Startle Elicitation: Stimulus Parameters, Recording Techniques, and Quantification

Berg, Wendy K.; Balaban, Marie T.

doi:10.1017/cbo9780511665523.004

Cited by 78 publications

(64 citation statements)

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“…Startle blink amplitude was calculated as the difference between the maximum of the rectified EMG signal in a time window of 20 to 150 seconds after startle stimulus presentation and the median of the 50 milliseconds before the upstroke of the blink response. 13 Blink responses were coded as missing if the EMG fluctuated by Ͼ30% of the blink amplitude during 50 seconds before the onset of the blink response and if no typical blink response was detectable (together, Ͻ8% of the trials). 13 EMG amplitudes of the startle reactions were logarithmically transformed.…”

Section: Discussionmentioning

confidence: 99%

“…Three salt-resistant subjects were excluded from analysis, because Ͻ50% of their startle trials could be scored by the criteria described below. 13 All subjects underwent routine physical examination, laboratory evaluation, and phenotypic characterization regarding their blood pressure response to a dietary salt-loading/ restriction protocol described elsewhere. 14,15 To assess parental history of hypertension, written information was obtained from the parents' family physicians.…”

Section: Subjectsmentioning

confidence: 99%

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Enhanced Affective Startle Modulation in Salt-Sensitive Subjects

et al. 2001

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Abstract-Salt-sensitive normotensive men exhibit an enhanced pressor response to mental stress. Although an enhanced pressor response is associated with higher affective startle modulation in men, an association between salt sensitivity of blood pressure and affective startle modulation has not been studied so far. We studied reactivity to mental stress and startle modulation in 14 salt-sensitive healthy white male students and 14 salt-resistant control subjects, who were well matched for age, body mass index, physical fitness, and family history of hypertension. Subjects performed a computerized information-processing task under time pressure (manometer test), while heart rate and blood pressure were continuously registered. In a separate session, subjects viewed a series of 42 pictures of the International Affective Picture System (IAPS), varying in pleasure and arousal, while acoustic startle probes were administered randomly, and electromyogram activity of the orbicular eye muscle was continuously recorded. Startle modulation was calculated as the difference between startle responses under negative and positive affective stimuli. In contrast to salt-resistant subjects, salt-sensitive subjects showed significantly enhanced startle amplitudes under negative stimuli and diminished amplitudes under positive stimuli. Thus, salt-sensitive subjects displayed a significantly higher startle modulation than did salt-resistant subjects (PϽ0.05). Subjective ratings of the presented IAPS pictures did not differ between the groups. The increased startle modulation of salt-sensitive subjects suggests an enhanced activity of the central nucleus of the amygdala. This enhanced central nervous responsiveness may contribute to higher sympathetic pressor reactivity and, thus, to the later development of hypertension in salt-sensitive individuals.

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Section: Discussionmentioning

confidence: 99%

Section: Subjectsmentioning

confidence: 99%

Enhanced Affective Startle Modulation in Salt-Sensitive Subjects

et al. 2001

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“…Indeed, several earlier studies have shown that schizophrenia patients treated with typical antipsychotic medication exhibited significantly less P50 suppression than did patients receiving atypical antipsychotics Becker et al, 2004;Adler et al, 2004). Specifically, patients receiving clozapine (Tandon and Jibson, 2003;Adler et al, 2004) or olanzapine (Berg and Balaban, 1999) had superior suppression levels relative to those treated with typical antipsychotic medication. Moreover, Nagamoto et al (1996) reported that schizophrenia patients, who therapeutically responded to clozapine after 1 month of treatment also showed enhanced P50 suppression levels.…”

Section: P50 Suppressionmentioning

confidence: 98%

Haloperidol Differentially Modulates Prepulse Inhibition and P50 Suppression in Healthy Humans Stratified for Low and High Gating Levels

Csomor

Stadler

Feldon

et al. 2007

Neuropsychopharmacol

102

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Schizophrenia patients exhibit deficits in sensory gating as indexed by reduced prepulse inhibition (PPI) and P50 suppression, which have been linked to psychotic symptom formation and cognitive deficits. Although recent evidence suggests that atypical antipsychotics might be superior over typical antipsychotics in reversing PPI and P50 suppression deficits not only in schizophrenia patients, but also in healthy volunteers exhibiting low levels of PPI, the impact of typical antipsychotics on these gating measures is less clear. To explore the impact of the dopamine D 2 -like receptor system on gating and cognition, the acute effects of haloperidol on PPI, P50 suppression, and cognition were assessed in 26 healthy male volunteers split into subgroups having low vs high PPI or P50 suppression levels using a placebocontrolled within-subject design. Haloperidol failed to increase PPI in subjects exhibiting low levels of PPI, but attenuated PPI in those subjects with high sensorimotor gating levels. Furthermore, haloperidol increased P50 suppression in subjects exhibiting low P50 gating and disrupted P50 suppression in individuals expressing high P50 gating levels. Independently of drug condition, high PPI levels were associated with superior strategy formation and execution times in a subset of cognitive tests. Moreover, haloperidol impaired spatial working memory performance and planning ability. These findings suggest that dopamine D 2 -like receptors are critically involved in the modulation of P50 suppression in healthy volunteers, and to a lesser extent also in PPI among subjects expressing high sensorimotor gating levels. Furthermore, the results suggest a relation between sensorimotor gating and working memory performance.

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“…The startle response is a brainstem reflex elicited by a sudden stimulus (Berg & Balaban, 1999). The response to the startle-eliciting stimulus is modified by the prior presentation of a weaker stimulus, called a prepulse, an effect most often referred to as prepulse inhibition, or PPI (Blumenthal, 1999).…”

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confidence: 99%