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Keywords:

  • Prepulse inhibition;
  • Self-action;
  • Temporal window

Abstract

  1. Top of page
  2. Abstract
  3. Method
  4. Results
  5. Discussion
  6. References

A startle reflex to a startle pulse is inhibited when preceded by a prestimulus. We introduced a key-press action (self-action) or an 85 dB noise burst as a prestimulus, followed by a 115 dB noise burst as a startle pulse. We manipulated temporal offsets between the prestimulus and the startle pulse from 30–1,500 ms to examine whether self-action modulates the startle reflex and the temporal properties of the modulatory effect. We assessed eyeblink reflexes by electromyography. Both prestimuli decreased reflexes compared to pulse-alone trials. Moreover, the temporal windows of inhibition were different between the types of prestimuli. A faster maximal inhibition and narrower temporal window in self-action trials suggest that preceding self-action inhibits the startle reflex and allows prediction of the coming pulse in different ways from auditory prestimuli.

Studies using an experimental paradigm that rapidly presents paired stimuli provide insight into how sensory systems select specific sensory inputs and filter out others. A conventional paired stimuli presentation consists of a prestimulus and a subsequent stimulus with varying stimulus onset and is used to demonstrate sensory system-operating characteristics in terms of the modulatory effect of prestimulus presentation on the response and the perceptual experience of the subsequent stimulus. Prepulse inhibition (PPI) is a representative example of a modulatory effect that is used to study sensory processing in both normal and patient populations, including patients with schizophrenia (for a review, Braff, Geyer, & Swerdlow, 2001). PPI is a phenomenon whereby a startle reflex to a startle pulse is inhibited when the pulse is preceded by a weaker prepulse (Graham, 1975). PPI is generally regarded as a psychophysiological measure of “sensorimotor gating,” which filters out redundant and irrelevant sensory information to regulate the vast amount of incoming sensory inputs (Graham, 1975; for a review, Braff et al., 2001; Filion, Dawson, & Schell, 1998). In this context, the inhibitory effect of a prepulse on startle suggests that sensory systems gate out (suppress) startle stimulus information to protect prepulse processing against the distraction stemming from startle reflexes. PPI deficit (weak inhibition) is regarded as a stable trait marker for schizophrenia (Braff et al., 1978, 2001).

Many previous studies examined the effects of various prepulse types on the startle reflex to characterize sensorimotor gating properties. For example, sound pressure level differences between a background noise and an auditory prepulse (Flaten, Nordmark, & Elden, 2005; Franklin, Moretti, & Blumenthal, 2007) and the intensity, duration, and sensory modality (acoustic, visual, or tactile) of a prepulse (for a review, Filion et al., 1998) all modulate the startle reflex. Specifically, stimulus onset asynchrony (SOA) between a prepulse and a startle pulse is important in determining whether the inhibitory effect of the prepulse occurs (Braff et al., 2001; Graham, 1975). For auditory PPI, maximal inhibitory effects occur at 60–120 ms SOA, reflecting an automatic sensorimotor gating mechanism (Braff, Grillon, & Geyer, 1992). Furthermore, the startle reflex is facilitated at longer SOAs of approximately 2 s (prepulse facilitation) in healthy populations, reflecting a classical activation effect by the reticular activating system, as well as attention or orienting to incoming information (Graham, 1975). These temporal properties are very robust and have been replicated in a large body of research (Braff et al., 2001). In addition, previous studies reported different temporal properties for the effects of visual and tactile prepulse on the auditory startle reflex; a reflex facilitation occurs at SOAs less than 100 ms, and a maximal inhibition was delayed (120–250 ms) compared to auditory PPI (for a review, Neuman, Lipp, & Pretorius, 2004).

In the context of conventional PPI as described above, we used a conventional auditory prepulse and a self-action (i.e., key pressing) as a preceding stimulus. The inhibition of the startle reflex by self-action suggests that sensory systems use self-action–related signals (signal preceding self-action or/and sensory signal arising from self-action itself) to regulate or filter out sensory inputs spatiotemporally adjacent to self-action. In a previous study on the startle reflex to electrical stimulation, Ison, Sanes, Foss, and Pinckney (1990) reported that self-stimulation inhibited the electromyography (EMG) amplitude of a late reflex component R2. Reports on event-related potentials (ERP) in electroencephalography (EEG) to auditory stimulation describe similar inhibitory effects of self-stimulation on N1 amplitude (Lange, 2011; Schafer & Marcus, 1973). Moreover, Martikainen, Kaneko, and Hari (2005) reported similar inhibitory effects on auditory N1 amplitude in the auditory cortex using magnetoencephalography (MEG). Differences between previous studies and the present work are related to stimulus sensory modalities (electrical or auditory stimulus), the ability to induce the startle reflex, and measurement modalities (EEG, MEG, or EMG). Although many EEG and MEG investigations have almost exclusively used nonstartle auditory stimuli to examine the inhibitory effect of self-action, the small number of previous studies on the startle reflex have not elucidated the effect of self-action on the auditory startle reflex. Here, we will show that we can generalize the inhibitory effect of self-action on both startle and nonstartle auditory stimuli. Since the 1980s, research into the neural pathways underlying the auditory startle reflex has demonstrated that the auditory reflex is generated by the caudal brainstem (Leitner, Powers, & Hoffman, 1980; Swerdlow, Caine, Braff, & Geyer, 1992). Thus, we suggest that self-related signals are available at the relatively lower levels of sensory processing carried out by the caudal brainstem. The present study allows us to discuss, from the perspective of psychophysiological indices, how sensory information flow would be regulated depending on whether a preceding event is self-generated or presented externally.

We also manipulated temporal delay (SOA) between the preceding stimulus and the startle pulse to characterize the temporal properties of auditory startle reflex inhibition. Although many previous studies on response inhibition by self-action focused on inhibition amplitude, we aimed to address differential sensitivity to SOA manipulation between experimenter-controlled and self-generated stimulus delivery. Distinct temporal properties are assumed to indicate that different information processes are associated with response inhibition between experimenter-controlled and self-generated preceding events. Thus, we investigated how sensory systems temporally associate preceding stimuli with following startle pulses and how they subsequently modulate responses to the pulse, thereby providing hints regarding sensory system-operating properties.

In the present work, we considered the large body of auditory PPI studies in healthy controls and people with schizophrenia and used auditory startle pulses and eyeblink reflex measurements to assess the inhibitory effect of self-action on the startle reflex. Notably, patients with schizophrenia often have deficits in monitoring situations in which they move their bodies by themselves, as well as abnormal sensory processing of sensory startle stimuli that PPI indicates. It is possible that deficits in processing self-action–related signals appear as non- or weak inhibitory effects by self-action. Thus, we aimed to explore a new psychophysiological method to reflect deficits to distinctively process externally and self-generated sensory information in schizophrenia (e.g., Frith, 2005; Ford & Mathalon, 2012).

Method

  1. Top of page
  2. Abstract
  3. Method
  4. Results
  5. Discussion
  6. References

Participants

Participants were 26 healthy students (15 males and 11 females) at Tohoku Fukushi and Tohoku University who were paid to complete the study. Their average age was 21.08 years (age range, 19–28 years). To obtain reliable startle reflexes and its inhibition, we excluded six participants (five males and one female) from subsequent data analysis because their mean EMG amplitudes were < 45 μV in pulse-alone trials. Among the six participants, one had considerable body movements that resulted in noisy data, and one fell asleep during the measurements. We obtained written informed consent from all participants according to the guidelines of the Ethical Committee of Tohoku Fukushi University and the Declaration of Helsinki.

Experimental Stimuli and Apparatus

All stimuli were constructed using MATLAB 2007a (The MathWorks Inc., Natick, MA) and Cogent Graphics software packages (http://www.vislab.ucl.ac.uk/cogent.php). A prepulse (20 ms, 85 dB sound pressure level [SPL] broadband white noise) and startle pulse (40 ms, 115 dB SPL broadband white noise) with near instantaneous rise/fall times were presented through headphones (DR-531, Elega Acous Co., Ltd., Tokyo, Japan). Background white noise was presented over loudspeakers (Eclipse TD508II, Fujitsu Ten Ltd., Kobe, Japan) and had an intensity of 70 dB SPL under the headphones. A red bull's eye (1.0° × 1.0°, 39.65 cd/m2) was presented on a computer monitor (60 Hz vertical refresh rate, 2007FPb, Dell, Austin, TX). The prepulse and startle pulse were presented in three conditions. In the pulse-alone condition, only the startle pulse was presented. In the prepulse-pulse condition (standard prepulse condition), the prepulse was presented at various SOAs of 30, 60, 120, 240, 480, 960, and 1,500 ms relative to startle pulse presentation. In the self-action condition, participants pressed an assigned key with their index finger in a self-paced manner, which signaled a startle pulse presented at SOAs of 30, 60, 120, 240, 480, 960, and 1,500 ms relative to the key press.

Six pulse-alone trials were conducted at the beginning (block 1) and end of the experiment (block 10). Half of blocks 2 to 9 were in the prepulse condition, and half were in the self-action condition. Three prepulse-to-pulse trials or self-action-to-pulse trials for each of seven SOA conditions were pseudorandomly conducted for 21 trials per block. The kinds of blocks (i.e., standard prepulse or self-action condition) were alternated within each participant's session, and the order was counterbalanced across participants. These blocks also included six “no-auditory stimulus” (auditory stimulus including prepulse and startle pulse) trials for blocks 1 and 10 or three for blocks 2 to 9. Intertrial intervals ranged from 9–23 s (mean = 16 s) for the pulse-alone and standard prepulse conditions. For the self-action condition, participants were asked to press an assigned key with their right or left index finger at a self-paced rate of approximately 10–20 s. The order of responding fingers was counterbalanced across participants, and they were also instructed to avoid counting the intervals.

EMG Recording and Analysis

One of two 6-mm gold electrodes (Model F-E6GH, Grass Technologies, West Warwick, RI) were positioned 1 cm lateral to and 0.5 cm below the lateral canthus of the right eye and a second electrode was positioned 1.5 cm below and slightly medial to the first electrode (Braff et al., 1992). Electrode resistances were below 5 kΩ. A ground electrode was placed behind the right ear over the mastoid. EMG activity was amplified with a digital multipurpose EEG (EE5514 SYNAFIT 5000, NEC, Tokyo, Japan) and band-pass filtered (5–1000 Hz). Raw EMG data were full-wave rectified and integrated with a 5-ms time constant using BIMUTAS II (Kissei Comtec Co. Ltd., Matsumoto, Japan). Sampling on each trial began 100 ms prior to startle pulse onset and continued for 250 ms after startle pulse onset. An integrated EMG peak amplitude was scored as the maximum EMG amplitude during a window of 20–100 ms after a startle pulse onset minus the baseline, where EMG amplitudes were averaged for the 20 ms immediately after the onset. Trials were rejected if baseline EMG in the first 20 ms was not stable, but < 2% of trials were rejected. Prestimulus inhibition (%) of EMG amplitude was defined as the following mathematical expression: PSI (%) = (1 − [mean EMG amplitude in the standard prepulse or self-action condition/mean EMG amplitude in the pulse-alone condition]) × 100.

Procedure

Each participant was seated in a recliner approximately 57 cm away from the monitor and instructed to sit still with his/her eyes open and to focus on a fixation point. EMG traces were recorded in a moderately lit and sound-attenuated room. Participants were told that they would hear a variety of sounds. The experiment consisted of a 5-min acclimation period with the background noise followed by the first five test blocks, rest, a second 5-min acclimation period, and the remaining five blocks.

Results

  1. Top of page
  2. Abstract
  3. Method
  4. Results
  5. Discussion
  6. References

Figure 1 shows mean prestimulus inhibition (PSI) for each condition across participants. A value of 0% indicates that the prestimulus (prepulse or self-action) had no inhibitory effect on the startle reflex.

figure

Figure 1. Mean prestimulus inhibition (%) for each condition. The dotted line indicates no inhibition, the area above the line indicates inhibition, and the area below the line indicates facilitation. Error bars denote the standard error of the mean (n = 20).

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Analysis of PSI

We assessed habituation with paired t tests of EMG amplitudes between the pulse-alone blocks (1 and 10). Results showed that EMG amplitude in block 10 was significantly lower than that in block 1, t(19) = 3.63, p = .002, Cohen's d = 0.95, suggesting that there was significant habituation.

We conducted one-sample t tests to examine whether the PSI (%) values for each condition were significantly different from zero. This allowed us to test whether each prestimulus preceding the SOAs inhibited the startle reflex. The t tests were corrected for multiple comparisons by using a false discovery rate correction of q = 0.05 (Benjamini & Hochberg, 1995). For the standard prepulse condition, startle EMG activity was significantly inhibited in the range of the 30–1,500 ms SOAs: for 30–960 ms, t(19) = 8.94, 18.23, 13.69, 5.35, 8.23, and 7.22, p < .0001, d = 3.02, 5.99, 4.45, 1.83, 2.68, 2.38; for 1,500 ms, t(19) = 2.39, p = .02, d = 0.83. For the self-action condition, startle EMG activity was significantly inhibited at the 30 and 240 ms SOAs: for 30 ms, t(19) = 2.98, p = .008, d = 1.05; for 240 ms, t(19) = 2.95, p = .008, d = 1.06. The inhibition was marginally significant for 60 ms, t(19) = 2.17, p = .04, d = 0.80; for 120 ms, t(19) = 2.01, p = .06, d = 0.71. Inhibition was not significant for SOAs over 480 ms.

Analysis of Temporal Properties

Next, we conducted a repeated measures two-way analysis of variance with the factors of prestimulus type (standard prepulse or self-action) and SOA. The Huynh–Feldt corrections were used to adjust probabilities for repeated-measures effects with more than two levels. The main effect of prepulse type was significant, F(1,19) = 39.70, p < .001, ε = 1.00, η2 = 0.68, indicating that the inhibitory effect elicited by the standard prepulse was larger than that induced by the self-action. The main effect of SOA was significant, F(1,19) = 20.32, p < .001, ε = .54, η2 = 0.52. The interaction between these two factors was also significant, F(6,114) = 3.00, p = .045, ε = .44, η2 = 0.14. To further assess the temporal dependency of the inhibitory effect, post hoc analysis (Ryan's method) was performed. The results showed that the inhibitory effect in the standard prepulse condition was larger than that in the self-action condition for all SOA conditions > 30 ms, p < .001 (only for 240 ms, p = .006), d = 1.27, 1.26, 0.57, 1.24, 1.01, and 0.67 for increasing SOAs, respectively. Moreover, in the standard prepulse condition, the inhibitory effect was larger for the 60 and 120 ms SOAs than for the 30 and 960 ms SOAs, all p < .001, d = 1.19 (60 ms > 30 ms), d = 1.31 (60 ms > 960 ms), d = 1.12 (120 ms > 30 ms), d = 1.23 (120 ms > 960 ms); it was also larger in the 30–960 ms SOAs compared to the 1,500 ms SOA, p < .001 (only for 960 ms, p = .004), d = 0.78, 1.62, 1.57, 0.76, 0.98, and 0.62 for increasing SOAs, respectively. For the self-action condition, the inhibitory effect was larger for the 30 ms SOA compared to the 480 and 960 ms SOAs, p = .003 and < .001, d = 0.48 and 0.57, respectively; larger in the 240 ms SOA compared to the 960 ms SOA, p = .001, d = 0.52; and larger in the 30–960 ms SOAs compared to the 1,500 ms SOA, p < .001 (p = .002 for 480 ms, p = .01 for 960 ms), d = 0.82, 0.67, 0.64, 0.79, 0.44, and 0.35 for increasing SOAs, respectively.

Discussion

  1. Top of page
  2. Abstract
  3. Method
  4. Results
  5. Discussion
  6. References

In the present study, we tested whether a preceding self-action inhibited the startle blink reflex to an auditory startle pulse. We further characterized the temporal relationship between a preceding prepulse or a preceding self-action and a startle pulse for reflex inhibition. On the basis of these results, we will discuss commonalities and differences in the inhibitory effect elicited by conventional auditory prepulse and preceding self-action.

One of the main findings was that the startle blink reflex was inhibited by preceding self-action, as well as by a conventional auditory prepulse, suggesting that sensory systems regard preceding self-action as a kind of prepulse to inhibit the startle reflex. This finding is consistent with that of previous studies on the inhibitory effect of psychophysiological responses associated with self-action (Ison et al., 1990; Martikainen et al., 2005; Schafer & Marcus, 1973). Therefore, the inhibitory effect by self-action is common to both the nonstartle response reported in previous studies and the startle reflex generated at relatively earlier levels of sensory processing in regions such as the brainstem.

Here, we discuss how self-action inhibits the startle reflex. Some previous studies on the self-action inhibitory effect have suggested that self-action and cueing techniques enable participants to predict when an auditory stimulus will occur (Lange, 2011; Meincke, Topper, & Hoff, 2000; Schafer, Amochaev, & Russell, 1981; Schafer & Marcus, 1973) and facilitates reduced psychophysiological responses. The concept of temporal predictability itself is not dependent on the type of cueing, such as self-action or other cueing techniques. Schafer and colleagues emphasized the importance of temporal predictability or foreknowledge on the basis of similarly reduced ERP component (P1, N1, P2, N2, and P3) amplitudes in both self-action (Schafer & Marcus, 1973) and numerical cueing conditions (countdown to stimulus presentation; Schafer et al., 1981). However, Lange (2011) explicitly demonstrated different N1 amplitudes to self-generated tones and predictable visually cued tones, which implies that reduced ERP component amplitudes by self-action cannot be adequately accounted for by temporal predictability. Bäß, Jacobsen, and Schröger (2008) reported that reduced N1 amplitudes in ERP were dependent on whether a tone was externally or self-generated but not on temporal predictability. In the present study, participants had difficulty accurately predicting the onset timing of startle pulses because various SOAs were randomly presented in each trial. Therefore, the inhibitory effects in both the standard prepulse and self-action conditions may not be entirely accounted for by temporal predictability. We should consider other factors besides temporal predictability to explain the inhibitory effect by self-action. We will describe these factors in the context of temporal profiles of the inhibitory effects later in the Discussion.

The second important finding of this study is the significant difference in inhibition between the prepulse and self-action conditions. Regarding different inhibitory effects, on the basis of EEG studies (e.g., Lange, 2011), one might expect a larger inhibitory effect for the self-action condition than for the conventional prepulse because self-action is assumed to provide more precise timing information. However, we observed a larger inhibitory effect for the conventional prepulse condition than for the self-action condition. Similar studies showed that self-action inhibited approximately 15–50% of EMG amplitude in cutaneous and tap-elicited startle eyeblink measurements (Cohen et al., 1983; Ison et al., 1990; however, 63% inhibition in Meincke et al., 2000). Meanwhile, conventional PPI studies reported approximately 50–80% inhibition (for a review, Filion et al., 1998), but another study found that it reached 100% (Braff et al., 2001). Therefore, we speculate that the smaller inhibitory effect in the self-action condition might be common to inhibition by self-action in startle eyeblink measurements. Information associated with self-action helped predict that a sensory consequence of self-action would occur and served to reduce the impact of the consequence, whereas excessive consequence intensity (i.e., a stimulus property to startle participants) might be neither sufficiently predicted nor received as a sensory consequence of self-action. Further research is needed to confirm why inhibition by self-action is weaker than that by standard prepulse. Moreover, it is necessary to consider high arousal levels and the possibility of different habituations between the self-action and the prepulse conditions, because participants were asked to actively press a key.

The final finding in this study is the inhibitory effect of temporal differences between the prepulse and preceding self-action conditions. For the prepulse, the inhibitory effect was maximal at SOAs of 60–120 ms and was observed for all SOAs used in this study. These results are consistent with many previous PPI and sensorimotor gating studies (Braff et al., 2001). Meanwhile, the degree of inhibition by self-action reached a maximum at an SOA of 30 ms, and the inhibitory effect disappeared for the 480 ms SOA. In a related vein, Cohen et al. (1983; Experiment 1) reported that self-action maximally inhibited the mean eyeblink amplitude induced by glabella tap at SOAs of 0–50 ms, and the inhibitory effect persisted for less than 500 ms. In line with the present findings, many psychological and psychophysiological studies using different measurement modalities reported that such response inhibition was maximal soon after self-action and mostly declined less than 500 ms after self-action (MEG, Aliu, Houde, & Nagarajan, 2009; positron emission tomography, Blakemore, Frith, & Wolpert, 2001; fMRI, Leube et al., 2003; tickliness rating, Blakemore, Frith, & Wolpert, 1999; but see Lange, 2011, for wider temporal window of N1 suppression of the ERP). Sato and Yasuda (2005) explicitly measured the sense of self-agency by using the questionnaire item “I was the one who produced the tone.” They reported that the sense of self-agency sharply decreases as time intervals between self-action and tone increase. Although it may be necessary to carefully examine the mechanisms underlying various psychophysical measures, the present results suggest potential differences in inhibitory processing between self-action and conventional prepulse conditions. In particular, the characteristics of fast maximal inhibition and relatively short-lived inhibition may reflect a sort of specific inhibitory process associated with self-action. On a related note, Blumenthal and colleagues reported an inhibitory effect of a tactile prepulse (passive stimulation of the thenar eminence of the right hand) on the auditory startle reflex (Blumenthal & Gescheider, 1987; Blumenthal & Tolomeo, 1989). In these studies, startle reflex was facilitated around SOAs of 50 ms. Auditory startle reflex inhibition was shown at SOAs of 200–300 ms and became weaker at longer SOAs. Compared to an auditory prepulse, the delayed inhibition by a tactile prepulse is assumed to be affected by the transmission time delay for tactile input from the hand to midbrain (Blumenthal & Tolomeo, 1989). Similarly, the transmission delay might also delay the reduction of the inhibitory effect by self-action with a similar transmission time. Although we cannot directly compare those findings with the present results because of differences in stimulus quality, we speculate that, despite the transmission time delay, maximal inhibition by self-action at SOAs less than 50 ms may be useful as a psychophysiological index to distinguish between external preceding stimulus and self-action.

Regarding the inhibitory process associated with self-action, Cohen et al. (1983) suggested the possibility that the participants' expectation (temporal predictability and foreknowledge) and motor command (i.e., the neural command that produces an intended motor action) may contribute to eyeblink reflex inhibition by self-action. If only the participant's expectation determines the inhibitory effect, the inhibitory effect induced by the participant's mental set or expectation will persist for approximately 3 s after a signal to predict when a startle pulse comes (e.g., Hackley & Graham, 1984). However, we observed the inhibitory effect of self-action for SOAs less than 480 ms. Therefore, as Cohen et al. (1983) stated, we must consider the role of motor command besides temporal predictability that elicits inhibition. Here, we consider monitoring self-generated action and its consequences, known as “self-monitoring” (Frith, 2005). During the self-monitoring of action, proprioceptive feedback associated with self-action and sensory consequences of self-action can be predicted by motor commands that we intend to issue (Frith, 2005). The prediction (or forward modeling) might be used to label self-action and its consequence and to differentiate self-generated stimuli from externally generated stimuli (Blakemore & Frith, 2003). In this context, any predictable sensory consequences (e.g., startle pulse) produced by our actions might be attenuated and therefore have less impact on sensory systems (Blakemore, Rees, & Frith, 1998; Frith, 2005; Wenke & Haggard, 2009). In the present study, the fast maximal inhibition (at the minimum SOA of 30 ms) could occur in the self-action condition because the consequence of self-action might be predicted by motor commands before the presentation of a startle pulse. Blakemore et al. (1998) suggested that the predictability of sensory stimuli is a general phenomenon in that humans detect spatiotemporal patterns of sensory stimuli but are unable to distinguish whether the sensations are produced by self-actions or external events. Thus, the inhibitory effect by self-action may be explained in terms of the combination of the participant's predictability and self-action monitoring.

The findings of the present study may provide insight into a new “self-related” psychophysiological marker for schizophrenia. Patients with schizophrenia have deficits in recognizing self in action (Frith, 2005) and attribute the consequences of their own intentional actions to the intentions of others (Haggard, Martin, Taylor-Clarke, Jeannerod, & Franck, 2003). Therefore, they might have difficulty in relating self-action to spatiotemporally adjacent sensory stimuli as the consequence of self-action to adjust and reduce their responsiveness. This deficit might manifest as reduced inhibitory effects, such as reduced S2 (Meincke et al., 2000) and reduced N1 suppression (Ford, Gray, Faustman, Roach, & Mathalon, 2007; Ford & Mahtalon, 2012) by self-action. Thus, the self-action inhibition of the startle reflex in the present study may be useful as a rapid screening tool for deficits of predicting self-action and its consequences in schizophrenia, in combination with an established trait maker for sensorimotor gating deficits represented by PPI.

Collectively, the present findings clearly indicate that self-action works as a preceding stimulus for inhibiting the startle reflex to a subsequent auditory startle pulse, similar to a standard auditory prepulse. The amplitude of reflex inhibition by self-action is smaller than that elicited by an auditory prepulse. The smaller inhibition is consistent with previous findings on the startle reflex (Cohen et al., 1983; Ison et al., 1990); however, whether the small inhibition of the startle reflex is reliable and specific to self-action modulation still needs to be determined. Importantly, inhibition by self-action is maximal at the smallest SOA of 30 ms and more short-lived than that elicited by the auditory prepulse. These temporal characteristics are consistent with those reported in previous studies on sensory modulation by self-action using various psychological and psychophysiological measurements. We suggest that these characteristics are realized by predicting sensory consequences of self-action via the motor commands we intend to issue.

References

  1. Top of page
  2. Abstract
  3. Method
  4. Results
  5. Discussion
  6. References