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Michael Davis - One of the best experts on this subject based on the ideXlab platform.
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Acoustic Startle reflex in rhesus monkeys: a review.
Reviews in the neurosciences, 2008Co-Authors: Michael Davis, Elena A. Antoniadis, David G. Amaral, James T. WinslowAbstract:Modulation of the acoustic Startle response is a simple and objective indicator of emotionality and attention in rodents and humans. This finding has proven extremely valuable for the analysis of neural systems associated with fear and anxiety. Until recently, there have been few efforts to develop acoustic Startle measurement in non-human primates. Here we review recent work in which whole body acoustic Startle amplitude has been measured in rhesus monkeys. Initial studies revealed that the amplitude of whole body Startle in monkeys, as in rodents and humans, is directly proportional to acoustic stimulus intensity and gradually habituates with repeated exposures. Presentation of a weak acoustic stimulus 25-5,000 msec before a Startle stimulus reduces Startle amplitude by 40-50% depending on inter-stimulus interval length (prepulse inhibition). We have also measured significant fear-potentiated Startle in the presence of a visual stimulus after pairing it with an inescapable pulse of pressurized air (fear-potentiated Startle). This effect was reduced by diazepam and morphine, but not by buspirone. Ibotenic acid-induced lesions of the amygdala prevented the acquisition of fear-potentiated Startle but, remarkably, did not prevent the expression of fear-potentiated Startle when fear conditioning was carried out prior to the lesion. Finally, we have developed an objective measure of fear inhibition in monkeys using a novel conditioned inhibition procedure identical to one used in rats and humans. Our data demonstrate that acoustic Startle in non-human primates successfully bridges rodent and human research. The opportunity now emerges to link concepts developed in rodents to the more complex neuroanatomical and cognitive processes common to monkeys and humans.
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role of the primate amygdala in fear potentiated Startle effects of chronic lesions in the rhesus monkey
The Journal of Neuroscience, 2007Co-Authors: Elena A. Antoniadis, Michael Davis, James T. Winslow, David G. AmaralAbstract:In experiment 1, we assessed the role of the primate amygdala and hippocampus in the acquisition of learned fear measured with fear-potentiated Startle. Three groups of six rhesus monkeys were prepared with bilateral ibotenic acid lesions of the amygdaloid complex and the hippocampus or were sham operated. Selective ibotenic acid lesions of the amygdala, but not the hippocampus, blocked the acquisition of fear-potentiated Startle. In experiment 2, we assessed the role of the primate amygdala in the expression of fear-potentiated Startle. Surprisingly, animals that sustained amygdala damage after they successfully learned fear-potentiated Startle expressed normal fear-potentiated Startle, despite a complete amygdala lesion based on magnetic resonance imaging assessments. These results suggest that although the amygdala is necessary for the initial acquisition of fear-potentiated Startle, it is not necessary for the retention and expression of fear-potentiated Startle. These findings are discussed in relation to the role of the amygdala in emotional learning and in cross-species comparisons of emotional behavior.
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Acoustic Startle, prepulse inhibition, and fear-potentiated Startle measured in rhesus monkeys.
Biological psychiatry, 2002Co-Authors: James T. Winslow, Lisa A. Parr, Michael DavisAbstract:Abstract Background: Modulation of the acoustic Startle response is a simple and objective indicator of emotionality and attention in rodents and humans. This finding has proven extremely valuable for analysis of neural systems associated with fear and anxiety. Until recently, there have been few efforts to develop acoustic Startle measurement in nonhuman primates. We report here development of a whole-body acoustic Startle protocol in rhesus monkeys. Methods: Eight juvenile rhesus monkeys were tested in a new whole-body (somatic) acoustic Startle protocol. Startle responses were assessed in three paradigms: 1) stimulus intensity-response amplitude, 2) prepulse inhibition (PPI), and 3) fear-potentiated Startle. Results: Initial studies revealed that the amplitude of whole-body Startle in monkeys, as in rodents and humans, is directly proportional to acoustic stimulus intensity and gradually habituates with repeated exposures. Presentation of a weak acoustic stimulus 45–2020 msec before a Startle stimulus reduces Startle amplitude by 40%–50%, depending on interstimulus interval length (PPI). We have also measured significant potentiated Startle amplitude in the presence of a visual stimulus after pairing it with an inescapable pulse of pressurized air (fear-potentiated Startle). Conclusions: Our data demonstrate that acoustic Startle in nonhuman primates successfully bridges rodent and human research in two broad areas: stimulus-response relationships and behavioral plasticity represented by habituation, PPI, and fear potentiation. The opportunity now emerges to link concepts developed in rodents to the more complex neuroanatomical and cognitive processes common to monkeys and humans.
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Fear: Potentiation of Startle
International Encyclopedia of the Social & Behavioral Sciences, 2001Co-Authors: Michael DavisAbstract:The fear-potentiated Startle paradigm measures conditioned fear by an increase in the amplitude of the acoustic Startle reflex elicited in the presence of a cue previously paired with shock. Fear-potentiated Startle is blocked selectively by drugs that reduce fear in humans, making it a valid test of conditioned fear in rats. The conditioned stimulus in rats activates the central nucleus of the amygdala through a pathway involving the auditory or visual thalamus, which projects via the perirhinal cortex to the amygdala. Pain information converges with conditioned stimulus information at the amygdala via parallel pathways from the posterior intralaminal nuclei of the thalamus and the insular cortex. Certain glutamate antagonists infused into the basolateral amygdala block the acquisition, but not the expression, of fear-potentiated Startle, suggesting that this may be the site of plasticity during fear acquisition. The central nucleus of the amygdala projects directly and indirectly to the acoustic Startle pathway so as to modulate the Startle response. Fear-potentiated Startle also can be measured in humans, using the eyeblink component of the Startle reflex. Thus far, there is a close correspondence between results gathered in rats and humans, and the amygdala seems to be involved in fear-potentiated Startle in humans.
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double dissociation between the involvement of the bed nucleus of the stria terminalis and the central nucleus of the amygdala in Startle increases produced by conditioned versus unconditioned fear
The Journal of Neuroscience, 1997Co-Authors: David L Walker, Michael DavisAbstract:The amplitude of the acoustic Startle response is reliably enhanced when elicited in the presence of bright light (light-enhanced Startle) or in the presence of cues previously paired with shock (fear-potentiated Startle). Light-enhanced Startle appears to reflect an unconditioned response to an anxiogenic stimulus, whereas fear-potentiated Startle reflects a conditioned response to a fear-eliciting stimulus. We examine the involvement of the basolateral nucleus of the amygdala, the central nucleus of the amygdala, and the bed nucleus of the stria terminalis in both phenomena. Immediately before light-enhanced or fear-potentiated Startle testing, rats received intracranial infusions of the AMPA receptor antagonist 2, 3-dihydroxy-6-nitro-7-sulphamoylbenzo(F)-quinoxaline (3 microg) or PBS. Infusions into the central nucleus of the amygdala blocked fear-potentiated but not light-enhanced Startle, and infusions into the bed nucleus of the stria terminalis blocked light-enhanced but not fear-potentiated Startle. Infusions into the basolateral amygdala disrupted both phenomena. These findings indicate that the neuroanatomical substrates of fear-potentiated and light-enhanced Startle, and perhaps more generally of conditioned and unconditioned fear, may be anatomically dissociated.
Christian Grillon - One of the best experts on this subject based on the ideXlab platform.
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the benzodiazepine alprazolam dissociates contextual fear from cued fear in humans as assessed by fear potentiated Startle
Biological Psychiatry, 2006Co-Authors: Christian Grillon, Johanna M.p. Baas, Daniel S Pine, Shmuel Lissek, Megan Lawley, Valerie Ellis, Jessica LevineAbstract:Background The Startle reflex is potentiated by aversive states. It has been proposed that phasic Startle potentiation to a threat cue and sustained Startle potentiation to contextual stimuli reflect distinct processes mediated by different brain structures. The present study tested the hypothesis that alprazolam would reduce the sustained Startle potentiation to contextual threats but not the Startle potentiation to a threat cue. Methods Sixteen healthy subjects received each of four treatments: placebo, .5 mg of alprazolam, 1 mg of alprazolam, and 50 mg of diphenhydramine (Benadryl) in a crossover design. Participants were exposed to three conditions, including one in which predictable aversive shocks were signaled by a cue, a second in which shocks were administered unpredictably, and a third condition in which no shocks were anticipated. Acoustic Startle were delivered regularly across conditions. Results Phasic Startle potentiation to the threat cue in the predictable condition was not affected by alprazolam. In contrast, the sustained increase in Startle in the predictable and unpredictable conditions was reduced significantly by the high dose of alprazolam. Conclusions Startle responses to an explicit threat cue and to an aversive context are psychopharmacologically distinct, suggesting that they may represent functionally dissociable aversive states.
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families at high and low risk for depression a three generation Startle study
Biological Psychiatry, 2005Co-Authors: Christian Grillon, Virginia Warner, Jeffrey Hille, Kathleen R Merikangas, Gerard E Bruder, Craig E Tenke, Yoko Nomura, Paul Leite, Myrna M WeissmanAbstract:Background Anxiety symptoms might be a vulnerability factor for the development of major depressive disorder (MDD). Because elevated Startle magnitude in threatening contexts is a marker for anxiety disorder, the present study investigated the hypothesis that enhanced Startle reactivity would also be found in children and grandchildren of individuals with MDD. Methods The magnitude of Startle was investigated in two tests (anticipation of an unpleasant blast of air and during darkness) in children (second generation) and grandchildren (third generation) of probands with (high risk) or without (low risk) MDD (first generation). Results Startle discriminated between the low- and high-risk groups. In the probands’ children, the high-risk group showed increased Startle magnitude throughout the fear-potentiated Startle test. In the probands’ grandchildren, a gender-specific abnormality was found in the high-risk group with high-risk girls, but not boys, exhibiting elevated Startle magnitude throughout the procedure. Conclusions Increased Startle reactivity in threatening contexts, previously found in patients with anxiety disorder and in children of parents with an anxiety disorder, might also constitute a vulnerability marker for MDD. These findings suggest that there might be common biologic diatheses underlying depression and anxiety.
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Comments on the use of the Startle reflex in psychopharmacological challenges: impact of baseline Startle on measurement of fear-potentiated Startle.
Psychopharmacology, 2002Co-Authors: Christian Grillon, Johanna M.p. BaasAbstract:A large body of experimental literature indicates that theStartle reflex is a sensitive measure of fear and anxiety. Inboth humans and animals, the Startle reflex is increasedwhen the Startle-eliciting stimulus is presented in thepresence of a cue that signals an aversive event, such as ashock (Davis and Astrachan 1978; Grillon et al. 1991). Inanimals, drugs that reduce anxiety in humans, such asdiazepam and buspirone, reduce this so-called fear-potentiated Startle effect (Davis et al. 1993). This findingsuggests that the fear-potentiated Startle methodology is auseful procedure to investigate the anxiolytic properties ofdrugs in humans. However, the emerging literature on theeffects of benzodiazepines on fear-potentiated Startle tothreat in humans has been contradictory. Benzodiazepineshave been shown to reduce fear-potentiated Startle insome studies (Bitsios et al. 1999; Riba et al. 2001), but notin others (Riba et al. 1999; Baas et al. 2002). In all thesestudies, fear-potentiated Startle was expressed as adifference score between Startle amplitude in the threatcondition minus Startle amplitude in a no threat controlcondition. The objective of this paper is to call attentionto the issue that difference scores may not always beappropriate to express fear-potentiated Startle. A problemwith difference scores is that they may be dependent onbaseline Startle levels, which are themselves affected(reduced) by the sedative side-effect of benzodiazepines(Rodriguez-Fornells et al. 1999). Possibly, a reduction ofabsolute fear-potentiated Startle by benzodiazepines couldbe due to a non-specific (i.e. non-anxiolytic) effect onbaseline Startle reactivity.The concern that differences in baseline levels mayaffect fear-potentiated Startle has been raised in theanimal literature (Davis 1992; Walker and Davis 2000). Apossible solution to equate baseline levels across drugconditions was proposed, namely using different Startleprobe intensities (Davis 1992). An additional concern iswhether the dynamics of the Startle system changes at theextremes of the scale (cf. floor and ceiling effects). Forthese reasons, one should be cautious in drawing defin-itive conclusions on the modulation of fear-potentiatedStartle by a pharmacological challenge that alters baselineStartle levels. In this report, we illustrate how differencesin baseline levels can affect fear-potentiated Startle.Consequently, decisions on how to express fear-potenti-ated Startle (e.g. difference score versus ratio) criticallyimpact the results.Little is known about the relationship between baselineStartle and fear-potentiated Startle. It is likely that changesin baseline values arise from a variety of factors that mayor may not affect the expression of fear-potentiatedStartle. Approaches based on difference scores are basedon the critical assumption that fear-potentiated Startle isadditive rather than multiplicative with respect to baselineStartle levels. In other words, a given absolute differencehas the same significance across levels of the scale (forinstance, the difference between 50 and 60 V is the sameas the difference between 200 and 210 V). The datapresented here show that this may not always be true.The way in which different factors interact to modulateStartle is not a statistical question, but an empirical one.Fear-potentiated Startle may be additive or multiplicative,depending on the factors that cause the change in baselineStartle. Only empirical studies can provide us with anunderstanding of the underlying mechanisms that affectbaseline Startle and its modulation. To illustrate this point,we reanalyzed data from a previous study. More specif-ically, we compared the impact of changes in baselineStartle levels on fear-potentiated Startle. Different baselineStartle levels were obtained by 1) dividing subjects into alow Startle and a high Startle group and 2) examining theeffect of habituation.
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fear potentiated Startle conditioning in humans explicit and contextual cue conditioning following paired versus unpaired training
Psychophysiology, 1997Co-Authors: Christian Grillon, Michael DavisAbstract: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.
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Fear-potentiated Startle in posttraumatic stress disorder.
Biological psychiatry, 1995Co-Authors: Charles A. Morgan, Michael Davis, Christian Grillon, Steven M. Southwick, Dennis S. CharneyAbstract:Exaggerated Startle is reputed to be one of the cardinal symptoms of posttraumatic stress disorder (PTSD); however, objective studies have given conflicting results as to whether or not Startle is increased in PTSD. The present study investigated Startle in PTSD during the threat of shock (fear-potentiated Startle). The eyeblink component of the Startle reflex was measured at various times preceding and following the anticipation of unpleasant electric shocks in 9 PTSD subjects and 10 age-matched, healthy controls. Startle amplitude was significantly greater during baseline and during shock anticipation in the PTSD subjects, compared to the controls. Habituation of the Startle reflex was normal. Because other studies in the literature, as well as in our own laboratory, have failed to find exaggerated Startle at baseline (i.e., absence of stress) in PTSD patients, it is unlikely that the present results reflect a chronic elevation of Startle in this group. Instead, the higher levels of Startle in the PTSD group probably resulted from a greater conditioned emotional response in this group, triggered by anticipation of electric shocks that generalized to the unfamiliar experimental context in which testing occurred. Hence, emotionally charged test procedures may be especially informative in distinguishing PTSD patients from other psychiatric diagnostic groups.
John S. Yeomans - One of the best experts on this subject based on the ideXlab platform.
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Kynurenate in the pontine reticular formation inhibits acoustic and trigeminal nucleus-evoked Startle, but not vestibular nucleus-evoked Startle
Neuroscience, 2004Co-Authors: Stephan Steidl, P Faerman, John S. YeomansAbstract:The Startle reflex is elicited by acoustic, trigeminal or vestibular stimulation, or by combinations of these stimuli. Acoustic Startle is mediated largely by ibotenate-sensitive neurons in the ventrocaudal pontine reticular formation (PnC). In these studies we tested whether Startle elicited by stimulation of different modalities is affected by infusion of the non-selective glutamate antagonist, kynurenate, into the PnC. In awake rats, Startle responses evoked by either acoustic or spinal trigeminal nucleus stimulation were inhibited by kynurenate, but not saline, infusions, with the most effective placements nearest PnC. In chloral hydrate-anesthetized rats, kynurenate in the PnC reduced trigeminal nucleus-evoked hindlimb EMG responses, but not vestibular nucleus-evoked Startle. Kynurenate in the vestibular nucleus had no effect on trigeminal nucleus-evoked Startle. These results indicate that trigeminal nucleus stimulation evokes Startle largely through glutamate receptors in the PnC, similarly to acoustic Startle, but vestibular nucleus-evoked Startle is mediated through other pathways, such as the vestibulospinal tract.
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tactile acoustic and vestibular systems sum to elicit the Startle reflex
Neuroscience & Biobehavioral Reviews, 2002Co-Authors: John S. Yeomans, Brian W Scott, Paul W. FranklandAbstract:The Startle reflex is elicited by intense tactile, acoustic or vestibular stimuli. Fast mechanoreceptors in each modality can respond to skin or head displacement. In each modality, stimulation of cranial nerves or primary sensory nuclei evokes Startle-like responses. The most sensitive sites in rats are found in the ventral spinal trigeminal pathway, corresponding to inputs from the dorsal face. Cross-modal summation is stronger than intramodal temporal summation, suggesting that the convergence of acoustic, vestibular and tactile information is important for eliciting Startle. This summation declines sharply if the cross-modal stimuli are not synchronous. Head impact stimuli activate trigeminal, acoustic and vestibular systems together, suggesting that the Startle response protects the body from impact stimuli. In each primary sensory nucleus, large, second-order neurons project to pontine reticular formation giant neurons critical for the acoustic Startle reflex. In vestibular nucleus sites, Startle-like responses appear to be mediated mainly via the vestibulospinal tract, not the reticulospinal tract. Summation between vestibulospinal and reticulospinal pathways mediating Startle is proposed to occur in the ventral spinal cord.
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Fear-potentiated Startle and electrically evoked Startle mediated by synapses in rostrolateral midbrain
Behavioral neuroscience, 1995Co-Authors: Paul W. Frankland, John S. YeomansAbstract:Startle amplitudes are increased when acoustic Startle responses are elicited in the presence of a stimulus that has previously been paired with shock. This "fear-potentiated" Startle response appears to be mediated via the caudal ventral amygdalofugal pathway to the brainstem. Electrical stimulation of this pathway evokes unconditioned Startlelike responses. Collision tests have shown that a monosynaptic connection from amygdala to midbrain mediates these responses. Collision tests here localize these synapses mediating electrically evoked Startlelike responses to the rostrolateral midbrain in awake rats. To test whether rostrolateral midbrain synapses also mediate fear-potentiated Startle, we lesioned cells in these sites with ibotenic acid. These lesions completely blocked fear potentiation of acoustic Startle. These same lesions did not block potentiation of Startle by d-amphetamine (6 mg/kg).
Terry D. Blumenthal - One of the best experts on this subject based on the ideXlab platform.
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Pre- and perinatal predictors of Startle eye blink reaction and prepulse inhibition in healthy neonates.
Psychophysiology, 2011Co-Authors: Harriet J. Huggenberger, Susanne E. Suter, Terry D. Blumenthal, Hartmut SchächingerAbstract:The present study examined the Startle eye blink reflex and prepulse inhibition (PPI) in 65 healthy term-born neonates. Although the Startle eye blink is already present at birth, some relevant neuronal structures are not fully mature. We therefore investigated the relationship between prenatal maturation and perinatal stress experience on Startle eye blink and PPI. Eye blinks were evoked by unilaterally presented acoustic broadband white noise (50 ms, 95 dB, prepulse 75 dB). Startle response magnitude and percent PPI were calculated for ipsilateral and contralateral side of stimulation. Neonates exhibited stronger Startle responses ipsilaterally than contralaterally, and a significant PPI. Neonates with more prenatal growth and less perinatal stress had greater Startle magnitudes. Neonates with more stress had more PPI contralaterally. Results suggest that Startle eye blinks may be useful as indicators of prenatal maturation and perinatal stress.
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state craving food availability and reactivity to preferred snack foods
Appetite, 2010Co-Authors: Jack W Rejeski, Terry D. Blumenthal, Gary D Miller, Morgan Lobe, Caroline Davis, Lauren BrownAbstract:The Startle response has been shown to be useful in studying reactivity to food cues. Following 6 h of food deprivation and exposure to neutral and food cues, we examined the role of state craving combined with both a short and long delay of consumption on affect and Startle reflex. Participants completed the PANAS, consumed a controlled early morning meal, and experienced 6 h of food deprivation. They then reported back to the laboratory, completed a second baseline PANAS, and had their baseline eyeblink EMG Startle responses to 100 dB(A) Startle probe assessed. Prior to and following the presentation of cues, Startle probes were presented and responses were recorded. The PANAS and state craving were also assessed after each cue. Food cues provoked higher levels of state craving than neutral cues and Startle responses failed to habituate as quickly to food cues as they did to neutral cues. In addition, cue exposure created the highest NA among high state cravers in the long delay of consumption group. Startle responses differed from NA in that with long delay Startle was high irrespective of state craving scores; in the short delay of consumption condition, Startle increased linearly with state craving. These results illustrate that state craving and expectations of food availability are important variables in understanding food-related cue reactivity.
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Prepulse inhibition decreases as Startle reactivity habituates.
Psychophysiology, 1997Co-Authors: Terry D. BlumenthalAbstract:In the present study, I investigated the effect of stimulus repetition on human Startle eyeblink reflex inhibition (PPI) by a prepulse. Participants were assigned to one of three groups (n = 14 each), in which they received 18 trials of (a) noise Startle stimuli presented alone or preceded by 1000-Hz tone prepulses, (b) Startle stimuli presented alone, or (c) prepulses presented alone. All participants then received 18 more trials of Startle stimuli presented alone or preceded by 1000-Hz tone prepulses, followed by 6 trials of Startle stimuli presented alone or preceded by 2000-Hz tone prepulses. As trials progressed, Startle eyeblink electromyogram magnitude habituated and PPI decreased. PPI was not affected by the repeated presentation of the prepulses alone but decreased with the repeated presentation of the Startle stimulus alone. Changes in the frequency of the prepulse had no significant effect on PPI. These data suggest that the reduction of PPI that is seen across trials is not due to habituation of the prepulse but is related to Startle reactivity in control trials, which is reduced by habituation.
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Prepulse effects on magnitude estimation of Startle-eliciting stimuli and Startle responses
Perception & psychophysics, 1996Co-Authors: Terry D. Blumenthal, Edward J. Schicatano, Jeremy G. Chapman, Christopher M. Norris, Edward R. ErgenzingerAbstract:The present studies investigated the relationship between prepulse effects on the modification of the brainstem Startle reflex and magnitude estimates of Startle-eliciting stimuli. In Experiment 1, Startle eyeblink responses were elicited in 24 students, half of whom were instructed to estimate the loudness of the Startle stimulus (actual intensities of 80, 90, and 100 dB) and half of whom were instructed to estimate the magnitude of their eyeblink. When weak acoustic prepulses preceded the Startle-eliciting stimulus, eyeblink amplitude was inhibited, and estimates of response magnitude decreased, but estimates of Startle stimulus magnitude decreased only when 100-dB Startle stimuli were presented. In Experiment 2, the same Startle stimuli were preceded on some trials by a vibrotactile prepulse to the hand. In conditions in which Startle amplitude was inhibited, Startle stimulus magnitude estimates were not affected. This suggests that the effect of acoustic prepulses on 100-dB Startle stimuli in Experiment 1 may have been due to loudness assimilation, an effect independent of the prepulse inhibition of Startle responding.
James T. Winslow - One of the best experts on this subject based on the ideXlab platform.
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Acoustic Startle reflex in rhesus monkeys: a review.
Reviews in the neurosciences, 2008Co-Authors: Michael Davis, Elena A. Antoniadis, David G. Amaral, James T. WinslowAbstract:Modulation of the acoustic Startle response is a simple and objective indicator of emotionality and attention in rodents and humans. This finding has proven extremely valuable for the analysis of neural systems associated with fear and anxiety. Until recently, there have been few efforts to develop acoustic Startle measurement in non-human primates. Here we review recent work in which whole body acoustic Startle amplitude has been measured in rhesus monkeys. Initial studies revealed that the amplitude of whole body Startle in monkeys, as in rodents and humans, is directly proportional to acoustic stimulus intensity and gradually habituates with repeated exposures. Presentation of a weak acoustic stimulus 25-5,000 msec before a Startle stimulus reduces Startle amplitude by 40-50% depending on inter-stimulus interval length (prepulse inhibition). We have also measured significant fear-potentiated Startle in the presence of a visual stimulus after pairing it with an inescapable pulse of pressurized air (fear-potentiated Startle). This effect was reduced by diazepam and morphine, but not by buspirone. Ibotenic acid-induced lesions of the amygdala prevented the acquisition of fear-potentiated Startle but, remarkably, did not prevent the expression of fear-potentiated Startle when fear conditioning was carried out prior to the lesion. Finally, we have developed an objective measure of fear inhibition in monkeys using a novel conditioned inhibition procedure identical to one used in rats and humans. Our data demonstrate that acoustic Startle in non-human primates successfully bridges rodent and human research. The opportunity now emerges to link concepts developed in rodents to the more complex neuroanatomical and cognitive processes common to monkeys and humans.
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role of the primate amygdala in fear potentiated Startle effects of chronic lesions in the rhesus monkey
The Journal of Neuroscience, 2007Co-Authors: Elena A. Antoniadis, Michael Davis, James T. Winslow, David G. AmaralAbstract:In experiment 1, we assessed the role of the primate amygdala and hippocampus in the acquisition of learned fear measured with fear-potentiated Startle. Three groups of six rhesus monkeys were prepared with bilateral ibotenic acid lesions of the amygdaloid complex and the hippocampus or were sham operated. Selective ibotenic acid lesions of the amygdala, but not the hippocampus, blocked the acquisition of fear-potentiated Startle. In experiment 2, we assessed the role of the primate amygdala in the expression of fear-potentiated Startle. Surprisingly, animals that sustained amygdala damage after they successfully learned fear-potentiated Startle expressed normal fear-potentiated Startle, despite a complete amygdala lesion based on magnetic resonance imaging assessments. These results suggest that although the amygdala is necessary for the initial acquisition of fear-potentiated Startle, it is not necessary for the retention and expression of fear-potentiated Startle. These findings are discussed in relation to the role of the amygdala in emotional learning and in cross-species comparisons of emotional behavior.
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Acoustic Startle, prepulse inhibition, and fear-potentiated Startle measured in rhesus monkeys.
Biological psychiatry, 2002Co-Authors: James T. Winslow, Lisa A. Parr, Michael DavisAbstract:Abstract Background: Modulation of the acoustic Startle response is a simple and objective indicator of emotionality and attention in rodents and humans. This finding has proven extremely valuable for analysis of neural systems associated with fear and anxiety. Until recently, there have been few efforts to develop acoustic Startle measurement in nonhuman primates. We report here development of a whole-body acoustic Startle protocol in rhesus monkeys. Methods: Eight juvenile rhesus monkeys were tested in a new whole-body (somatic) acoustic Startle protocol. Startle responses were assessed in three paradigms: 1) stimulus intensity-response amplitude, 2) prepulse inhibition (PPI), and 3) fear-potentiated Startle. Results: Initial studies revealed that the amplitude of whole-body Startle in monkeys, as in rodents and humans, is directly proportional to acoustic stimulus intensity and gradually habituates with repeated exposures. Presentation of a weak acoustic stimulus 45–2020 msec before a Startle stimulus reduces Startle amplitude by 40%–50%, depending on interstimulus interval length (PPI). We have also measured significant potentiated Startle amplitude in the presence of a visual stimulus after pairing it with an inescapable pulse of pressurized air (fear-potentiated Startle). Conclusions: Our data demonstrate that acoustic Startle in nonhuman primates successfully bridges rodent and human research in two broad areas: stimulus-response relationships and behavioral plasticity represented by habituation, PPI, and fear potentiation. The opportunity now emerges to link concepts developed in rodents to the more complex neuroanatomical and cognitive processes common to monkeys and humans.
