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At least 667 records · Page 37Linked to original sources

PubMed1997

The effects of clonazepam and vigabatrin in hyperekplexia.

Hyperekplexia is an autosomal dominant disorder caused by a point mutation in the alpha1 subunit of the glycine receptor, characterized by excessive startle responses followed by temporary generalized stiffness. Clonazepam, effective in open case studies, potentiates, through unknown mechanisms, the neurotransmitter gamma-aminobutyric acid (GABA). Vigabatrin increases GABA by inhibition of the GABA catabolic enzyme GABA-transaminase. Effects of clonazepam (1 mg for 1 day) and vigabatrin (1000 mg per day for 5 days) were investigated in a double-blind placebo-controlled cross-over study in 4 patients with hyperekplexia. The pharmacodynamic parameters were startle reflexes, studied 3 times during the day. At each time, 2 trains of 10 auditive stimuli (113 dB) were given at intervals of 10 and 60 s. Startle movements were quantified with summed areas of EMG-bursts of the orbicularis oculi, sternocleidomastoid, biceps and thenar muscles. The degrees of stiffness and drowsiness were quantified with visual analogue scores (VAS) 10 times during the day, by both the patient and the observer. Clonazepam, but not vigabatrin, reduced startle activity significantly in both paradigms. The degree of stiffness and drowsiness was not significantly influenced by either drug.

Acoustic Stimulation↗

PubMed1991

Temporal resolution of gaps in noise by the rat is lost with functional decortication.

In Experiment 1 (n = 8), the rat's ability to detect brief gaps in white noise was measured by gap-produced inhibition of an acoustic startle reflex, elicited 100 ms after the gap. After bilateral application of KCl to the cortex, gaps as long as 15 ms provided no reflex inhibition; in contrast, the inhibitory threshold was between 2 and 4 ms in the saline control condition. In Experiment 2 (n = 13), noise pulses of 40, 50, or 70 dB were presented 20-500 ms before the startle stimulus, and in Experiment 3 (n = 5) noise offsets occurred so that the startle stimulus was presented at the end of a 2-30-ms gap. Noise pulses and offsets both inhibited reflex expression equally in saline- and KCl-treated animals. Differences between the normal (saline) functions of noise offsets and gaps suggest additional sensory processing with the longer lead time. The loss of gap sensitivity after KCl application indicates that gap processing, unlike pulses and offsets, depends on cortical mechanisms.

Animals↗

PubMedDate not supplied

Prepulses reduce the pain of cutaneous electrical shocks.

OBJECTIVE: Both the startle reflex elicited by an intense acoustic or tactile stimulus and the perceived intensity of that stimulus can be diminished by a weak "prepulse" that precedes the startling stimulus. The present study examined whether prepulses can also diminish the pain produced by an intense electrical stimulus similar to that used to treat life-threatening cardiac arrhythmias in conscious patients with implantable cardioverter/defibrillators or transcutaneous pacemakers. METHODS: Perceptual and pain thresholds for electrical shocks to the arm were determined in 20 adults. Participants then rated the painfulness of 25 electrical shocks that were 1.5 times the pain threshold (mean shock intensity, approximately 160 V) and either presented alone or preceded (at 40-60 ms) by weak electrical prepulses equal to or 25% above the perceptual threshold. RESULTS: Prepulses significantly reduced the pain produced by the intense shocks. Individuals with the lowest pain thresholds experienced the greatest pain reduction with prepulses. In these more sensitive individuals, the most effective prepulses reduced perceived pain by 26% across the entire test session and by 54% in the initial block of five shocks. CONCLUSIONS: Prepulses may be useful in diminishing the pain associated with the therapeutic electrical shocks used to treat cardiac arrhythmias.

Adult↗

PubMed2004

Sensorimotor gating deficits in transgenic mice expressing a constitutively active form of Gs alpha.

Schizophrenia is a complex disorder characterized by wide-ranging cognitive impairments, including deficits in learning as well as sensory gating. The causes of schizophrenia are unknown, but alterations in intracellular G-protein signaling pathways are among the molecular changes documented in patients with schizophrenia. Using the CaMKIIalpha promoter to drive expression in neurons within the forebrain, we have developed transgenic mice that express a constitutively active form of G(s)alpha (G(s)alpha(*)), the G protein that couples receptors such as the D(1) and D(5) dopamine receptors to adenylyl cyclase. We have also generated mice in which the CaMKIIalpha promoter drives expression of a dominant-negative form of protein kinase A, R(AB). Here, we examine startle responses and prepulse inhibition of the startle reflex (PPI) in these G(s)alpha(*) and R(AB) transgenic mice. G(s)alpha(*) transgenic mice exhibited selective deficits in PPI, without exhibiting alterations in the startle response, whereas no deficit in startle or PPI was found in the R(AB) transgenic mice. Thus, overstimulation of the cAMP/PKA pathway disrupts PPI, but the cAMP/PKA pathway may not be essential for sensorimotor gating. G(s)alpha(*) transgenic mice may provide an animal model of certain endophenotypes of schizophrenia, because of the similarities between them and patients with schizophrenia in G-protein function, hippocampus-dependent learning, and sensorimotor gating.

Acoustic Stimulation↗

PubMed1999

Late onset startle induced tics.

Three cases of late onset Gilles de la Tourette's syndrome are presented. The motor tics were mainly induced by an unexpected startling stimulus, but the startle reflex was not exaggerated. The tics developed after physical trauma or a period of undue emotional stress. Reflex tics may occur in Gilles de la Tourette's syndrome, but have not been described in late onset Tourette's syndrome. Such tics must be distinguished from psychogenic myoclonus and the culture bound startle syndromes.

Adult↗

PubMed1998

Startle potentiation: shock sensitization, aversive learning, and affective picture modulation.

This study investigated the size of, and relationship between, different modulatory effects of aversive stimulation on the acoustic startle reflex. This reflex is potentiated by shock exposure and associative shock conditioning (in animals and human volunteers) and unpleasant pictures (in human volunteers). In this study, dramatic sensitization of the probe-startle response was observed after shock exposure but not after a control task. Magnitude of sensitization was significantly larger than associative shock conditioning and picture modulation effects (also significant). Sensitization and conditioning scores showed modest, significant correlations with one another but not with picture modulation scores, consistent with animal data showing that partially overlapping brain mechanisms (i.e., amygdaloid-reticular projections) mediate these effects. The present results also indicate that sensitization of startle in human volunteers is a relatively more robust defensive response to aversive stimulation.

Acoustic Stimulation↗

PubMed1997

Effects of physostigmine on the startle in guinea pigs: two mechanisms involved.

The effects of the acetylcholinesterase inhibitor physostigmine (PHY) on the auditory startle reflex in guinea pigs were studied. The dose-response curve of PHY appeared bell shaped, with a maximum effect dose of 0.3 mg/kg. In addition, PHY altered the shape of the startle response. The muscarinic antagonist scopolamine (SCO) increased the startle at PHY doses above 0.3 mg/kg without affecting the PHY-induced shape of the response. The decreasing part of the startle due to PHY could be mimicked by the cholinesterase inhibitor soman in combination with 0.3 mg/kg PHY. It appeared that the decreasing part of the dose-response curve at higher dose levels is caused by the cholinesterase inhibitory action of PHY and, in view of the SCO effect, is mediated by muscarinergic receptors. The increasing part of the curve is probably caused by an agonistic action of PHY on neuronal nicotinergic receptors, because the antagonist mecamylamine (20 mg/kg) antagonized the effects of 0.3 mg/kg PHY both on the deflection and shape of the startle.

Acoustic Stimulation↗

PubMed1999

A startle-probe methodology for investigating the effects of active avoidance on negative emotional reactivity.

This study introduces a new methodology for investigating the impact of active avoidance and behavioral control on defensive emotional reactivity using the startle reflex. A between-groups yoked design was devised that permitted manipulation of participants' perception of control over an aversive event (loud noise) while precisely controlling motor activity and noxious stimulation. Startle responses to tactile (airpuff) probes were compared during threat/performance trials and neutral trials. Results conclusively demonstrated cross-modal startle potentiation in the context of a continuous motor performance task. Also, consistent with prior research, heart rate increased with perceived control. However, behavioral control per se did not appear to mitigate defensive emotion as indexed by startle potentiation. These findings indicate that other parameters may mediate the efficacy of active coping in addition to control, and that the startle probe paradigm can provide a valuable tool for investigating these parameters in future research.

Adolescent↗

PubMed1998

Withdrawal from i.v. cocaine "binges" in rats: ultrasonic distress calls and startle.

Human cocaine abusers report that they experience intense anxiety during withdrawal from chronic use or "binging". Because the symptoms of cocaine withdrawal are not easily observed, it has been difficult to develop an adequate animal model for cocaine withdrawal that detects anxiety-like behavior. The objective of the present study was to examine the effects of continuous access to i.v. self-administered cocaine on ultrasonic vocalizations (USVs) induced by startling tactile stimuli as a possible animal model for cocaine withdrawal. Five days after implantation of a jugular catheter, rats were placed into self-administration chambers with access to cocaine (0.25 mg/infusion). Once the animal had a stable response rate over 3 days, on a fixed schedule of reinforcement (FR5), they were given unlimited access to cocaine (0.25 mg/infusion) for 48 or 12 h. Subsequently, animals were exposed to 18 air puffs (20 or 10 psi) at 6, 24, 72 h, 7 and 14 days after the "binge". Rats that self-administered cocaine for 48 h and were subsequently startled with 20 psi stimuli increased the number of automatically recorded ultrasonic distress calls and showed an enhanced startle response at 6 h after the last cocaine infusion when compared to handled controls. Animals that self-administered cocaine for 48 h and were subsequently startled with 10 psi stimuli showed increased USVs and an enhanced startle reflex at both 6 and 24 h after the unlimited access. Animals that self-administered cocaine for 12 h also showed an increase in ultrasonic distress calls and enhanced startle responses to 10 psi tactile stimuli when compared to handled controls. USVs during cocaine withdrawal may be interpreted to reflect affective distress during the first 24 h after the last cocaine infusion of 12 or 48 of continuous access to drug.

Animals↗

PubMed2005

Prepulse inhibition and fear-potentiated startle are altered in tissue inhibitor of metalloproteinase-2 (TIMP-2) knockout mice.

The ability to discriminate between potential dangers and recall those stimuli is essential for survival. This emotional learning requires the involvement of higher brain structures, including the amygdala, hippocampus and related cortical structures. Long-term changes in synaptic transmission and structure are important for the establishment and consolidation of fear memory. The structural changes associated with this synaptic plasticity likely require alterations in the composition of the extracellular matrix (ECM). ECM integrity is maintained by the opposing action of matrix metalloproteinases (MMPs) and their specific inhibitors, tissue inhibitors of metalloproteinases (TIMPs). To date, no studies have examined the role of MMPs or TIMPs in conditioned fear. Here, we show that neither male nor female mice deficient in TIMP-2 (knockout) exhibit prepulse inhibition of the startle reflex, suggesting deficits in pre-attentional sensorimotor gating. In addition, knockout mice and mice expressing a mutant truncated TIMP-2 (knock-down) show deficits in fear-potentiated startle. This is the first report of a phenotype for the TIMP-2(-/-) mice and suggests that TIMP-2 may play a role in the synaptic plasticity underlying learning and memory.

Acoustic Stimulation↗

PubMed2006

Prenatal exposure to a cannabinoid receptor agonist does not affect sensorimotor gating in rats.

Clinical evidence suggests that prenatal exposure to cannabis may be conducive to long-term neurobehavioral impairments in executive and attentional domains. Such sensorimotor alterations might be related to disorders in gating functions. Hence, the present study was undertaken to assess the effects of long-term prenatal exposure to WIN 55,212-2, a potent cannabinoid receptor agonist, on prepulse inhibition of the acoustic startle reflex, a well-validated paradigm to test sensorimotor gating. In utero exposure to WIN 55,212-2 (0.5, 1 mg/kg, from day 5 to 20 of gestation) failed to alter startle magnitude in rats in comparison with controls. Similarly, prepulse inhibition of the startle was not significantly affected by such treatment, regardless of the age when behavioral testing was carried out (40, 60 or 80 days). Interestingly, prenatal treatment with WIN 55,212-2 (0.5 mg/kg, from day 5 to 20 of gestation) induced no differences in the prepulse inhibition-disrupting effects of apomorphine (0.125, 0.25 mg/kg, s.c.) and dizocilpine (0.05, 0.1 mg/kg, s.c.), suggesting that a prenatal exposure to a cannabinoid receptor agonist is likely unable to affect sensitivity of sensorimotor gating substrates to dopaminergic agonists and NMDA receptor antagonists. Our results show that prenatal exposure to cannabis does not affect reflex reactivity to environmental stimuli, ruling out that the observed impairments in executive functions are to refer to sensorimotor gating alterations.

Acoustic Stimulation↗

PubMed1995

Psychophysiological responses as indices of affective dimensions.

The startle reflex, facial electromyogram (EMG), and autonomic nervous system responses were examined during imagery varying in affective valence and arousal. Subjects (N = 48) imagined affective situations during tone-cued 8-s trials. Startle blink magnitudes were larger and latencies faster during negatively valent than during positively valent conditions and during high-arousal than during low-arousal conditions. Greatest heart rate acceleration and fastest and largest skin conductance responses to startle probes occurred during high-arousal imagery. Zygomatic and orbicularis oculi facial muscle activities were higher during high-arousal imagery, whereas corrugator muscle activity was higher during low-arousal imagery. Zygomatic and corrugator activity also varied with emotional valence. The startle and facial EMG responses are most parsimoniously organized by the negative affect (NA) and positive affect (PA) dimensions, respectively. This NA/PA framework integrates previous research, dimensional theories of emotional behavior, and physiological assessment of pathological emotion.

Adult↗

PubMed1999

Effects of alprazolam on the acoustic startle response in humans.

In the present study, we assessed the effects of the potent benzodiazepine alprazolam on the human acoustic startle response in healthy volunteers. Eight undergraduate students received single oral doses of placebo and alprazolam 2 mg on 2 separate days, according to a double-blind balanced crossover design. Electromyographic activity of the orbicularis oculi muscle was recorded 5, 7 and 11 h after drug administration. At each recording time, subjects received 21 acoustic stimuli (1 KHz, 116 dB, 50 ms duration) separated by variable intervals (8-30 s, mean 16.5 s). Consistent with previous results obtained for diazepam in humans, alprazolam significantly reduced the amplitude of the startle reflex. A patent increase in onset latency was also observed, this being a novel effect not previously described for benzodiazepines in human studies. Both effects were maximum at 5 h after dosing, the startle response experiencing a recovery as the drug disappeared from systemic circulation. These results indicate a potent inhibitory effect of alprazolam on baseline startle at the dose used, with a robust time-dependent recovery of initial values effectively counteracting between-session habituation.

Adult↗

PubMed1998

Effects of threat of shock, shock electrode placement and darkness on startle.

Fear can be elicited by physically-presented explicit threat stimuli or by more static contextual stimuli that are not an immediate source of danger. Research in both humans and animals suggest that fear produced by these two types of stimuli represents separate processes mediated by different brain structures. The present study used the startle reflex methodology to examine affective responses elicited by an explicit threat cue signalling a period of shock anticipation and by two types of contextual stimuli; darkness and attaching the shock electrodes. As expected, shock anticipation potentiated startle (fear-potentiated startle). Startle was also facilitated by darkness and by the placement of shock electrodes. Further, darkness increased fear-potentiated startle to an explicit threat cue, but did not affect the facilitation of startle produced by attaching the shock electrodes. It is suggested that affective responses to contextual stimuli should be considered when investigating both normal and pathological fear.

Adult↗

PubMed2006

Contingency awareness and fear inhibition in a human fear-potentiated startle paradigm.

Fear-potentiated startle is defined as an increase in the magnitude of the startle reflex in the presence of a stimulus that was previously paired with an aversive event. It has been proposed that a subject's awareness of the contingencies in the experiment may affect fear-potentiated startle. The authors adapted a conditional discrimination procedure (AX+/BX-), previously validated in animals, to a human fear-potentiated startle paradigm in 50 healthy volunteers. This paradigm allows for an assessment of fear-potentiated startle during threat conditions as well as inhibition of fear-potentiated startle during safety conditions. A response keypad was used to assess contingency awareness on a trial-by-trial basis. Both aware and unaware subjects showed fear-potentiated startle. However, awareness was related to stimulus discrimination and fear inhibition.

Acoustic Stimulation↗

PubMed1993

Lack of a temporal gradient of retrograde amnesia in rats with amygdala lesions assessed with the fear-potentiated startle paradigm.

It is well known that lesions of the hippocampal formation produce a temporally graded retrograde amnesia for certain types of memory. A similar pattern of results has been reported with amygdaloid lesions in avoidance learning (K.C. Liang et al., 1982). The present study examined the effects of posttraining amygdaloid lesions using a Pavlovian conditioning task, fear-potentiated startle, in which the amplitude of the acoustic startle reflex is increased when elicited in the presence of a cue (e.g., a light) previously paired with footshock. Electrolytic lesions of the amygdala given either 6 or 30 days after training blocked the expression of potentiated startle, indicating no temporal gradient of amnesia over these intervals in this paradigm. The effects of amygdaloid lesions on different measures of aversive learning are discussed.

Amygdala↗

PubMed2006

Midbrain pathways for prepulse inhibition and startle activation in rat.

The midbrain is essential for prepulse inhibition (PPI) of the startle reflex, but the exact neural circuits for PPI are not yet determined. Electrical stimulation of the superior colliculus (SC) or pedunculopontine tegmentum was used to characterize the neurons and pathways that mediate PPI and the activation of startle that also occurs at higher currents in the same sites. Startle was inhibited by prepulses in most, but not all SC sites, with the lowest intensity sites in intermediate layers of SC. PPI latencies in SC sites were 4-6 ms longer than in inferior colliculus, intercollicular nucleus or pedunculopontine sites. Contrary to previous serial models, there must be two parallel midbrain pathways for PPI, a faster auditory pathway from inferior colliculus to pedunculopontine tegmentum, and a slower multimodal SC output for PPI. Double-pulse stimulation of SC sites shows that PPI results from direct stimulation of neurons with moderate refractory periods (0.4-1.0 ms), similar to SC neurons that mediate contraversive turning responses. By contrast, startle activation occurring at higher currents in all SC sites (even sites where PPI could not be elicited) results from stimulation of very short refractory period neurons (0.3-0.5 ms) and very long refractory period neurons (1.0-2.0 ms), with startle inhibition often found from 0.5-1.0 ms. Startle activation appears to result from stimulation of short refractory period neurons in deep SC layers that mediate fear-potentiated startle, plus long refractory period substrates in more dorsal SC sites.

Animals↗

PubMed1995

Axons and synapses mediating electrically evoked startle: collision tests and latency analysis.

Davis et al. proposed that the primary acoustic startle reflex is mediated by synapses in the ventral cochlear nucleus (VCN), lateral lemniscus (LL) and caudal pontine reticular formation (PnC). The collision test was used here to estimate the locations of synapses mediating startle-like responses in these sites, and the conduction times between and across these synapses. Conditioning (C) and test (T) pulses were delivered to pairs of sites in chloral hydrate anaesthetized rats, and current thresholds for, and latencies of, hindlimb EMG responses were determined. When sites are axonally connected, thresholds increase at the same positive and negative C-T intervals ('symmetric collision'), but when sites are connected by strong synapses, thresholds increase at asymmetric C-T intervals. (i) Asymmetric collisions between VCN and contralateral PnC centered on a C-T interval of + 0.5 ms suggest a monosynaptic connection in ventrolateral pons (VLP), near LL. (ii) Asymmetric collisions between VCN and contralateral medulla centered on a C-T interval of + 0.85 to + 1.0 ms suggest a disynaptic connection. (iii) Asymmetric collisions between VLP and ipsilateral medulla centered on a C-T interval of 0.2-0.4 ms suggest a monosynaptic connection in PnC, as shown previously in freely behaving animals [32]. (4) Symmetric collisions between VLP and rostral PnC, and between caudal PnC and medulla suggest fast axonal connections. Latency differences between electrode pairs were generally similar to collision-derived conduction times. From these, conduction times and transmission times were estimated for each axon bundle and synapse in the circuit.

Animals↗