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PubMedDate not supplied

Hyperekplexia and sudden neonatal death.

Fifteen patients with hyperekplexia were identified in 3 families; diagnostic clinical characteristics were defined which allowed for early recognition and treatment. During the first 24 hours of life, spontaneous apnea and sluggish feeding effort were observed. After the first 24 hours, surviving infants exhibited the hyperekplexic startle response to nose tapping. This startle response is characterized by sudden muscular rigidity, feeding-induced oropharyngeal incoordination, and poor air exchange often with apnea, persisting with repetitive nose tapping. Untreated infants experienced recurring apnea until 1 year of age. Three of 15 patients died unexpectedly during the neonatal period. Patients treated with clonazepam (0.1-0.2 mg/kg/day) had no serious apneic episodes and startle reflexes were diminished. The pathophysiologic mechanism for hyperekplexia remains obscure. Electroencephalographic studies were consistently normal. The response to and tolerance of benzodiazepines are striking in newborns and infants and suggest an aberrant central nervous system reflex as the etiology; therefore, hyperekplexia should be considered in the evaluation of neonates and infants with apnea, aspiration pneumonia, episodic muscular rigidity, hyperexcitability, and near-miss sudden infant death syndrome. The need for immediate monitoring of at-risk infants, observation for signs of hyperekplexia, and initiation of clonazepam in these patients are emphasized. Hyperekplexic startle response to nose tapping should be included in the routine examination of all newborns.

Apnea↗

PubMed2002

Addressing the specificity of affective startle modulation: fear versus disgust.

Previous research is equivocal regarding whether startle reflex eyeblink is specifically sensitive to the emotion of fear, or is more generally influenced by the valence dimension of emotion. Thirty-five undergraduate participants (17 male) viewed 60 pictures from five affective categories (pleasant, neutral, fear, disgust-blood, and disgust-other). Bilateral eyeblink EMG responses to acoustic startle probes were assessed during 2/3 of picture presentations, and 1/3 of intertrial intervals. Left corrugator and levator EMG responses to no-startle pictures were also examined. Supporting an emotional valence model of affective startle modulation, the startle potentiation effect was not specific to fear materials. In fact, women, but not men, had larger startles during disgust compared with fear pictures. Both corrugator and levator EMG responses were greater to disgust than fear stimuli. These findings limit the generalizability of corrugator as an index of all negative emotions and extend evidence for the specificity of levator to disgust.

Adolescent↗

PubMed2001

Startle and sensorimotor gating in rats lacking CCK-A receptors.

Otsuka Long Evans Tokushima Fatty (OLETF) rats lack CCK-A receptors because of a genetic mutation. Previous studies have shown that CCK-A receptors seem to play a role in the regulation of prepulse inhibition (PPI) of the startle reflex, an operational measure of sensorimotor gating. This study investigated baseline and drug-disrupted PPI in OLETF rats and their non-mutant counterparts, Long Evans Tokushima Otsuka (LETO) rats. Baseline PPI did not differ significantly between the two rat genotypes but OLETF rats exhibited a higher acoustic startle response compared to LETO rats. Amphetamine (2 mg/kg), and the non-competitive NMDA antagonist, dizocilpine (0.1 mg/kg), disrupted PPI in LETO rats but not in the OLETF rats. Apomorphine (0.5 mg/kg) failed to disrupt PPI in both LETO and OLETF rats, and haloperidol (0.5 mg/kg) produced a comparable facilitation of PPI in both groups. In a separate study, OLETF rats were found to be less sensitive to the locomotor stimulating effects of amphetamine. These results suggest that CCK-A receptors play a significant role in the behavioral effects of amphetamine and dizocilpine. The PPI response of OLETF rats to amphetamine and dizocilpine is similar to normal rats pretreated with atypical antipsychotics, suggesting that CCK-A receptors may play an important role in the restoration of drug-disrupted PPI by antipsychotics.

Acoustic Stimulation↗

PubMed2000

GABA in the deep layers of the superior Colliculus/Mesencephalic reticular formation mediates the enhancement of startle by the dopamine D1 receptor agonist SKF 82958 in rats.

GABA transmission in the deep layers of the superior colliculus/deep mesencephalic reticular formation (deep SC/Me) mediates several motor responses, including those expressed after systemic administration of dopamine agonists. In the present study we examined the role of the deep SC/Me in the modulation of the acoustic startle reflex and its enhancement by the dopamine D(1) agonist SKF 82958. Rats were implanted with bilateral cannulas into the deep SC/Me or superficial layers of the SC (super SC) and 1 week later were infused with various compounds. The GABA(A) antagonist bicuculline (0, 5, and 10 ng) produced a dose- and time-dependent enhancement of startle after infusion into the deep SC/Me, but not the super SC. Infusion of the GABA(A) agonist muscimol (0.1 microg) into the deep SC/Me, but not the super SC, blocked the enhancement of startle by systemic SKF 82958 (1 mg/kg) but had no effect on baseline startle by itself. This effect was not produced by infusion of the D(1) antagonist SCH 23390(1 microg) or the glutamate antagonist NBQX (0.1 microg). Deposits of FluoroGold into the deep SC/Me, combined with immunohistochemistry for glutamic acid decarboxylase (GAD), confirmed a direct GABAergic input from the substantia nigra pars reticulata (SNr) to the deep SC/Me. These results suggest that GABA tone in the deep SC/Me modulates the expression of startle as well as the enhancement of startle by dopamine D(1) agonists. On the basis of these data and previous work, we have proposed a striatonigral-tectal-reticular neural pathway mediating the effects of dopamine D(1) agonists on startle.

Acoustic Stimulation↗

PubMed1996

Effects of the PCP analog dizocilpine on sensory gating: potential relevance to clinical subtypes of schizophrenia.

Prepulse inhibition (PPI) of the acoustic startle reflex, a measure of sensory gating, is reduced in schizophrenic patients. Dopamine agonists and NMDA receptor antagonists such as phencyclidine (PCP) can disrupt PPI in animals, consistent with both the dopamine and glutamate hypotheses of schizophrenia. In this study, we sought to further characterize the effects of the NMDA antagonist dizocilpine on acoustic startle modulation. Fischer 344 rats were tested after one of three doses of dizocilpine (0.05, 0.2, and 0.5 mg/kg) and assessed for PPI as well as for alterations in baseline startle and prepulse facilitation (PPF). Results showed complete disruption of PPI for each inhibitory trial type after 0.2 and 0.5 mg/kg of dizocilpine. Baseline startle and PPF were enhanced by the low dose but decreased with the moderate and high doses of dizocilpine. Although dizocilpine caused alterations in prepulse modulation of startle similar to dopamine agonists, some effects differ. Unique effects of dizocilpine on sensory gating are discussed in terms of their potential for discriminating subtypes of schizophrenic illness with different underlying pathophysiology.

Animals↗

PubMedDate not supplied

Behavioral evaluations in developmental toxicity testing: MARTA survey results.

During 1991, the Middle Atlantic Reproduction and Teratology Association (MARTA) conducted a survey of laboratories performing behavioral evaluations as part of GLP developmental toxicity studies. This survey was conducted to determine the extent to which an "industry standard" had evolved for behavioral test batteries. The most commonly used developmental parameters were eye opening, pinna unfolding, and sexual maturation (physical landmarks); surface righting, pupil constriction, and nonautomated acoustic startle (reflexive landmarks). Locomotor activity was used by 80% of the laboratories. The majority (76%) of laboratories conducted at least one learning and/or retention evaluation; nearly one-fourth of the laboratories routinely performed two. The most common learning tests were watermaze (primarily a simple two-choice discrimination task) and passive avoidance. Automated startle paradigms (habituation, prepulse modification, and/or startle elicitation) were evaluated by 28% of the laboratories. This survey showed a remarkable similarity in methodology across laboratories and a progressive increase in the number of GLP studies that included behavioral assessments. The results indicate that behavioral tests have become a common component of developmental toxicity assessments of pharmaceuticals.

Animals↗

PubMed1998

Fear-potentiated startle in adolescent offspring of parents with anxiety disorders.

BACKGROUND: The startle reflex and its potentiation by aversive states was used as a possible vulnerability marker for anxiety disorders in adolescent offspring of parents with this condition. METHODS: The participants were 39 low-risk adolescents (16 male/23 female) with a parental history of no psychiatric disorder and 35 high-risk adolescents (18 male/17 female) with a parental history of anxiety disorders. The magnitude of startle was examined at baseline and during anticipation of an aversive stimulus (fear-potentiated startle). RESULTS: Startle was found to discriminate between children at high and low risk for anxiety disorders; however, different abnormalities for high-risk male and female subjects were observed. Startle levels, overall, were elevated among high-risk female subjects, whereas high-risk male subjects exhibited greater magnitude of startle potentiation during aversive anticipation. CONCLUSIONS: Startle reactivity may serve as a vulnerability marker for the development of anxiety disorders. With its basic grounding in animal and human behavioral research, startle may enhance our understanding of the underlying neurobiological bases of human anxiety states.

Adolescent↗

PubMed1998

Dependence on smoking and the acoustic startle response in healthy smokers.

Recent data from nicotine-dependent rats (14) and healthy smokers (18) would suggest that nicotine withdrawal modulates the acoustic startle reflex in a way similar to that of fear (5,20). We examined this directly using nonsmokers and healthy smokers who had no deprivation, brief deprivation (2-3 h), or prolonged deprivation (15 h). Groups differences in heart rate (HR), alveolar carbon monoxide (CO) levels, and desire and craving for cigarettes confirmed the presence of smoking withdrawal. However, there were no significant differences in the magnitude of the baseline startle response among the differently deprived smokers or between the smokers and the nonsmokers. Subsequent startle tests were carried out in the smokers during repeated sequences of preparing a cigarette for smoking (smoking cues) and then smoking. Whereas we did find statistically significant interactions of smoking deprivation with smoking cues and with renewed smoking, there was only weak confirmation of a priori predictions of motivational effects of smoking cues or of smoking. We conclude that smoking dependence may not affect the acoustic startle response itself; modulation seems to occur, but only after experience with the test situation. Discussed were possible mechanisms of this modulation in both humans and animals and further application of the startle response for providing interdisciplinary assessments of the motivational effects of nicotine withdrawal.

Acoustic Stimulation↗

PubMed1993

Effects of haloperidol and SCH 23390 on acoustic startle and prepulse inhibition under basal and stimulated conditions.

1. Adult Sprague-Dawley rats underwent startle testing for assessment of baseline startle amplitude and prepulse inhibition (PPI) of the startle reflex. 2. Animals were tested after administration of either: saline, a selective D1 dopamine (DA) receptor antagonist, a relatively selective D2 DA antagonist, or combined low dose D1 and D2 antagonists. 3. Changes due to antagonists were assessed with and without administration of the D1/D2 agonist apomorphine. 4. Testing without apomorphine stimulation showed that both D1 and D2 antagonists reduce baseline startle and enhance PPI. Further, the two antagonists exhibited a synergistic interaction. 5. Testing with apomorphine showed that D1 and D2 antagonists reduce apomorphine-induced startle enhancement. Again, the two exhibited a synergistic interaction. 6. For PPI, the D2 but not D1 antagonist reduced the apomorphine effect. However, the D1 antagonist potentiated the effect of the D2 antagonist.

Acoustic Stimulation↗

PubMed1979

Temporal integration of acoustic stimulation obtained in reflex inhibition in rats and humans.

An acoustic stimulus (S1) presented just before reflex elicitation inhibits reflex expression. The present studies questioned whether inhibition provided by initial stimuli of various durations conforms to established temporal integration functions. Initial stimuli were noise bursts varying in duration (2, 20, or 200 msec) and intensity (55 or 85 dB). Eliciting stimuli (S2) for rats were intense tone bursts, which elicited the acoustic startle reflex, and for humans electrotactile stimuli to the forehead, which elicited the eye blink. Findings revealed that inhibition was greater with the 85-dB S1 stimulus and increased linearly with log increases in duration. These latter data suggest that the acoustic substrate for reflex inhibition has a long-time constant. There was one exception to this general finding. For seven (of nine) human subjects, inhibition declined when the duration of the 85-dB S1 was increased from 20 to 200 msec. Postexperimental questioning and video monitoring suggest that this anomaly resulted from a reflex enhancing arousal process.

Acoustic Stimulation↗

PubMed1997

Fear-potentiated startle conditioning in humans: explicit and contextual cue conditioning following paired versus unpaired training.

Conditioned fear in response to explicit and contextual cues was examined using the startle reflex in three groups of participants over two sessions separated by 4-5 days. The conditioned stimulus (CS) was paired with an aversive unconditioned stimulus (US) (shock) during conditioning in the paired but not in the unpaired group. In the reaction time (RT) group, the US was a nonaversive visual signal for an RT task. In the paired group, the CS potentiated startle in the postconditioning phase. This conditioned response was fully retained over the retention interval. There was no substantial change in baseline startle (startle delivered in the absence of CS). By contrast, startle was not potentiated by the CS in the unpaired group, but baseline startle was increased from Session 1 to Session 2. In the RT group, startle was not affected by the CS, and baseline startle was reduced from Session 1 to Session 2. These results suggest that paired presentations of a CS and an aversive US result in conditioned fear in response to the CS but little contextual fear, whereas unpaired presentations of a CS and US leads to poor explicit cue conditioning but substantial contextual fear.

Adolescent↗

PubMed2002

The relative detectability for mice of gaps having different ramp durations at their onset and offset boundaries.

The effect on gap detectability of varying noise fall time (FT) and rise time (RT) of the gap boundary ramps was examined in mice using reflex modification audiometry, measuring inhibition of acoustic startle reflexes by variously shaped gaps just preceding reflex expression. In experiment 1 (n = 12) inhibition increased up to near-asymptotic values with longer FT (0, 1, 2, 3, 5, or 10 ms) and QT (quiet time, 0 to 13 ms), with a 2:1 trade-off between FT and QT. In experiment 2 (n = 24) inhibition increased for any RT above 0 ms (2, 3, 5, or 7 ms) if QT= 1 ms, but diminished with increased RT when QT = 3 or 8 ms. Enhanced detectability for subthreshold gaps by longer ramps results from their extending the apparent gap duration. The negative effect of increased RT for threshold gaps suggests the importance for gap detection of the stronger neural responses to sharp edges at the end of the gap shown previously in the mouse inferior colliculus. These effects are specific to gaps: inhibition for fixed (70-dB SPL) or varied level pulses (30 to 60 dB) was unaffected by varying the ramped edges (experiments 3 and 4, n = 9).

Animals↗

PubMed1995

A functional analysis of the age-related degeneration in the Fischer 344 rat.

We have previously described how the expression of photoreceptor cell degeneration in the Fischer 344 rat is affected by age, retinal topography, and gender. Degeneration in the central and equatorial regions progresses linearly with age throughout the life span of the animal, while the periphery of the male is subject to sudden and dramatic losses of cells in the superior hemisphere after 12 months and in the inferior hemisphere after 18 months of age. The purpose of the present study was to determine how this degeneration affected retinal function and visual ability in the male Fischer 344 from 3 to 24 months of age. Functional testing included the electroretinogram (ERG, measuring both a-wave and b-wave amplitudes and implicit times) and the behavioral method of startle reflex modification (RM, which measures the degree to which a light flash inhibits the response to an immediately subsequent loud noise). All of the functional measures showed a decline with age, but varied in their time course. ERG amplitudes showed a linear decline in amplitude over the entire age range. In contrast, the implicit times of the ERG waves and the degree to which the light flash inhibited the startle reaction both showed a slight maturation in function (faster implicit times and greater inhibition) from 8 or 12 months of age. After 18 months of age, the implicit time showed a significant increase and the startle response showed a significant decrease. This study shows how visual function correlates with the histopathological changes seen in age-related retinal degeneration.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1996

Intracerebroventricular infusion of the CCKB receptor agonist pentagastrin potentiates acoustic startle.

The acoustic startle reflex is increased by stimuli associated with aversive events (such as the delivery of shock) and so has been used as a sensitive index of 'anxiety' or 'fear'. Administration of cholecystokininB (CCKB) receptor agonists produces a constellation of behaviors associated with 'anxiety' in laboratory animals and humans. Here, intracerebroventricular infusions of the CCKB agonist, pentagastrin (0, 1, 10, 100 nM), produced a long-lasting, dose-related potentiation of acoustic startle responses. Similar infusions of pentagastrin had no effect on locomotor activity over the same time course, showing that changes in startle responses following infusions of pentagastrin are not due to nonspecific changes in motor activity.

Acoustic Stimulation↗

PubMed1998

Effects of stimulus modality and task condition on blink startle modification and on electrodermal responses.

Participants in Experiments 1 and 2 performed a discrimination and counting task to assess the effect of lead stimulus modality on attentional modification of the acoustic startle reflex. Modality of the discrimination stimuli was changed across subjects. Electrodermal responses were larger during task-relevant stimuli than during task-irrelevant stimuli in all conditions. Larger blink magnitude facilitation was found during auditory and visual task-relevant stimuli, but not for tactile stimuli. Experiment 3 used acoustic, visual, and tactile conditioned stimuli (CSs) in differential conditioning with an aversive unconditioned stimulus (US). Startle magnitude facilitation and electrodermal responses were larger during a CS that preceded the US than during a CS that was presented alone regardless of lead stimulus modality. Although not unequivocal, the present data pose problems for attentional accounts of blink modification that emphasize the importance of lead stimulus modality.

Adolescent↗

PubMed2004

Endogenous kynurenic acid disrupts prepulse inhibition.

BACKGROUND: Recent studies show that endogenous levels of kynurenic acid (KYNA) are increased in the cerebrospinal fluid of schizophrenic patients. Prepulse inhibition (PPI) of the acoustic startle reflex is an operational measure of sensorimotor gating that is reduced in neuropsychiatric disorders, such as schizophrenia. Previous studies show that administration of N-methyl-D-aspartate (NMDA) receptor antagonists, such as phencyclidine or MK-801, leads to deficits in sensorimotor gating that mimic those observed in schizophrenic patients. METHODS: The present study examined the effects of the endogenous NMDA receptor antagonist KYNA on startle and PPI in rats. Elevation of endogenous brain levels of KYNA was achieved through intraperitoneal (IP) administration of kynurenine (100 mg/kg), the precursor of KYNA, or by intravenous administration of PNU 156561A (10 mg/kg). RESULTS: A fourfold increase in brain KYNA levels, as induced by kynurenine or PNU 156561A, significantly reduced PPI. There were no differences in startle magnitudes between control rats and drug-treated rats. The disruption of PPI was restored by administration of the antipsychotic drugs haloperidol (.2 mg/kg, IP) or clozapine (7.5 mg/kg, IP). CONCLUSIONS: The present results suggest that brain KYNA serves as an endogenous modulator of PPI and are consistent with the hypothesis that KYNA contributes to the pathophysiology of schizophrenia.

Acoustic Stimulation↗

PubMed2001

Conditioned inhibition of fear-potentiated startle and skin conductance in humans.

Conditioned inhibition of classical conditioning was investigated with the startle reflex and the skin conductance response (SCR) in humans using a serial presentation of the conditioned inhibitor (X) and of the conditioned stimulus (CS). The unconditioned stimulus (US) was a shock. During conditioning, participants were presented with two different reinforced CS (A, B) and with X preceding A (noted X-->A). During X-->A, A was not reinforced with the US. During the summation test, B, X-->B, and Y-->B were presented (Y was a new stimulus that tested the specificity of the inhibitory properties of X). B was not reinforced during the summation test. A, B, X, and Y were lights of different colors. Participants were divided into a low and a high anxious group based on the TPQ (C.R. Cloninger, 1987). In the low anxious group, conditioned startle potentiation and SCR responses to A were inhibited when X preceded A (noted A(XA)). This differential responding to A and A(XA) emerged earlier with the SCR than with startle. During the summation test, the inhibitory properties of X did not transfer to B. In the high anxious group, there was only a differential SCR to A and A(XA). X did not inhibit startle potentiation to A.

Adolescent↗

PubMed1989

Implementation of a primary screen for developmental neurotoxicity.

A battery of tests to evaluate physical growth/development and neurobehavioral function was conducted with 78 litters of control Sprague-Dawley rats given purified water by intubation. The objectives of this study were to optimize test methods and to document the range and variability of the experimental endpoints. Data are presented for maternal evaluations (body weight gain, food consumption), gestation length, litter size, and postnatal survival. Pup body weight was used to assess postnatal somatic growth rate from birth to 85 days of age, while whole and regional brain weight measurements at 7, 28, and 85 days provided a more specific measure of physical growth relevant to a neurobehavioral study. Physical landmarks of development evaluated were pinna unfolding, incisor eruption, and eye opening while reflex landmarks of development evaluated were the negative geotaxis and pupillary reflexes. The mean percentage of litters acquiring a physical trait or reflex increased sigmoidally with age, and the data suggest that the potential to detect developmental delays would be optimal when ca. 90% of control litters reach the test landmark. Functional evaluations were arranged according to four testing subsets so that each litter was evaluated in each test (1 pup/sex/litter), but repeated testing on pups was minimized. Auditory and tactile startle reflexes, as well as prepulse inhibition, were measured at ages 22 days and 60-64 days and found to increase with age. A passive avoidance paradigm (age 40-43 days) was used to assess exploratory behavior (approach) and memory (avoidance). Swimming performance in a water maze was used to evaluate learning. In this test, escape times and error rates improved to their highest level by five or six trials and showed acceptable degrees of variability. Spontaneous motor activity was monitored for 23 hr at age 54-61 days to evaluate exploratory activity, photoperiod entrainment, and catecholamine-induced locomotion (amphetamine challenge). Finally, landmarks of sexual maturation (balanopreputial separation evident at 45 days of age, vaginal perforation evident at 33 days) and estrous cyclicity (4.8 cycles per 21 days) were evaluated as measures of reproductive neuroendocrine function. In sum, the test battery provided an efficient yet comprehensive screen for evaluating effects on physical growth/development and neurobehavioral function which meets practical criteria for preclinical testing of pharmaceutical agents.

Animals↗