Fear-potentiated startle: Relationship to the level of state/trait anxiety in healthy subjects

Grillon, Christian; Ameli, Rezvan; Foot, Michael; Davis, Michael T.

doi:10.1016/0006-3223(93)90094-t

Cited by 164 publications

(106 citation statements)

References 24 publications

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“…Recently, Fullana et al [26] predicted but did not find that individuals at opposite extremes in terms of BIS scores (as measured by SP[SR]Q) would show significant differences in magnitude and time course of fear-potentiated startle that involved the threat of a shock. Previously, Grillon et al [34] found the same results. As for the SCL results discussed above [30], but much more specifically so, these SR findings question the relationship between amygdala reactivity and BIS sensitivity originally proposed by Kagan and Snidman [21].…”

Section: Neurobiologysupporting

confidence: 70%

Behavioral inhibition: A neurobiological perspective

Morgan

2006

Curr Psychiatry Rep

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Behavioral inhibition (BI) during early childhood has been associated with subsequent development of anxiety disorders. However, understanding of the neuroanatomical substrates of BI in humans generally has not kept pace with that of anxiety disorders. Recent interpretations and implementations of Gray's and Kagan's concepts of BI are examined from the perspective of current neurobiological models. Particular attention is given to evidence pointing to conceptual and operational limitations of self-report scales purported to measure trait BI in adults, and especially to inconsistent correlations between such behavioral inhibition system (BIS) scores and amygdala and autonomic responses to fear- or startle-inducing stimuli. Evidence showing a dissociation of both BI and trait anxiety from the amygdala is considered. Possible reasons for the poor association between BIS and trait anxiety self-report scale scores and predicted physiological outputs of the BIS are identified. Reasons to distinguish between the neural bases of BI as against trait anxiety also are discussed. The need to critically examine the role of the amygdala in BI and trait anxiety, as well as to consider other brain areas that appear to be involved in subserving these emotional traits, is emphasized.

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Section: Neurobiologysupporting

confidence: 70%

Behavioral inhibition: A neurobiological perspective

Morgan

2006

Curr Psychiatry Rep

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“…After Pavlovian fear conditioning, rats showed an increased startle response [Davis and Astrachan, 1978]. The paradigm of the fear potentiated-startle reaction has been shown in controls [summarized in Lang et al, 1990]; increased fear-potentiated startle values (compared to controls) have been found in patients with PD [Grillon et al, 1994], and healthy subjects with high trait anxiety [Grillon et al, 1993]. In this study only safety conditions were used.…”

Section: Discussionmentioning

confidence: 97%

“…Increased startle in a nonthreat condition is found in simple phobics [Hamm et al, 1991] and in Vietnam veterans with post-traumatic stress disorder (PTSD) [Butler et al, 1990;Morgan III et al, 1995. Other studies did not find increased startle in healthy subjects with high state/trait anxiety [Grillon et al, 1993], panic patients [Grillon et al, 1994], or Vietnam veterans with PTSD [Grillon et al, 1998] in the baseline condition. Prepulse inhibition (PPI) has been widely used as a neurophysiological measure of the early preattentive stages of information processing and is used as an operational measure of sensorimotor gating Swerdlow et al, 1992].…”

Section: Introductionmentioning

confidence: 94%

Prepulse inhibition deficits in patients with panic disorder

Ludewig²,

et al. 2002

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Prepulse inhibition (PPI) is an operational measure of sensorimotor gating that is reduced in several neuropsychiatric disorders that are characterized by deficits in inhibition or gating of intrusive or irrelevant stimuli. Clinically, panic disorder (PD) patients have been described as having difficulties in inhibition of responding to sensory and cognitive events. Because such difficulties may be due to failures in early stages of information processing, we examined PPI in patients with PD. Acoustic startle reactivity, habituation, and PPI (30-, 60-, 120-, 240-, and 2,000-ms interstimulus intervals) were assessed in patients with panic disorder (m/f = 10, 10) and age- and gender-matched healthy controls (m/f = 11, 10). PD patients were assessed with structured clinical interview for DSM-IV criteria with benzodiazepine treatment as an exclusion criterion. Panic disorder patients exhibited normal startle reactivity, reduced habituation, and significantly reduced PPI in the 30-, 60-, and 240-ms prepulse conditions. Within the PD group, the patients with high trait and state anxiety exhibited less PPI than patients with low trait and state anxiety. Furthermore, in PD patients, decreased PPI correlated significantly with high trait but not state anxiety. These data indicate that early stages of sensory information processing are abnormal in patients with PD. These observed deficits in PPI could reflect a more generalized difficulty in suppressing or gating information in panic disorder. The correlation between high trait anxiety and deficient PPI supports the hypothesis that sensorimotor gating abnormalities are an enduring feature of subjects with PD.

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“…The startle reflex in humans is increased in the presence of cues signaling danger and decreased if elicited in a pleasant or rewarding emotional context (Vrana et al, 1988;Grillon et al, 1993). Likewise rodents show increased startle in the presence of cues paired with shock (Davis, 1992) and drugs that increase anxiety (Frankland et al, 1997) and decreased startle in the presence of cues paired with food (Schmid et al, 1995) or rewarding brain stimulation (Steidl et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

The Nucleus Accumbens is not Critically Involved in Mediating the Effects of a Safety Signal on Behavior

Josselyn

Falls

Gewirtz

et al. 2004

Neuropsychopharmacol

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Although considerable progress has been made towards understanding the neural systems mediating conditioned fear, little is known about the neural mechanisms underlying conditioned inhibitors of fear (or safety signals). The present series of experiments examined the involvement of the nucleus accumbens (NAC) in mediating the effects of safety signals on behavior using a conditioned inhibition of fear-potentiated startle paradigm. Neither increasing dopaminergic nor decreasing glutamatergic function in the NAC altered the magnitude of conditioned fear or conditioned inhibition of fear in rats. Furthermore, large pre-or post-training electrolytic lesions of the NAC did not affect acquisition or expression of fear-potentiated startle or conditioned inhibition of fear-potentiated startle. Taken together, these data suggest that the NAC is not critically involved in the acquisition or expression of fear-potentiated startle or conditioned inhibition of fear-potentiated startle. Previous research has implicated the NAC in 'reward-attenuated startle' in which presentation of a stimulus paired with food decreased startle responding. The present results, therefore, indicate important neural dissociations between the processing of appetitive and safety signals, even though behavioral studies and learning theories have suggested that these two forms of learning share some commonalities.

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Fear-potentiated startle: Relationship to the level of state/trait anxiety in healthy subjects

Cited by 164 publications

References 24 publications

Behavioral inhibition: A neurobiological perspective

Behavioral inhibition: A neurobiological perspective

Prepulse inhibition deficits in patients with panic disorder

The Nucleus Accumbens is not Critically Involved in Mediating the Effects of a Safety Signal on Behavior

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