symmetrical collision effect, i.e. a loss of summation at the same positive and negative stimulus intervals, indicating a continuous connection between the vestibular nucleus and ventromedial medulla in mediating vestibular startle. By contrast, combining trigeminal nucleus stimulation with ventromedial medulla stimulation resulted in an asymmetric collision effect when the trigeminal nucleus stimulation preceded ventromedial medulla stimulation by 0.5 ms, suggesting that a monosynaptic connection between the trigeminal nucleus and ventromedial medulla mediates trigeminal startle. We propose that the vestibulospinal tracts participate strongly in mediating startle produced by activation of the vestibular nucleus. The convergence of the vestibulospinal tracts with the reticulospinal tract within the spinal cord therefore provides the neural basis of cross-modal summation of startling stimuli.

Acoustic Stimulation↗
PubMed2002

Electromyographical differentiation between the acoustic blink and startle reflex. Implications for studies investigating startle behavior.

Recent evidence suggests that electromyographic activity in the orbicularis oculi muscle occurring in response to sudden acoustic stimuli consists of two overlapping components: the blink and the startle reflex. The aim of the present study was to identify these two components in acoustically elicited eyeblink responses and to analyze their differential modulation by weak acoustic prepulses. The prevalence, latency and amplitude characteristics of double EMG peaks in pulse-alone and prepulse-pulse trials (PP) with 30 ms and 100 ms interstimulus intervals were assessed in 16 healthy volunteers.EMG responses with two peaks were registered in 42.6 % of the pulse-alone trials and in 56.2 % of the PP30 and 48.7 % of the PP100 trials, respectively. Prepulse inhibition of the amplitude was greater for the second peak (14.2 % (P2) vs. -11.5 % (P1) in PP30 trials; 62.6 % (P2) vs. 32.3 % (P1) in PP100 trials), resulting also in higher P1/P2 amplitude ratios in prepulse-pulse trials (P1/P2: 62.9 % in pulse-alone, 92.6 % in PP30 and 100.1 % in PP100 trials). In conclusion, double peaks are a common phenomenon in human studies of acoustically elicited blink responses. It is postulated that the first peak represents the auditory blink reflex, whereas the second peak corresponds to the startle reflex, which may be more susceptible to prepulse inhibition. This complexity should be taken into account in clinical studies of the modulation of the startle reflex.

Acoustic Stimulation↗
PubMed1987

[Comparison of the reflex responses to unexpected stimulation (startle reflexes) in freely moving and chloralose-anesthetized cats].

Comparative study of startle reflexes recorded electromyographically in the same cat was performed under two different experimental conditions: in freely moving animal and after chloralose-anesthesia. A remarkable similarity in the component composition and temporal parameters (latency, duration) of the EMG responses in these two cases was found. The data obtained suggest the functional similarity of startle reflex discharges in freely-moving and anesthetized cats as well as the identity of their corresponding neural mechanisms.

Acoustic Stimulation↗
PubMed2006

The monotonic dependency of prepulse inhibition of the acoustic startle reflex on the intensity of the startle-eliciting stimulus.

Prepulse inhibition (PPI) of the acoustic startle reflex is a translational behavioural paradigm for the assessment of sensorimotor gating deficit which has been demonstrated in a number of neuropsychiatric conditions. PPI refers to the reduction of the reflexive startle response to a 'pulse' stimulus when its presentation is shortly preceded by a weak 'prepulse' stimulus. We have recently examined the expression of PPI as a function of the startle-eliciting 'pulse' stimulus intensity in mice and in humans. One major discrepancy that emerged was the finding that healthy human subjects, unlike normal mice, did not show a clear monotonic reduction of PPI magnitude (as indexed by % reduction in startle reactivity) with increasingly intense pulse stimulus. This lack of correspondence between species may potentially weaken the translational power of the PPI paradigm. Here, we re-examined this issue in 31 healthy subjects across three levels of pulse stimulus intensity (95, 105 and 115 dB). A clear linear reduction of PPI as a function of pulse intensity was revealed when subjects failing to respond to the lowest pulse stimulus were excluded. Inclusion of such non-responders, on the other hand, resulted in a trend towards an inverted U-shape function as reported previously. The present study thus clarifies an apparent divergence between mouse and man, and provides important qualification to the "First Law of Reflex Modification" proposed by Hoffman and Ison which suggests that the absolute reduction in startle reactivity resulting from a prepulse stimulus preceding the startle-eliciting pulse stimulus is fixed by the prepulse intensity regardless of the pulse stimulus intensity.

Acoustic Stimulation↗
PubMed1989

Footshock-induced sensitization of electrically elicited startle reflexes.

The acoustic startle reflex can be facilitated by the presentation of a train of footshocks presented in rapid succession (footshock sensitization). Acoustic startle is a short-latency reflex mediated by a neural circuit consisting of the ventral cochlear nucleus (VCN), ventral nucleus of the lateral lemniscus (VLL), the nucleus reticularis pontis caudalis (RPC), and the spinal cord. The present study sought to determine the point along this pathway where footshocks might ultimately alter neural transmission to affect startle response. Rats were implanted bilaterally with stimulating electrodes in either the VCN, VLL, or RPC. Startle could be elicited acoustically with a noise burst or electrically with a single-pulse stimulus to either the VCN, VLL, or RPC before and after a train of ten 0.6-mA, 500-ms shocks presented at a rate of 1 shocks/s. Startle elicited acoustically or electrically in the VCN or VLL was significantly elevated following shocks. In contrast, startle elicited from the RPC showed no sensitization, even though startle elicited acoustically from the same animals during the same test session was facilitated. These data suggest that footshock sensitization ultimately alters transmission in the startle circuit at the RPC.

Acoustic Stimulation↗
PubMed1991

Effects of anxiety drugs on the modification of the acoustic startle reflex by noise gaps.

The acoustic startle reflex was modified by presenting gaps (0-30 ms) in a continuous noise (70 dB) before the startle eliciting stimulus. The effects of midazolam (0.4-1.8 mg/kg, IP), DMCM (0.1-0.4 mg/kg, IP), buspirone (5-20 mg/kg, PO), 8-OH-DPAT (0.5-8 mg/kg, IP), and clonidine (0.009-0.08 mg/kg, IP) on startle amplitudes (reflecting sensorimotor reactivity) on the one hand, and on gap inhibition of the startle reflex (a measure of temporal acuity) on the other hand, were investigated. The results showed that midazolam and clonidine attenuated sensorimotor reactivity dose-dependently. DMCM had no systematic effect on sensorimotor reactivity. Buspirone and 8-OH-DPAT increased sensorimotor reactivity dose dependently. Furthermore, midazolam and clonidine did not affect the neuronal systems underlying inhibition of the startle reflex. In contrast, DMCM and buspirone increased inhibition dose-dependently, and 8-OH-DPAT first increased and then decreased inhibition of the startle reflex. The possibility that drug-induced behavior affected the startle reflex was discussed.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2006

Influence of individual differences in the Behavioral Inhibition System and stimulus content (fear versus blood-disgust) on affective startle reflex modulation.

Inconsistencies among affective startle reflex modulation studies may be due to differences in the startle potentiation produced by the specific content of the images used, to individual differences in sensitivity to negative stimuli, or to the interaction of both factors. To explore this interaction, 52 undergraduates obtaining extreme scores on a self-report measure of the Behavioral Inhibition System (BIS) participated in an affective startle reflex modulation paradigm. A significant interaction between BIS group (high versus low) and image content emerged from the MANOVA. Comparing startle magnitude between fear and pleasant images, low BIS participants did not seem to show startle potentiation, whereas high BIS participants did. Both groups displayed potentiated startle during blood-disgust images. The present results suggest the importance of considering personality variables and their interaction with image content in the affective startle modulation paradigm.

Adult↗
PubMed1991

Effects of subchronic d-amphetamine on prepulse and gap inhibition of the acoustic startle reflex in rats.

Prepulse inhibition of the startle reflex has been used as an animal model for information processing deficits found in some types of schizophrenia. These deficits may be mediated by hypersensitive dopaminergic systems. In the present study, the effects of subchronic d-amphetamine administration [2 mg/kg intraperitoneally (IP)] on prepulse and gap inhibition of the startle reflex were compared to the effects of acute amphetamine and saline administration on startle inhibition. Results of three experiments are reported. The first two experiments were used to select prestimulus parameters sensitive to changes in stimulus intensity on the one hand, and prestimulus parameters sensitive to temporal aspects of stimulus processing on the other hand. Because schizophrenics have problems with the temporal sequencing of information, prestimulus inhibition of the startle reflex was expected to be more pronounced when prestimulus processing depended predominantly upon temporal factors. Results supported this hypothesis, although the effects of d-amphetamine were found at near detection threshold duration only. Subchronic amphetamine had no effect on the neuronal mechanisms underlying inhibition of the startle reflex by prestimuli. The results also suggested that a careful selection of duration and intensity of the prestimulus may increase the sensitivity of the prestimulus-startle paradigm for the effects of drugs, for example.

Acoustic Stimulation↗
PubMed1998

Lesions of the bed nucleus of the stria terminalis block sensitization of the acoustic startle reflex produced by repeated stress, but not fear-potentiated startle.

1. The effects of lesions of the bed nucleus of the stria terminalis (BST) on the acquisition of conditioned fear were examined. In Experiment 1, BST lesions did not block acquisition of fear-potentiated startle to an explicit visual conditioned stimulus (CS) over 20 days of training. However, BST lesions blocked a gradual elevation in baseline startle also seen over the course of training. 2. The gradual increase in baseline startle was replicated in Experiment 2 without the presence of an explicit CS, using unoperated subjects. Experiment 2 showed that the elevation was due to repetitive exposure to shock, because unshocked control subjects did not show any elevation over sessions. 3. In Experiment 3, lesions of the BST did not disrupt rapid sensitization of the startle reflex by footshock, showing that different neural substrates underlie sensitization of startle by acute and chronic exposure to footshock. 4. These data indicate that the BST, despite its anatomical continuity with the amygdala, is not critically involved in the acquisition of conditioned fear to an explicit CS. Nevertheless, the BST is involved in mediating a stress-induced elevation in the startle reflex. This suggests that the BST and the CeA, which constitute part of the "extended amygdala" have complementary roles in responses to stress.

Acoustic Stimulation↗
PubMed1995

The acoustic startle reflex: neurons and connections.

The startle reflex protects animals from blows or predatory attacks by quickly stiffening the limbs, body wall and dorsal neck in the brief time period before directed evasive or defensive action can be performed. The acoustic startle reflex in rats and cats is mediated primarily by a small cluster of giant neurons in the ventrocaudal part of the nucleus reticularis pontis caudalis (RPC) of the reticular formation. Activation of these RPC neurons occurs 3-8 ms after the acoustic stimulus reaches the ear. Undetermined neurons of the cochlear nuclei activate RPC via weak monosynaptic and strong disynaptic connections. The strong disynaptic input occurs via neurons of the contralateral ventrolateral pons, including large neurons of the ventrolateral tegmental nucleus that integrate auditory, tactile and vestibular information. RPC giant neurons, in turn, activate hundreds of motoneurons in the brain stem and the length of the spinal cord via large reticulospinal axons near the medial longitudinal fasciculus. To hindlimb motoneurons, monosynaptic connections from the reticulospinal tract are weak, but disynaptic connections via spinal cord interneurons are stronger and show temporal facilitation, like the startle response itself.

Animals↗
PubMed1993

NMDA and non-NMDA antagonists infused into the nucleus reticularis pontis caudalis depress the acoustic startle reflex.

The neural pathway that mediates the acoustic startle reflex has been proposed; however, the pharmacology underlying this reflex is less well known. The present study examined the role of excitatory amino acid receptors at the level of the nucleus reticularis pontis caudalis, a brainstem nucleus obligatory for the whole body startle reflex and implicated as the locus where extrinsic systems such as the amygdala may act to modulate acoustic startle. Twenty-nine rats, chronically implanted with bilateral cannulae aimed at the nucleus reticularis pontis caudalis, were tested to assess the effects of gamma-D-glutamylglycine (DGG), DL-2-amino-5-phosphonopentanoic acid (AP5), and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) on the amplitude of the acoustic startle reflex. Local infusion of each of the 3 compounds significantly reduced startle amplitude by as much as 70-80%. AP5 and CNQX attenuated startle over a dose range which indicated that the reticularis pontis caudalis may be much more sensitive to these compounds than other nuclei along the primary startle pathway. These results suggest that, at the level of the nucleus reticularis pontis caudalis, an excitatory amino acid neurotransmitter may mediate acoustic startle, and that both NMDA and non-NMDA receptor subtypes may be important for the expression of the acoustic startle reflex.

2-Amino-5-phosphonovalerate↗
PubMed1993

Startle reflex facilitation as a function of classical eyeblink conditioning in humans.

I investigated whether classical eyeblink conditioning increases the activating effect of the conditional stimulus (CS) on the relevant alpha motoneuron pool in the facial nucleus. The activating effect was measured by the reflex modification method, where startle reflexes, sharing the facial nerve motor pathway with conditional and unconditional eyeblink reflexes, were elicited in the presence of reinforced and nonreinforced CSs (CS+ and CS-). To reduce influences of conditional arousal on startle, a weak airpuff to the eye was used as unconditional stimulus and relatively short stimulus onset asynchronies (SOAs) of 300 and 600 ms were used in three startle tests presented while conditioning was in progress. Two groups (N = 72) received 100% or 0% reinforcement (Groups 100 and 0) of a tone CS+. The CS- was not reinforced. Three startle tests, consisting of acoustic startle probes presented alone and after CS+ and CS- onset, were conducted early, middle, and late in conditioning. Results showed increased startle reflex facilitation after CS+ onset in the late startle test in Group 100, indicating that startle increased as a function of classical conditioning. Although reflex facilitation at the 300-ms SOA in Group 100 is consistent with the hypothesis that CS presentations activated motoneurons in the facial nucleus, the present study cannot itself definitively support this hypothesis. Reflex facilitation at the 600-ms SOA in Group 100 could be influenced by conditional arousal.

Adolescent↗
PubMed1986

Audiogenic startle reflex of man and its relationship to startle syndromes. A review.

The normal human audiogenic startle reflex is defined from a review of the literature, substantiated by a current investigation of normal subjects, and clarified pathophysiologically by a discussion of animal experimentation. The basic information is used to evaluate critically a variety of syndromes loosely termed 'startle' in the past. A new classification of startle syndromes is proposed.

Adult↗
PubMed1983

Development changes in pharmacological responsivity of the acoustic startle reflex: effects of picrotoxin.

Using the acoustic startle reflex as the behavioral measure, qualitatively different responses to the GABA antagonist picrotoxin were obtained in developing rats before and after 21 days postnatal (PN) age. Dose-dependent increases in acoustic startle were seen following picrotoxin in PN day 15-16 rat pups. In contrast, dose-dependent decreases in startle following picrotoxin were observed in adult rats. The switch from excitation to inhibition of startle was found to occur abruptly on PN day 21. Excitatory responses to picrotoxin were also found in adult rats following localized infusions of picrotoxin into lumbar spinal cord regions, but not into the forebrain. These results give evidence that picrotoxin-sensitive sites that modulate increases in startle reflex behavior mature first and are analogous to sites in the adult spinal cord, whereas picrotoxin-sensitive sites that modulate decreases in startle reflex behavior mature later (greater than or equal to PN day 21) and are localized in more rostral brain areas.

Acoustic Stimulation↗
PubMed1999

Cochlear and trigeminal systems contributing to the startle reflex in rats.

The startle reflex is evoked by strong acoustic or tactile stimuli, or by electrical stimulation of acoustic or tactile pathways. To dissociate the contributions of acoustic and tactile pathways, stimulating electrodes were placed in adjacent cochlear and trigeminal nuclei. The currents needed to evoke startle-like responses were an order of magnitude lower in ventral trigeminal sites (12-80 microA for a 0.1-ms pulse) than in cochlear nucleus sites (150-800 microA). At low threshold sites in both areas, brief acoustic stimuli were followed 0-4 ms later by a single electrical pulse and the current required to evoke startle was measured at several interstimulus intervals. Summation between the acoustic and electrical stimuli for startle was strong in both cochlear and trigeminal sites. Collision effects were found in the anteroventral cochlear nucleus when the electrical stimulus followed the ipsilateral acoustic stimulus by 2.0 ms, suggesting that acoustic startle is mediated by axons in the anteroventral cochlear nucleus. Collision effects were found at 4.0 ms if the electrical stimulus was presented in the contralateral pontine reticular formation, suggesting that acoustic signals mediating startle mainly cross to the pontine reticular formation. Collision effects were not found in medial or posterior sites in the cochlear nucleus, or trigeminal sites, suggesting that the neurons that mediate startle in these sites do not mediate acoustic startle. Therefore, acoustic startle is mediated through high threshold cochlear nucleus sites, while low threshold sites are non-acoustic, probably as a result of trigeminal or vestibular stimulation.

Acoustic Stimulation↗