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At least 19 recordsLinked to original sources
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↗
PubMed1992

5-Hydroxytryptamine 1a receptor agonists block prepulse inhibition of acoustic startle reflex.

Presentation of a nonstartling stimulus (prepulse) 100 msec before a startle-eliciting auditory stimulus (pulse) reduces startle reflex amplitude in mammals. Prepulse inhibition of acoustic startle reflex is smaller in schizophrenics than in nonschizophrenics, a phenomenon that has been hypothesized to reflect sensorimotor gating deficits underlying schizophrenic psychosis. Five 5-hydroxytryptamine1a (5-HT1a, serotonin) receptor agonists: 8-hydroxy-2-(di-n-propylamino) tetraline (8-OHDPAT), 5-methoxydimethyltryptamine, buspirone, gepirone and ipsapirone, were tested for effects on prepulse inhibition and startle reflex amplitude in rats. All five agents reduced prepulse inhibition at doses that had no effect on startle reflex amplitude or motor activity. Reduction of prepulse inhibition by 8-OHDPAT was antagonized by (-)propranolol, a 5-HT1a receptor antagonist, and partially by haloperidol, a dopamine D2 receptor antagonist, but not by ketanserin or methysergide, 5-HT2 receptor antagonists. 8-OHDPAT did not reduce prepulse inhibition in subjects pretreated with reserpine or tetrabenazine to deplete neuronal amines, but interpretation of this result is complicated because reserpine and tetrabenazine given alone reduced prepulse inhibition. The results indicate that 5-HT1a receptor agonists block prepulse inhibition of acoustic startle reflex, possibly via dopaminergic mechanisms.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1977

Psilocybin: biphasic dose-response effects on the acoustic startle reflex in the rat.

The startle reflex was measured in 7 groups of 10 rats each after intraperitoneal injection of saline or 0.25, 0.50, 0.75, 1.0, 2.0, 4.0 or 8.0 mg/kg psilocybin. Low doses (0.75-2.0 mg/kg) increased startle amplitude whereas high doses (4.0-8.0 mg/kg) depressed startle. Selected low (0.71 mg/kg) or high (5.70 mg/kg) doses of psilocin also had a biphasic dose-response effect on startle comparable in magnitude to equimolar doses of psilocybin. This biphasic dose-response relationship of the indole hallucinogen, psilocybin, on startle is consistent with the hypothesis that startle is increased when the firing rates of midbrain raphe neurons are selectively inhibited but is depressed when neurons postsynaptic to raphe cells are also inhibited.

Acoustic Stimulation↗
PubMed1975

Acoustic startle reflexes in the rat during consummatory behavior.

Auditory startle reflexes were elicited in thirsty rats when they were drinking water or were between drinking boutsmthe reaction was greater during drinking, this enhancement developing over the first few seconds after drinking onset. The startle reaction was lowest immediately after the termination of drinking. Reflex enhancement was reduced when thirsty rats drank milk rather than the more preferred water. The reflex was smaller with increased water deprivation, but enhancement produced by drinking was apparent at all levels of deprivation studied, satiety to 4-days deprivation. The inhibitory effect of a preliminary stimulus was not affected by consummatory behavior. Attention is drawn to suggestive parallels between these behavioral effects and other consequences of consummatory activity, primarily having to do with electrophysiological events and arousal processes

Acoustic Stimulation↗
PubMed1992

Effects of the serotonin releasers 3,4-methylenedioxymethamphetamine (MDMA), 4-chloroamphetamine (PCA) and fenfluramine on acoustic and tactile startle reflexes in rats.

The substituted amphetamines 4-chloroamphetamine (PCA), 3,4-methylenedioxymethamphetamine (MDMA) and fenfluramine (FEN) share the common neurochemical action of acutely releasing central serotonin (5-HT), and yet their behavioral effects are quite different. The present study evaluated the effects of these compounds on acoustic and tactile startle reflexes. PCA and MDMA were qualitatively similar in producing dose-related increases in acoustic and tactile startle reflexes that were slow in onset, but sustained throughout the 3.5-hr test session. Changes in motor activity did not account for the observed excitation of startle. In marked contrast to MDMA and PCA, FEN did not alter tactile startle and tended to depress acoustic startle. The excitatory effect of 20 mg/kg of MDMA was prevented by the 5-HT uptake blockers MDL 27,777A and fluoxetine. MDMA excitation was not affected by a dose of the dopamine antagonist haloperidol that attenuated the startle-enhancing effect of d-amphetamine. MDMA excitation was greatly attenuated by a general depletion of central 5-HT produced by prior intraventricular injection of the 5-HT neurotoxin 5,7-dihydroxytryptamine. PCA and MDMA excitations of startle were attenuated in rats specifically depleted of spinal 5-HT or in rats with radio frequency lesions of the dorsal raphe nucleus. Thus, PCA and MDMA have similar prolonged excitatory effects on startle reflexes that are mediated by ascending (dorsal raphe) and descending (spinal) pathways, whereas FEN differs in its lack of excitation of startle. Differences in the neurochemical properties of these compounds or their patterns of 5-HT release may underlie their different behavioral profiles.

5,7-Dihydroxytryptamine↗
PubMed1979

Startle reflex habituation in children with cerebral palsy.

Two groups of children (9 with cerebral palsy and 10 normals, matched for sex and age) participated in a study of the startle reflex. Each child was instructed to press a button as soon as possible after the onset of a visual stimulus on a box on the table at which they were seated. During some of the trials, a sudden and intense auditory stimulus (85 dB) was presented concomitantly with the onset of the visual stimulus, and effects on reaction time recorded. Mean reaction time of normal children was significantly faster than that of the group with cerebral palsy. The magnitude of disruption associated with the first startle stimulus presentation was signicantly greater for cerebral palsied children. The course between groups of habituation to the startle stimuli was not significantly different. Data support the hypothesis that startle reflexes of children with cerebral palsy are more marked than are those of normal children.

Acoustic Stimulation↗
PubMed1992

Corticotropin-releasing factor: long-lasting facilitation of the acoustic startle reflex.

Intracerebroventricular infusion of corticotropin-releasing factor (CRF) (0.1-1.0 micrograms) produced a pronounced, dose-dependent enhancement of the acoustic startle reflex in rats. This excitatory effect began about 20-30 min after infusion, grew steadily over the 2 hr test period, and lasted at least 6 hr. Higher doses of CRF (10 micrograms) often produced marked facilitation and then inhibition of startle that oscillated repeatedly with a period of 10-20 min. CRF-enhanced startle did not result from an increase in sensitization produced by repetition of the startle stimulus or from a blockade of habituation. Peripheral injections of the autonomic ganglionic blockers hexamethonium (10 mg/kg) or chlorisondamine (3 mg/kg) slightly attenuated the magnitude of CRF-enhanced startle, suggesting a partial role of peripheral sympathetic activation. Intracerebroventricular infusion of the CRF antagonist alpha-helical CRF9-41 (alpha hCRF; 25 or 50 micrograms) blocked CRF-enhanced startle when infused 5 min prior to CRF, indicating a central site of action. CRF-enhanced startle also was reversed when alpha hCRF was given 90 min after infusion of CRF. This suggests that exogenously applied CRF remains in the brain for a very long time after administration or that CRF given exogenously initiates a process that results in a long-lasting activation of endogenous CRF. Because the startle reflex is elevated by both conditioned and unconditioned fear, these data lend further support to the idea that CRF infusion produces a behavioral state that resembles fear or anxiety. Because startle is mediated by a well-defined neural pathway, CRF-enhanced startle may provide a useful behavioral assay to analyze the neural systems upon which exogenous CRF acts to produce its behavioral effects.

Acoustic Stimulation↗
PubMed1977

Correlation of the startle reflex and Mauthner cell auditory responses in unrestrained goldfish.

Stainless-steel electrodes were implanted near the left or right. Mauthner cells (M-cells) of goldfish to determine if these cells can initiate the startle reflex evoked by a brief sinusoidal sound stimulus. Recordings of the M-cell extracellular spike were obtained for the duration of 10 experiments. Fish with chronic implants were allowed to free-swim and exposed to at least 10 consecutive sound stimuli consisting of 2 cycles of 200 Hz. Seventy-three startle responses were analysed. In 34 cases the implanted M-cell electrode was contralateral to the contracting musculature, and in each of these cases, a M-cell spike preceded the EMG response by 1-1-2-1 ms. In the reamining 39 cases the electrode was ipsilateral to the active musculature, and the M-cell only fired in one of these trails. There were no startle responses and no M-cell firings in an additional 52 tests. Since the M-cell activates contralateral motoneurones, the results indicate it is responsible for initiation of the startle reflex.

Action Potentials↗
PubMed1992

Startle reflex habituation in functional psychoses: a controlled study.

The habituation of the startle reflex in a paradigm using electrical stimulation was studied in 17 psychotic patients and 18 healthy controls. The magnitude of the R2 component of the blink reflex differed between the groups (ANOVA, F = 5.81; P = 0.022) and during the course of trials (F = 25.72; P < 0.0001). Furthermore a statistically significant interaction of diagnosis x trials (F = 3.34; P = 0.022) emerged suggesting that an impairment in habituation of startle is present in patients but not in healthy controls despite a comparable reactivity.

Adolescent↗
PubMed1979

Tryptophan-free diet: effects on the acoustic startle reflex in rats.

In Experiment 1, body weights of rats fed a powdered tryptophan-free (TF) diet decreased monotonically during a 13-day period. Control animals fed the same diet supplemented with 0.5% L-tryptophan gained weight. The groups did not differ significantly in acoustic startle amplitude measured at 2, 4, 6, 7, 9, 11, and 13 days despite a 28% decrease in whole-brain serotonin in the TF rats. In Experiment 2, daily intubation of rats with a syrup form of each diet maintained the two groups' body weights at comparable levels. TF diet intubation decreased whole-brain serotonin by 64% and produced significantly elevated startle amplitudes, which returned to control levels when 0.5% L-tryptophan was added to the diet. Changes in whole-brain serotonin level preceded changes in startle amplitude by several days. In Experiment 3, acute injections of 125 mg/kg L-tryptophan significantly reduced the startle amplitude of TF diet intubated rats and significantly raised their brain serotonin levels. The results show that acoustic startle reflex is increased by a TF diet, provided the animals receive adequate nourishment, and suggest that this facilitation may result from depletion of brain serotonin.

Acoustic Stimulation↗
PubMed1979

Modulation of the acoustic startle reflex in humans in the absence of anticipatory changes in the middle ear reflex.

If a weak tone precedes an intense tone, then the acoustic startle eyeblink reflex elicited by the stronger stimulus is inhibited. It has been suggested that the leading stimulus gives rise to a protective middle ear reflex that attenuates the effective intensity of the second. This hypothesis was tested and disproved. In seven subjects intense tone bursts sufficient to elicit both intratympanic and eyeblink responses were presented sometimes alone and sometimes preceded at various lead times (25 to 400 msec) by a weak tone. The weak tone inhibited the amplitude of the eye blink to the strong tone, maximally at intervals of 100 to 200 msec, but was never seen to produce any of the anticipatory impedance changes that would be characteristic of middle ear reflex activity during the interval between the two stimuli.

Adolescent↗
PubMed1992

Lesions of the central nucleus of the amygdala, but not the paraventricular nucleus of the hypothalamus, block the excitatory effects of corticotropin-releasing factor on the acoustic startle reflex.

Intracerebroventricular (icv) infusion of corticotropin-releasing factor (CRF) was previously found to produce a long-lasting, dose-dependent (0.1-1.0 microgram) increase in the amplitude of the acoustic startle reflex. The present study sought to determine where in the CNS CRF acts to increase startle. Intracisternal infusion of CRF (0.1-1.0 microgram) increased startle with a time course and magnitude similar to that produced by icv CRF, unlike intrathecal infusion, which produced a small, more rapid enhancement of startle. While lesions of the paraventricular nucleus of the hypothalamus had no effect on icv CRF-enhanced startle, bilateral lesions of the central nucleus of the amygdala significantly attenuated the excitatory effect of icv CRF but had no effect on intrathecal CRF-enhanced startle. Even though lesions of the amygdala blocked icv CRF-enhanced startle, local infusion of CRF into the amygdala did not significantly elevate startle. The present data indicate that the amygdala is part of the neural circuitry required for icv CRF to elevate startle, but does not appear to be the primary receptor area where CRF acts. The involvement of the amygdala in icv CRF-enhanced startle is consistent with the hypothesis that both the amygdala and CRF are critically involved in fear and stress.

Acoustic Stimulation↗
PubMed1992

Auditory startle reflex in post-traumatic stress disorder patients treated with clonazepam.

Manifestations of acute hyperarousal in the Post-Traumatic Stress Disorder (PTSD) have been assimilated with panic attacks. This study examines the auditory startle reflex in PTSD patients treated with clonazepam, a benzodiazepine with anti-panic properties. PTSD patients treated with clonazepam did not differ from drug-free PTSD patients in the magnitude and the habituation rate of their responses to an auditory startle, with both groups showing abnormally slow habituation. It is suggested that the mechanisms underlying phasic hyperarousal in PTSD might differ from those which have been implied in the genesis of panic attacks.

Adult↗
PubMed1992

Human startle reflex: technique and criteria for abnormal response.

Because quantitative norms for the normal audiogenic startle response to repeated stimuli have not been previously reported, we now describe a technique for eliciting the startle response and analysing its habituation with repeated stimuli. We used binaural 105 dB tones delivered in 5 blocks of 4 tones. Successive blocks were separated by a 5 min period without tones stimuli and had progressively shorter inter-stimulus intervals (ISIs) beginning with 5 min in the first block and reducing to 1 min in the final, fifth block. We contrast the response and its habituation in a group of 8 normal subjects with that in a patient with clinically exaggerated startle. Based on the differences observed, we propose that the following criteria may be used to ascertain an abnormally increased startle response: (1) excessive duration of the myogenic response; (2) persistence of extracranial responses after the initial two blocks of stimuli; and (3) reduced habituation of the response (as measured by decreases in response duration and in the area under the curve of rectified EMG for the orbicularis oculi myogenic response). Our patient was abnormal on each of these measures. This result is consistent with past qualitative reports which have indicated that abnormal startle is associated both with excessive startle and with subnormal habituation. Study of further patients with hyperekplexia will be necessary to either confirm our data or modify our proposed criteria.

Acoustic Stimulation↗