This study of contextual and explicit threat cue modulation of SR as a function of N in adolescence, a risk factor for anxiety and depressive disorders, yielded two main findings. First, within the explicit threat cue paradigm, the potentiating effects of N on SRs were larger during late safe and early danger trials than during early safe (furthest from threat) and late danger (closest to threat) trials. Also, N potentiated anxiety ratings for the initial baseline and context conditions, and the explicit threat cue paradigm. These findings are broadly consistent with other evidence for enhanced responding to contexts associated with threat in individuals with anxiety disorders and those at risk for such disorders due to familial anxiety or depression (4
). Second, N potentiated SRs in males but not in females across the entire experiment, regardless of phase, block or condition, even though females judged the muscle contraction as more arousing and unpleasant than males.
The electrical muscle stimulator was successful in generating explicit threat cue modulation of SRs, with larger SRs during danger than safe phases, and during late versus early trials. Also, N interacted with phase and probe time in modulating SRs, such that N tended to potentiate SRs more during late than early trials within safe phases but potentiated SRs more during early than late trials within danger phases. Conceivably, results from the safe phases represent a gradient of contexts associated with threat, with the modulating effects of N strongest in the late trials that represented closer proximity to threat by virtue of matching the timing of the contraction during danger phases. In contrast, within danger phases, the effects of N were stronger in early trials, representing the context of threat, than late trials, representing closest proximity to an explicit threat cue.
That N did not modulate SRs during closest proximity to threat (i.e., late threat trials) is consistent with previous evidence for lack of explicit threat cue modulation by risk status (8
). Also, this finding reflects the “strong situation” effect (32
), in which anxious patients and controls respond similarly to intense threat, when anyone would be expected to show neurobiologically imperative fear responses, whereas only anxious individuals respond more strongly to less intense aversive stimuli. Moreover, our finding that N did not modulate SRs during when furthest from threat (i.e., early safe trials) parallels findings in baseline conditions when participants are reassured that no aversive stimulus will be presented (2
). This may represent the other side of the “strong situation” when no-one would be expected to show neurobiologically imperative fear responses.
At least two alternative explanations exist. First is nonspecific arousal created by repeated exposure to startle probes. Second is slowed habituation as a function of higher levels of N. However, the differential effects of N across late safe and early threat trials, versus early safe and late threat trials, during which the startle stimuli were constant variables, suggests that the effects of N are not solely attributable to non-specific arousal. This same effect also rules out the slowed habituation explanation, as late versus early trials were not confounded with order effects.
In contrast to hypotheses, N did not potentiate SRs more so in the presence of a contextual cue than in its absence. However, context modulation of SR in general (i.e., larger SRs during context than baseline conditions) was not observed prior to the explicit threat cue paradigm. Conceivably, initial context modulation of SR was offset by insufficient habituation during the first baseline condition, when only nine startle probes were delivered. Additionally, threat of an ‘unknown’ aversive biceps contraction implied by attachment of the muscle contraction electrodes and instructional set may have been insufficiently aversive to generate contextual modulation; a possibility that is supported by lower anxiety ratings for the context than the baseline condition. Direct experience with the biceps contraction contributed to context modulation, since SRs and anxiety ratings were larger for the context than baseline condition following the explicit threat cue paradigm. N also modulated SR in general across the second baseline and context conditions, although main effect was accompanied by a Sex and N interaction.
Indeed, throughout the entire experiment, N potentiated SRs in males but not in females. Thus, N related to defensive reactivity in males but not females, regardless of phase, block or condition. Prior evidence showed elevated baseline SRs in female but not male offspring of anxious/depressed parents/grandparents (8
). Conceivably, familial emotional disorders and N confer risk differently for males versus females. Additionally, the effects of N upon SRs might be moderated by other variables in females, such as stronger family history. Moreover, sex differences in prior studies were confounded by age, as females were significantly older than males in one study (8
) and high risk samples were significantly older than low risk samples in another (9
). Thus, risk due to familial anxiety and depressive disorders versus N may be conferred at different developmental stages in males versus females. Clearly, replication of these findings is required before such speculations can be tested.
Our measure of SCRs was to the startle stimulus per se (29
) rather than to emotional stimuli, which may explain why we did not observe effects of N upon SCR that have been reported elsewhere (34
). A limitation of this study is that an uncertain number of muscle stimulations with threat of increasing intensity (akin to threat of shock procedures, 33) was not as anxiety-provoking as intended; subjective anxiety for the explicit threat cue paradigm was only moderate. On the other hand, anxiety was rated once the paradigm was complete and may have underestimated ongoing anxiety. Ongoing measurement of anxiety, such as via a dial-and-pointer at designated times without disrupting task procedures, would be valuable in future studies. Another limitation was that order effects and habituation may have deflated SRs during danger phases (which always followed safe phases) and context conditions (which always followed baseline conditions). Furthermore, selection biases from participation rates may have impacted generalizability of the findings, although Ps in the startle experiment did not differ appreciably from remaining Ps. Finally, further investigation of the role of ethnicity and sex in SRs, that possibly contributed to overall site differences herein, is warranted.
In conclusion, N enhanced SRs to startle probes more during contexts intermediary to threat than conditions furthest from threat and conditions closest to threat within an explicit threat cue paradigm. Thus, N modulated SRs when at partial risk but not when at full risk for threat. These findings may indicate that greater defensive responding to contexts associated with threat is a pathway through which N confers risk for anxiety and depressive disorders. Longitudinal investigation will elucidate the degree to which such patterns of SRs are predictive of anxiety disorders. Finally, the finding that N modulated SRs across the entire experiment in males and not females may be indicative of sex specific effects of risk factors.