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PubMed2005

Relationship of prepulse inhibition of the startle reflex to attentional and executive mechanisms in man.

Prepulse inhibition (PPI) of the startle reflex at short lead intervals is thought to reflect the operation of a preattentive "sensorimotor gating" mechanism, which suggests that processing of the prepulse stimulus should not be modulated prior to its inhibitory effects on startle. To test this hypothesis, we examined whether PPI is affected following habituation to the prepulse. PPI was measured in two sessions associated with either the presence (habituation condition) or the absence (control condition) of prepulse repetition. There was a trend for prepulse repetition to reduce the effectiveness of that prepulse in inhibiting the startle response. We also explored the relationship of PPI to scores in tests of selective and sustained attention and planning ability. Overall PPI performance was correlated to performance indices of planning ability and there was a trend level correlation with scores in selective but not sustained attention tests. These preliminary results merit further investigation.

Acoustic Stimulation↗

PubMed1997

Repeated stress, like vasopressin, sensitizes the excitatory effects of corticotropin releasing factor on the acoustic startle reflex.

In the rat, evidence now suggests a neurotransmitter function for the neuropeptides arginine vasopressin (AVP) and corticotropin releasing factor (CRF), implicating them in various autonomic, behavioral, and neuroendocrine responses to stress. Repeated AVP/CRF release in the pituitary portal circulation, due to stress, sensitizes and potentiates the release of ACTH from the anterior pituitary. Using a neuroanatomically well-defined behavior, the acoustic startle reflex in the rat, we sought to determine whether an interaction between AVP, CRF and stress might also occur centrally as measured by increased behavioral sensitivity to AVP or CRF given directly into the brain. The first experiment tested whether repeated intraventricular (i.c.v.) infusion of AVP would lead to an increase in the excitatory effect of a subthreshold dose of AVP on the acoustic startle reflex when infused 48 h later. Different groups of rats were infused with various doses of AVP (0.3, 3, or 30 ng) or vehicle on Day 1 and tested for startle over the next 60 min. On Day 2, 48 h later, all animals were infused with a single dose of AVP (300 pg) and tested for startle. Infusion of AVP on Day 1 did not increase startle consistently at any dose, but did lead to a sensitized excitatory effect of AVP on startle on Day 2 which was non-monotonically related to the dose of AVP given on Day 1. Experiment 2 tested whether AVP on Day 1 would sensitize the excitatory effects on startle of CRF given i.c.v. on Day 2. Different groups of rats were infused i.c.v. with various doses of AVP (10, 30, 100, 300 pg) or vehicle on Day 1. On Day 2, 48 h later, all rats were infused with a subthreshold dose of CRF (0.25 microg). Infusion of AVP on Day 1 led to a sensitized excitatory effect of CRF on startle on Day 2 which was non-monotonically related to the dose of AVP given on Day 1. In experiment 3, we tested whether footshocks given on Day 1 would sensitize the excitatory effect of CRF on startle tested 48 h later. Different groups were given footshocks (0.2, 0.4, 0.8, 1.6 mA) on Day 1. On Day 2, 48 h later, all rats were infused with a subthreshold dose of CRF (0.25 microg). Footshocks given on Day 1 led to a sensitized excitatory effect of CRF on startle on Day 2 which was non-monotonically related to the intensity of footshock on Day 1. Taken together, these results suggest that an interaction between AVP, CRF and stress may occur centrally, consistent with other studies showing similar interactions peripherally. This may provide a model system for analyzing how prior stress leads to enhanced behavioral reactions to subsequent stressors and a mechanism to explain dysregulation of the stress response.

Acoustic Stimulation↗

PubMed1984

Startle reflex inhibition in the rat: its persistence after extended repetition of the inhibitory stimulus.

Startle reflexes to intense sound bursts are inhibited by weak stimuli that briefly precede their elicitation. In three experiments the startle stimulus (a 110-dB SPL tone burst) was presented 100 ms after the final link in a train of stimuli, the length of the train varying from 1 to 1,000, its repetition rate varying from 1 per s to 10 per s, and its constituents being 40 dB or 50 dB white noise bursts of 25 ms duration. Inhibition was invariant across train length and repetition rate. In a final experiment the startle stimulus was presented a variable interval after the final link, from 40 ms to 1280 ms, with 1 or 100 noise bursts (50 dB) in the train. Inhibition developed more rapidly following the last member of the 100-stimulus train, suggestive of a "priming" or sensitization effect of stimulus repetition, but its overall strength and subsequent rate of decay were not different in the two conditions. The general persistence of inhibition following these extended series of stimuli reveals that reflex inhibition must be the outcome of a fixed and obligatory process associated with sensory input.

Acoustic Stimulation↗

PubMed1995

Prepulse inhibition of the acoustic startle reflex using visual and auditory prepulses: disruption by apomorphine.

The amplitude of the acoustic startle reflex can be reduced reliably when preceded at short intervals by a weak stimulus (prepulse) which itself does not elicit startle. The magnitude of this prepulse inhibition effect is attenuated by several dopamine agonists, such as apomorphine, especially when there is a relatively small difference between the intensity of the prepulse and the intensity of the background noise over which the prepulse is superimposed. One goal of the present experiment was to test the generality of this disruptive effect of apomorphine on prepulse inhibition by using either an auditory prepulse that included both a change in intensity and a change in frequency relative to the background noise or a visual prepulse stimulus. Apomorphine reduced auditory prepulse inhibition when induced by a small change in stimulus intensity, but not when induced by a change in both intensity and frequency. Apomorphine consistently reduced visual prepulse inhibition with a complete blockade at 100-ms test interval. However, it did not fully block the usual reduction in startle onset latency or even attenuate the increase in startle amplitude when a visual prepulse was presented 5, 10 or 15 ms before the startle stimulus. Consistent with conclusions from other laboratories using auditory prepulse inhibition, these data suggest that apomorphine did not prevent the animal from detecting prepulse presentation under conditions where the drug completely blocked prepulse inhibition. Moreover, they indicate that the blockade of prepulse inhibition by apomorphine was independent of prepulse modality, adding generality to the original finding. Visual prepulse inhibition may be a useful alternative procedure for evaluating the effects of drugs on this attentional process.

Acoustic Stimulation↗

PubMed1989

Neural substrates for long-term habituation of the acoustic startle reflex in rats: a 2-deoxyglucose study.

Autoradiography with [14C]2-deoxyglucose was used to examine the functional activity of the rat brain during long- and short-term habituation of the acoustic startle reflex. Long-term habituated rats, when compared to short-term rats, showed an enhanced metabolic activation of the auditory system, with the exclusion of thalamocortical levels. Regional metabolic increases were also located within the cerebellum and its major input-output structures. In contrast, the midbrain reticular formation and its ascending thalamocortical activating system showed a widespread metabolic suppression. The findings provide the first map of structures in a mammalian brain with learning-related metabolic alterations dependent on long-term habituation.

Acoustic Stimulation↗

PubMed1999

Dopamine antagonists in the orbital prefrontal cortex reduce prepulse inhibition of the acoustic startle reflex in the rat.

Schizophrenia is characterized by, among other things, (a) information processing deficits that have been indexed by a number of measures, including deficits in prepulse inhibition (PPI) of the acoustic startle reflex; and (b) pathophysiology of the frontal lobe. Recent studies have implicated the prefrontal cortex (PFC) in the modulation of PPI in rats. These studies suggest that dopamine (DA) ablation of the PFC (using 6-OHDA) leads to disruption of PPI. To better understand the role of DA type 1 (D1) and type 2 (D2) receptors in the modulation of PPI, we investigated the effects of two pharmacologically distinct DA antagonists on the modulation of PPI. Microinjection of SCH23390 (a D1 antagonist) into the orbital PFC markedly decreased PPI (at 0.1, 0.5, and 1.5 microg), whereas raclopride (a D2 antagonist) decreased PPI at some doses (0.1 and 0.5 mg/ml) but not at others (5.0 microg). We conclude that both D1 and D2 receptors mediate the cortical modulation of PPI.

Acoustic Stimulation↗

PubMed1995

The effects of different doses of caffeine on habituation of the human acoustic startle reflex.

Research in this laboratory showed that caffeine (4 mg/kg) delays habituation of the acoustic startle reflex in humans. The present study examined the effects of 2- and 6-mg/kg doses of caffeine on acoustic startle habituation in moderate-high and low caffeine users. Eyeblink responses to 30 trials of 85-dB noise stimuli were measured beginning 30 min after oral ingestion of either placebo or 2 or 6 mg/kg of caffeine. The 2-mg/kg dose of caffeine delayed startle habituation in both moderate-high and low caffeine users. The 6-mg/kg dose produced no differential effects on startle responding from placebo. In moderate-high users, following habituation, startle responding was smaller in the placebo condition compared to both caffeine conditions. In low users there were no differences in posthabituation responding between doses, suggesting that this dose effect is dependent on a history of chronic caffeine usage.

Acoustic Stimulation↗

PubMed1995

Affective modulation of the startle reflex in schizophrenic patients.

Startle-elicited blinks were measured during the presentation of affective slides in order to investigate emotional responsiveness in 24 male healthy subjects and 34 male schizophrenic patients. Although the two groups did not differ with regard to their subjective and autonomic responses to the slide stimuli, there was a significant difference between the groups in their responses to the startle probes. Patients rated low in affective expression showed a linear response pattern comparable to that of normal controls with largest amplitudes during unpleasant slides and smallest during pleasant slides. Patients without apparent deficit in affective expression showed a quadratic relationship with smaller blink amplitudes during both pleasant and unpleasant slides. Diminished affective expression rated on the basis of a clinical interview is not associated with a general attenuation of the blink reflex or of its modulation by exposure to emotional slides. Thus, we found no indication of an impairment in the perception of affective stimuli nor of reduced appreciation of pleasant stimuli (anhedonia) in these patients.

Adult↗

PubMed1989

Prepulse rise time and startle reflex modification: different effects for discrete and continuous prepulses.

The rise time of an auditory prepulse was varied to determine whether the onset transient of the prepulse is of primary importance in the modification of the acoustic startle reflex. In Experiment 1, 20-ms long discrete prepulses were presented at a lead time of 150 ms, and prepulse rise time was varied from 0.1 to 20 ms. Although all prepulses resulted in decreased response amplitude (inhibition of startle), varying rise time from 0.1 to 20 ms had no effect on reflex modification. These results suggest that the startle response is not sensitive to prepulse rise time changes in the range used here. In Experiment 2, continuous prepulses (in which lead time equals duration) were presented. Several of these prepulses had a lead time of 150 ms and rise times ranging from 0.1 to 150 ms, whereas others had a rise time of 0.1 ms and lead times of 50 to 150 ms. The results showed that only the fast-rising, 50-ms lead time prepulse decreased response amplitude, with the other prepulses having no effect on amplitude, relative to control responding. Rise time changes generally had no effect on responding, but responses were larger at longer lead times than at shorter lead times. Response probability was inhibited by fast-rising prepulses at lead times of 50 to 130 ms. Together with the results of Experiment 1, these findings suggest that startle reflex inhibition is determined by the onset of a prepulse, and that this inhibition is not sensitive to small changes in prepulse rise time.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed2004

Influence of neonatal short-term reduction in brainstem alpha2A-adrenergic receptors on receptor ontogenesis, acoustic startle reflex, and prepulse inhibition in rats.

Neonatal treatments can disrupt prepulse inhibition (PPI) of startle response later in life. Alpha2A-adrenergic receptors (alpha2A-ARs) regulate the release of brain neurotransmitters that may influence PPI. The authors examined the effects of short-term reduction in the neonatal brainstem alpha2A-ARs on subsequent development of this receptor system and acoustic startle reflex in rats. Administration of antisense oligodeoxynucleotide complementary to the alpha2A-ARs on Days 2-4 of life reduced receptor expression in the brainstem by Day 5. The treatment increased alpha2-AR numbers in the cortex, hippocampus, and amygdala at 40 days of age, and in cortex and hypothalamus at 90 days of age. Transient increases in hippocampal and amygdalar alpha2-ARs were accompanied by attenuation of acoustic startle response and impairment of PPI.

Adrenergic alpha-Antagonists↗

PubMed2006

Lateralization of the startle reflex circuit in humans: an examination with monaural probes following unilateral temporal lobe resection.

Startle reflex (SR) modulation elicited by monaural probes during affective picture viewing was investigated in patients following left temporal lobectomy (LTL; n = 8) and right temporal lobectomy (RTL; n = 10) and in controls (n = 18). All patients had undergone anteromedial temporal lobe (ATL) resection. LTL participants exhibited attenuated overall SR magnitude. Affective SR modulation in controls was significant for left ear probes, at both eyes, but not for right ear probes. RTL but not LTL participants displayed significant startle attenuation during pleasant picture viewing. Results suggest that monaural startle probes primarily activate structures in the ipsilateral ATL and that the ATLs are interconnected, with the left ATL more critical in perceiving arousing properties of affective stimuli, necessary for affective SR modulation.

Adult↗

PubMed2003

Nicotine and ethanol enhancements of acoustic startle reflex are mediated in part by dopamine in C57BL/6J mice.

Nicotine has been shown to have additive as well as antagonistic effects on behavior stimulated by ethanol. Here, we examine the effects of nicotine, ethanol, and the coadministration of each drug on acoustic startle responding in C57BL/6J mice. Mice were tested at a range of decibel levels (80-115 dB, 5 dB increments), with administration of 0.031, 0.062, 0.125, and 0.25 mg/kg nicotine or 0.5, 1.0, 1.5, and 2.0 g/kg ethanol. Nicotine and ethanol each caused an increase in the acoustic startle response at the highest and lowest doses tested, respectively. Mecamylamine, a nicotinic receptor antagonist, administered in combination with nicotine or ethanol attenuated these increases in acoustic startle responding. Nicotine and ethanol, administered together, did not produce greater enhancement of startle than when administered alone. Haloperidol (1 mg/kg) was administered in combination with nicotine or ethanol to investigate if dopamine modulated nicotine or ethanol enhancement of acoustic startle. It was found that the increase in acoustic startle responses observed with ethanol or nicotine was attenuated by haloperidol. Thus, ethanol or nicotine may enhance the acoustic startle reflex through a common dopaminergic mechanism.

Acoustic Stimulation↗

PubMed2005

The effects of temporary inactivation of the core and the shell subregions of the nucleus accumbens on prepulse inhibition of the acoustic startle reflex and activity in rats.

The nucleus accumbens can be dissociated into at least two subregions: a 'core' and a 'shell'. Using temporary chemical inactivation of these subregions, we investigated whether they are differentially involved in the regulation of prepulse inhibition (PPI) of the acoustic startle reflex and activity. For this purpose, rats were bilaterally implanted with guide cannulae aimed at either the core or the shell and infused with the GABA(A) receptor agonist muscimol (0.5 microg/0.2 microl per side). The control group consisted of vehicle infused and unoperated rats. To ascertain the region selectivity of the infusions, 0.2 microl of [3H]muscimol was infused into either the core or the shell of an additional group of rats. The behavioral results demonstrated that in comparison to the control group, inactivation of the core led to a loss of the prepulse intensity dependency of PPI. Moreover, core inactivation resulted in akinesia directly after infusion, but in hyperactivity 24 and 72 h thereafter in contrast to the control group. In both experiments, inactivation of the shell was ineffective compared to controls. Analysis of the autoradiograms revealed that the spread of drug into the other subregion was minimal, supporting the region selectivity of the inactivation. These results lend further support to the existence of a functional dissociation between the core and the shell, with the former being preferentially involved in PPI and locomotion. The persistent hyperactivity after the muscimol infusion into the core could be explained by compensatory mechanisms taking place in the nucleus accumbens.

Akathisia, Drug-Induced↗

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↗

PubMed1981

Effects of alpha-MSH and beta-endorphin on startle reflex in rat.

Twelve rats received peripheral injections (20 micrograms/rat) of alpha-MSH, beta-endorphin or the vehicle solution and were subsequently tested for the motor and cardiac responses to repeated presentations of intense acoustic stimuli. Each subject received all treatments in a counterbalanced order with 3-day periods between each session. beta-Endorphin tended to decrease the amplitude of the habituated motor startle reflex, while alpha-MSH produced a slight increase in basal heart rate during the habituation session. Neither peptide had any effect on the cardiac response to intense acoustic stimulation. The effects of the two peptides were not directly antagonistic but they are consistent with the hypothesis that complex attentional processes were facilitated by MSH/ACTH fragments and inhibited by the endorphins.

Animals↗

PubMed2006

Antipsychotics improve Delta9-tetrahydrocannabinol-induced impairment of the prepulse inhibition of the startle reflex in mice.

Recently, cannabinoid receptor agonists have been reported to impair prepulse inhibition (PPI) of the startle reflex. In the current study, we examined the effect of Delta9-tetrahydrocannabinol (THC), the principal psychoactive component of cannabis, on the PPI, and found that THC (10 mg/kg, i.p.) impaired the PPI concomitant with a decrease in the startle response. Antipsychotics such as haloperidol (0.3 mg/kg, i.p.) and risperidone (0.1 mg/kg, i.p.), which are potent dopamine D2 receptor antagonists, and SR141716 (10 mg/kg, i.p.), a CB1 cannabinoid receptor antagonist, reversed these THC-induced PPI deficits. Moreover, THC (10 mg/kg) increased dopamine (DA) release in the nucleus accumbens but not medial prefrontal cortex over a 50-100-min period (time of PPI test) after treatment, and SR141716 (10 mg/kg) reversed this increase in DA release induced by THC. These results suggest that dopaminergic hyperfunction in the nucleus accumbens may be involved in THC-induced PPI deficits.

Acoustic Stimulation↗

PubMed2000

Antipsychoticlike effects of amoxapine, without catalepsy, using the prepulse inhibition of the acoustic startle reflex test in rats.

BACKGROUND: The dibenzoxazepine amoxapine was introduced as an antidepressant but has shown antipsychoticlike activity in a number of animal screening tests. A recent positron emission tomography study showed a 5-HT(2)/D(2) receptor occupancy profile of amoxapine that is very similar to that of established atypical antipsychotics. Schizophrenics display deficits in sensory gating mechanisms, such as prepulse inhibition (PPI) of the acoustic startle reflex. A similar deficit can be produced by dopamine (DA) and by 5-HT(2A/C) receptor agonists in rats. Antipsychotic compounds reverse this effect. METHODS: Effects of amoxapine on apomorphine- or 1-(2, 5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI)-induced disruption of PPI were studied in adult male Sprague-Dawley rats. The extrapyramidal side effect (EPS) liability of amoxapine was assessed using the inclined grid catalepsy (CAT) test. Statistical analyses were performed by analysis of variance (ANOVA) for fully repeated measures (PPI) and by the Kruskal-Wallis one-way ANOVA by ranks (CAT). RESULTS: Apomorphine (0.5 mg/kg) produced a significant reduction in PPI compared with the case of rats in the saline control group. Pretreatment with amoxapine (10 mg/kg) significantly attenuated the apomorphine-induced disruption of PPI. DOI (0.5 mg/kg) significantly reduced PPI compared with saline controls. Pretreatment with amoxapine (5 or 10 mg/kg) produced a significant attenuation of the DOI-induced disruption of PPI. Amoxapine by itself did not alter PPI. Amoxapine (5 or 10 mg/kg) did not produce CAT. CONCLUSIONS: The DA D(2)/5-HT(2) receptor antagonist amoxapine produced an antipsychoticlike reversal of both apomorphine- and DOI-induced disruption of PPI. Furthermore, the same doses of amoxapine that reversed disruption of PPI did not produce CAT. The results confirm and lend further support to the results of previous studies on amoxapine, suggesting that amoxapine might possess antipsychotic activity with little propensity for producing EPS.

Acoustic Stimulation↗

PubMed2006

Neurophysiology of nocturnal enuresis: evoked potentials and prepulse inhibition of the startle reflex.

Nocturnal enuresis is a genetically determined maturational disorder of the central nervous system. Lack of arousal and an inhibition deficit of the micturition reflex have been found as the main dysfunctions leading to wetting during sleep. Both are mediated by nuclei in the brainstem. Therefore, evoked potentials (brainstem auditory evoked potential [BAEP], visual evoked potential [VEP], event-related late acoustic-evoked potential [P300]), and the prepulse inhibition (PPI) of the startle reflex were assessed to further evaluate the brainstem deficit compared with cortical function. Thirty-seven children with nocturnal enuresis, aged 8 years to 14 years 8 months (mean age 10y 7mo [SD 1y 10mo]; 27 males, 10 females) were compared with 40 controls (mean age 10y 7mo [SD 1y 6mo]; 17 males, 23 females). Left interpeak latencies I-III and I-V of the BAEP were increased in children with nocturnal enuresis. VEP measures did not differ between patients and controls. However, children with a positive family history of enuresis showed a shorter latency towards N75 and P100 than children without such a family history. P300 and PPI measures did not differ. We conclude that this strongly supports the postulation of a maturational deficit of the brainstem in nocturnal enuretic children. The increased interpeak latencies I-III and I-V of the BAEP support the hypothesis of an arousal deficit mediated by delayed maturation of brainstem function. Differences in VEP latencies might point towards functional cortical differences in children with a family history of nocturnal enuresis.

Arousal↗