2012. Vol.3, No.9, 666-674
Published Online September 2012 in SciRes (
Copyright © 2012 SciRes.
Spatial Negative Priming, but Not Inhibition of Return, with
Central (Foveal) Displays*
Eric Buckolz, Lyndsay Fitzgeorge, Stephanie Knowles
School of Kinesiology, The University of Western Ontario, London, Canada
Email: ebuckolz,,
Received June 2nd, 2012; revised July 4th, 2012; accepted August 2nd, 2012
The view persists that the inhibition of return (IOR) and the spatial negative priming (SNP) phenomena
may be produced by a common “orientation inhibition” mechanism (e.g., Christie & Klein, 2001), held to
arise during the processing of peripherally delivered (parafoveal) visual events. Both IOR and SNP effects
are present when responding to recently to-be-ignored distractor events is delayed. Since an SNP effect
has been produced using centrally located distracters (visual angle of about 2.5˚ or less), a common
mechanism view would require that these locations generate orientation inhibition, which then cause of
the SNP effect. We report past results and an experiment that reject the common mechanism view. Sub-
jects completed four tasks; two, 1-response tasks, using either central (Task 1) or peripheral (Task 2: IOR)
event locations, and two, 4-response tasks, again, using central (Task 3: SNP-central) or peripheral (Task
4: SNP-peripheral) locations. Trials occurred in pairs; first the prime (a target or a distractor), then the
probe (target only). Critically, neither distractor- nor target-occupied prime locations produced either in-
hibitory (SNP effect) or positive after-effects, respectively, in Task 1. Seemingly, centrally located events
do not generate orientation inhibition and so, unlike the IOR effect, this inhibition does not cause the
SNP-central phenomenon.
Keywords: Centrally Positioned Events; Orientation Inhibition; Spatial Negative Priming
Inhibitory after-effects are a consequence of an earlier act of
inhibition that interferes with later related processing (Tassinari,
Aglioti, Chelazzi, Marzi, & Berlucchi, 1987). The spatial nega-
tive priming effect (SNP; Tipper, Weaver, Cameron, Brehaut,
& Bastedo, 1991) and the inhibition of return phenomenon
(IOR; Posner, Rafal, Choate, Vaughn, & Cohen, 1985) are ex-
emplars of such inhibitory after-effects that arise as a result of
location processing; location being salient in SNP but not in
IOR tasks. Debate is ongoing as to whether the SNP and IOR
after-effects result from distinct (e.g., Fitzgeorge & Buckolz,
2008) or similar (e.g., Christie & Klein, 2001; Milliken, Tipper,
Houghton, & Lupianez, 2000) underlying processing. Our ob-
jective here is to again engage the “distinct exemplars” debate;
first, by presenting a brief review of some existing research that
supports the distinct exemplars position and second, by report-
ing an experiment that further embraces this viewpoint.
Resolving the distinct exemplars uncertainty does have some
importance. It should reduce confusion among studies render-
ing apparently discordant results because one has incorrectly
assumed IOR and SNP to be either the same or different phe-
nomena (e.g., see Chao, 2009). In a more practical vein, inhibi-
tory after-effect tasks are increasingly being used to identify
cognitive deficits (e.g., Verhaeghen & DeMeersman, 1998). So
it is essential that we understand what processing is being chal-
lenged by each of these tasks in order to avoid misdiagnoses.
The approach here to the distinct exemplars issue regarding
prior research is straightforward. We examine how inhibition
associated with distractor processing, which creates inhibitory
after-effects, likely arises in SNP and IOR tasks. Distinct ex-
emplars would be indicated if inhibition production mismatches,
the reverse holding if they match.
The Inhibition of Return (IOR) Effect
With the basic IOR task, trials are presented in pairs; first the
cue trial and then the target trial; henceforth, called the “prime”
and “probe” trials, respectively, to be consistent with SNP ter-
minology. Participants usually focus on a central fixation point
positioned midway between two possible peripheral event loca-
tions (i.e., subtending visual angles of greater than about 2.5˚).
An uninformative, to-be-ignored stimulation (e.g., luminance
elevation) is then delivered at one of the peripheral locations on
the prime trial and is followed by a single target stimulus on the
probe (sometimes preceded by an intervening central stimula-
tion). Individuals indicate their detection of the probe target by
executing a known response (e.g., a keyboard button press) as
quickly as possible. When the time delay between successive
trials is short (<200 - 300 msec), probe target reaction times are
smaller when it appears at the previously cued than at the for-
merly uncued position. This ordinal relationship is reversed
with longer inter-trial delays, and is commonly referred to as
the IOR effect (Posner & Cohen, 1984).
A basic tenet of most IOR explanations is that the IOR-
producing ingredients evolve during the perceptual processing
associated with peripherally positioned (parafoveal) distractor
(or target) events (cues). This processing includes the automatic
generation of an orienting response plan aimed at visiting the
*This research was supported by an operating grant to the first author and a
Doctoral Scholarship to the second author from the Natural Sciences and
Research Council of Canada.
stimulation source. Orienting response plans may involve atten-
tion (Posner & Cohen, 1984), oculo-motor (Rafal, Calabresi,
Brennan, & Sciolto, 1989) or head/neck (Corneil, Munoz,
Chapman, Admans, & Cushing, 2007) actions, or some combi-
nation of these, and are accompanied by the reflexive produc-
tion of orientation inhibition. When the original (stored) orient-
ing response plan is re-generated and retrieved by the probe
target when it appears at the prime-stimulated position, the
earlier formed orientation inhibition delays responding, relative
to when the probe target appears elsewhere (i.e., the IOR effect).
This version of IOR production may be viewed as somewhat
controversial in that it does not stipulate the conventional view
that the cued location itself is inhibited, which then contributes
to IOR generation. It is, nonetheless, a version that acknowl-
edges findings reported by Klein, Christie, and Morris (2005),
and subsequently replicated by Fitzgeorge and Buckolz (2009).
We present this work later.
We are aware that some details of IOR production remain
controversial (see Lupianez, Klein, & Bartolomeo, 2006; Rafal,
Davies, & Lauder, 2006, for reviews); however, we do not con-
sider them here because their resolution is not important for our
current needs. Rather, what we need agreed upon is that the
IOR effect results from the orientation inhibition that ultimately
arises during the perceptual processing of a peripheral stimula-
tion. Below, we illustrate that the SNP effect of current interest
arises via other means (i.e., during response-end processing),
consistent with the view that IOR and SNP are distinctly pro-
duced inhibitory after-effects.
The Spatial Negative Priming (SNP) Task/Effect
With SNP tasks, trials are again presented in pairs; first the
prime, and then the probe. Target and distractor events are pre-
sented at different locations, either singly or together on the
prime and probe trials, with each of these locations traditionally
being assigned their own manual response. Participants respond
by using the manual output assigned to the target-occupied lo-
cation, while attempting to ignore any distractor event that
might be present. Most commonly (but see Fitzgeorge, Buckolz,
& Khan, 2011), an SNP effect is registered when reaction time
is significantly longer when the probe target arises at a location
previously occupied by a distractor event (i.e., ignored-repeti-
tion trial) than when it occurs at a formerly unused location
(control trial) [e.g., Neill, Terry, & Valdes, 1994].
To be clear about our intentions here, we need to acknowl-
edge that past SNP procedures have used either “peripheral”
(i.e., SNP-peripheral: Chao, 2009; Christie & Klein, 2001;
Tipper, Brehaut, & Driver, 1990) or “central” (i.e., SNP-central:
e.g., Buckolz et al., 2008; Fitzgeorge & Buckolz, 2008; Fitz-
george et al., 2011; Guy, Buckolz, & Fitzgeorge, 2007; Guy,
Buckolz, & Khan, 2006; Guy, Buckolz, & Pratt, 2004; Neill et
al., 1994) event locations. Central locations subtend a visual
angle of about 2.5˚ or less so that delivered events fall wholly
or partially within the fovea area of the retina, while peripheral
locations naturally extend outside this area (i.e., parafoveally).
Because SNP-central and SNP-peripheral designs may have
different causes too (more on this later), they need to be distin-
guished from one another. Accordingly, we note that our pri-
mary intention is to contrast the causes of SNP-central and IOR
inhibitory after-effects, and so the SNP data considered herein,
unless otherwise indicated, has been derived from the SNP-
central procedure.
Our preferred explanation of the SNP-central inhibitory after-
effects is one mostly set out by Fitzgeorge et al. (2011). Briefly,
they proposed that the appearance of the prime-trial distractor
sets in motion automatic processing that includes the recogni-
tion of the prime distractor object (Fitzgeorge & Buckolz, 2008;
Fitzgeorge, 2009) and its location, along with the activation (A)
and subsequent inhibition (I) of the distractor location’s as-
signed response. Commensurate with this act of inhibition, the
distractor response becomes execution resistant (i.e., ER), a
feature that operates to prevent its future use. Along with the
prime distractor object/location, the distractor-response proc-
essing (i.e., AIER) is stored, and later reflexively retrieved
by the probe target on ignored-repetition (IR) trials, likely as a
result of the activation of the former prime distractor response
(Edgar, 2011). Overcoming ER takes time, causing RT(IR) to
be delayed, thereby producing the SNP effect. Incidentally, the
existence of a distractor-response ER feature is supported by
the fact that under free choice conditions, subjects showed an
aversion to choosing the prime distractor response in favour
of the control response (Edgar, 2011; Fitzgeorge et al., 2011).
In short, SNP-central is caused by distractor-response inhibi-
In the foregoing account, unlike for the IOR effect, orienta-
tion inhibition played no role in SNP-central production. The
notion that centrally positioned, distractor-occupied locations
are not associated with orientation or location inhibition is
somewhat new, and is also critical to the argument that IOR and
SNP-central likely have distinct causes. Thus, we briefly re-
count the related literature on this matter next.
SNP-Central Data: On th e Absence of
Orientation/Location Inhibition
Many:1 (M:1) Location-to-Response Mappings. A key fea-
ture of these M:1 mappings is that they isolate the impact of the
prime distractor response’s ability to produce inhibitory after-
effects, independent of any contribution from its related prime
distractor location. In this case, the probe target appears at a
new location while the prime distractor response is required
(i.e., a distractor response repeat [DRR] trial). Reaction time for
a DRR trial is significantly longer than when a control response
is used (Edgar, 2011; Guy et al., 2006), showing that the inhib-
ited prime distractor-response contributes to SNP-central gen-
eration. More important, though, is the fact that RT(DRR) size
significantly exceeds RT(IR). This shows that central, distrac-
tor-occupied prime locations are not associated with orientation
or location inhibition, and so these types of inhibition do not
contribute to SNP-central production. If anything, it seems
re-occupied prime distractor locations seem to produce a facili-
tation effect on latency.
Target-Repeat vs Control Trial Latencies
Although smaller in size than for the usual distractor-target
trial, an IOR effect does materialize at responded-to, prime-trial
target locations (i.e., called “target-target” trials) [e.g., Coward
et al., 2004; Fitzgeorge & Buckolz, 2009; Taylor & Klein, 2000;
Welsh & Pratt, 2006]. Presumably, the latency benefits of repe-
tition (and/or inhibition absence) counter but do not fully offset
the inhibitory after-effects attributed to orientation inhibition on
target repeat trials. Christie and Klein (2001), relying mainly on
target + distractor prime and probe trial results, did report in-
stances in their declared SNP task where prime target locations
Copyright © 2012 SciRes. 667
exhibited significant inhibitory after-effects. On this basis, and
having explained dissenting results, they concluded that IOR
and SNP had comparable causes. It is possible, however, that
the target-target slowing observed by Christie and Klein oc-
curred because they used an SNP-peripheral procedure. This
possibility is supported by the fact that a target-repeat facilita-
tion rather than an interference effect is observed with central
locations in SNP tasks. This held both when target plus dis-
tractor (e.g., Buckolz et al., 2008; Guy et al., 2006; Fitzgeorge,
2009; Fitzgeorge & Buckolz, 2008) or target-only probe trials
had been employed (e.g., Guy et al., 1994). So, target-repeat
data do not implicate the involvement of orientation or location
inhibition for centrally delivered events. Hence, they do not
argue for IOR and SNP-central having a common production
Also bear in mind that the Christie and Klein (2001) data did
not rule out the involvement of response inhibition (Fitzgeorge
et al., 2011) as a contributor to their SNP effects. So, on this
account as well, their data do not unequivocally point to a
common mechanism for IOR and SNP-central.
The Vector (Center of Gravity) Model of IOR
Klein et al. (2005) were the first to report that when simulta-
neously presented distractor events were symmetrically posi-
tioned on either side of midline in the visual periphery, IOR
effects failed to materialize at these stimulated locations
(Fitzgeorge & Buckolz, 2009). This failure is further evidence
that distractor-occupied locations are not themselves inhibited,
albeit peripheral locations in this case. Additionally, these
failed IOR effects have altered the typical IOR explanation, a
possibility that needs to be acknowledged in the IOR vs
SNP-central distinct phenomena debate. The account is ap-
proximately as follows.
In the usual IOR procedure, a single exogenous stimulus
generates a vector (i.e., an orienting response) which is the
source of inhibition and which points to the stimulated position.
Alternately, paired stimulations produce a net vector that is
positioned midway between the two actual stimulation posi-
tions, which then serve as the center of inhibition, and from
which radiates a decreasing gradient of inhibition magnitude.
This manoeuver separates the true source of inhibition (i.e., the
net vector) from the cued locations. In so doing, it reveals that
distractor-occupied (cued) locations do not yield inhibitory
after-effects, which means that they are not themselves inhib-
ited (i.e., the IOR effect; RT[cued] = RT[uncued]). Hence, nei-
ther IOR nor SNP-central effects are caused by location inhibi-
tion. However, their causes would differ in that a cued periph-
eral location would generate an inhibitory vector, while it is
unlikely central stimulations do the same. This is supported by
the RT(DRR) > RT(IR) finding noted earlier (Edgar, 2011; Guy
et al., 2006), showing the prime distractor location unrelated to
inhibitory after-effects.
Finally, if IOR and SNP-central effects have a common
cause, the net vector influence should cause SNP-central values
to be smaller with target plus distractor than with distractor-
only prime trials. That is, different-side prime-trial presenta-
tions should have produced little or no measured inhibitory
after-effects1, reducing the SNP calculated value. This influ-
ence would be absent in with distractor-only primes. This did
not occur (Buckolz et al., 2008).
In sum, the existing literature indicates that the IOR and
SNP-central effects have distinct causes; the former generating
inhibition from peripheral location processing (inhibitory vector
“our term”/orientation inhibition) while, with the SNP-central
task, distractor-response inhibition solely produces the inhibi-
tory after-effects observed.
The Current Experiment
Four tasks were used, differing with regard to event location
(central [C], peripheral [P]) and to manual response number
(1-response [1-R] vs 4-response [4-R]). Prime trials contained
target or distractor event, the probe trial only the former (Buck-
olz et al., 2008). Theoretically, these Tasks represented a con-
tinuum of inhibition producing mechanisms: Task 1(C[1-R]) =
none (past research) or potential orientation inhibition/ vector
inhibition (to-be-tested), Task 2 (P[1-R]) = orientation inhibit-
tion, vector inhibition (IOR), Task 3 (C[4-R]) = response inhi-
bition (SNP-central), and Task 4 (P[4-R]) = orientation inhibit-
tion/vector inhibition + response inhibition.
Importantly, Task 1 can provide direct evidence that cen-
trally stimulated locations do not generate inhibitory after-ef-
fects (since this Task lacks the response processing held to
produce the SNP effect). This evidence would take the form of
the absence of an inhibitory after-effect altogether with this
Task, or if an observed inhibitory after-effect is accompanied
by equivalent RTs for target-repeat (TR) and control (CO) trials.
The latter follows from Coward, Poliakoff, O’Boyle, & Lowe
(2004). They proposed that the distractor-occupied location
forms a stronger bond with the location’s activated and subse-
quently inhibited response so that this response inhibition ex-
erts a stronger influence when the probe target occupies the
prime distractor location. This contributes to the production of
the IOR effect on distractor-target trials, a contribution that is
removed on target-repeat trials leaving only orientation inhibit-
tion to operate. Hence, an RT(target-repeat) = RT(control)
finding points to the absence of the latter inhibition type. The
uncertainty at this point is whether the proposal of Coward et al.
operates with central event presentations.
Furthermore, Task 4 (P[4-R]) will allow us to study the in-
teractive effects of orientation and response inhibition subse-
quent to distractor primes, comparing its after-effects with
those of Tasks 2 (P[1-R]) and 3 (C[4-R]). Also, following tar-
get primes in Task 4, we can examine opposing positive (repe-
tition) and negative (orientation inhibition) forces on latency
production. The RT(target-repeat[TR]) vs RT(Control[CO])
relationship will indicate which force, if any, prevails. Impor-
tantly, should RT(TR) < RT(CO) occur (Chao, 2009), the prac-
tice of using this inequality to signal the absence of orientation
inhibition would have to be discontinued.
1We were able to examine different-side target-plus-distractor prime trial
presentations with some SNP-central pilot data that used a 2.0 inter-trial
delay (n = 22) and target-plus-distractor probes. A significant SNP-central
effect (21 ms) was obtained, (t[21] = 2.64, p < 0.02, SD = 37.62), indicating
that central distractor locations do not generate inhibitory net vectors; oth-
erwise the SNP effect should have been absent. Hence, IOR and SNP-central
have different causes on this account.
Forty university undergraduate students, ranging in age from
20 - 30 years and with normal or corrected-to-normal vision,
Copyright © 2012 SciRes.
participated in this experiment.
The apparatus, procedures, and the various timing values
employed here have been used before (e.g., Fitzgeorge &
Buckolz, 2008; Fitzgeorge et al., 2011).
The input display was presented in a dimly lit room on a 47.5
cm computer screen, situated on a tabletop located 73.5 cm
above the floor. The display consisted of a fixation cross that
appeared in the center of the screen, accompanied on each side
by two horizontally-arranged bar markers that specified the
possible locations of the target (T) artdenoted L1 - L4 from left
to right. The fixation cross and each bar marker (denoted L1 -
L4 going left to right) measured 0.9 cm in width, were white in
colour and appeared against a black background. Bar markers
L2 and L3 were each separated from the fixation cross by a
distance of 2.3 cm, and so were separated from each other by a
distance of 4.6 cm, center to center. In turn, bar markers L1 and
L4 were separated from L2 and L3 by 0.5 cm, respectively.
Accordingly, the horizontal distance of each of these locations
from the fixation cross, center to center, was 3.7 cm, with a
total L1 to L4 distance of 7.4 cm, center to center. With their
chins resting on a chin rest platform for the entire experiment,
participants processed the input display from two viewing dis-
tances of 40 cm and 190 cm were used, producing approximate
visual angles of 7˚ - 11˚ (inner-outer bar markers) [peripheral or
exogenous locations] and of 1.5˚ - 2.2˚ (central or endogenous
locations). Location (peripheral vs central) was a within-sub-
jects variable.
In order to respond to the appearance of a target stimulus, all
participants sat with their forearms comfortably placed on a
desk top containing a stablized computer keyboard. Both a
1-response and a 4-response protocol were used (between-sub-
jects factor). Participants randomly assigned to the 1-response
case, placed the index finger of their dominant hand on key-
board button “B”, depressing this key as fast as possible to de-
note the detection of the target stimulus. The remaining par-
ticipants using the 4-response procedure, positioned the middle
and index fingers of their left and right hands on keyboard but-
tons “D”, “V”, “L” and “M”, respectively. These buttons were
assigned to their spatially compatible bar marker locations (L1,
L2, L4, L3, respectively). Participants then indicated their per-
ception of a target’s location by pressing the spatially corre-
sponding (assigned) button as quickly as possible, while taking
care to avoid errors. Both prime and probe trial target presenta-
tions required a manual response.
Four tasks were formed by crossing the levels of the Loca-
tion and Response Number factors: Task 1 (central locations,
1-response: C1-R), Task 2 (peripheral locations, 1-response:
P1-R—traditional IOR task), Task 3 (central locations, 4-re-
sponses: C4-R—traditional SNP task) and Task 4 (peripheral
locations, 4-responses: hybrid: P4-R—both IOR and SNP
causes potentially active).
Labels assigned to Trial 1 and Trial 2 pairings differ for IOR
and SNP tasks. Henceforth, the SNP terminology will be used
here (noting that the prime trial and probe trial SNP terms are
comparable to the cue-trial and target-trial labels used with IOR
research. As well, the ignored-repetition and target-repeat la-
bels used in SNP reports are analogous to the cue-target and
target-target trial terms employed in IOR research, respectively).
The prime trial unpredictably contained a target or a distractor
event, whereas, the probe predictably contained a target-only
stimulus (T or DT-only). The target and the distractor events
consisted of green and red rectangles, respectively, and were
the same size, 0.9 cm wide and 1.9 cm high. The prime and
probe events appeared equally often at all possible locations in
a balanced design.
All trials began with a warning tone (100 ms) whose offset
was followed by the appearance of the bar markers and fixation
cross on the computer screen. Participants were asked to direct
their gaze to the central fixation cross prior to the beginning of
each trial, thereafter, they were free to visually orient as they
wished. According to Rafal and colleagues (1989, Exp. 4;
2006), these instructions should not disrupt any peripheral in-
hibitory-after-effect. Two hundred milliseconds after this ap-
pearance, the prime-trial event, either a to-be responded to tar-
get or to-be ignored distractor and remained present for 157 ms.
A time period of 700 ms elapsed between the offset of the
prime-trial display and the presentation of the probe-trial
stimulus was delivered. The probe-trial again lasted for 157 ms.
The initiation of the probe-trial response caused the screen to
go blank and initiation an inter-trial interval of 1500 ms. Ter-
mination of the inter-trial interval coincided with the onset of
the warning tone which initiated the next trial-pair sequence.
Participants completed 512 trial pairs, 256 each with the fo-
veal and peripheral event presentations. Each 256 trial series
consisted of 128 trial-pairs beginning with a distractor event: 16
inside ignored-repetition, 16 outside ignored repetition, 48 in-
side control, and 48 outside control. The remaining 128 trial-
pairs began with a target event, resulting in 16 inside target-
repeat, 16 outside target-repeat, 48 inside control, and 48 out-
side control trials. Using the 1-response or the 4-response pro-
cedure, participants completed two experimental sessions, one
when the display appeared in the periphery and one when the
display appeared centrally. A session lasted about thirty min-
utes, and breaks were automatically offered after every 24 trial
pairs (a break approximately every 3 minutes). A trial series
was restarted when the subject pressed the space bar.
Participants were also told that trials would be presented in
pairs and that a new pair would begin following each tone oc-
currence. Participants were instructed as well to respond as
quickly as possible to target stimuli while ignoring any distrac-
tor event that might appear. Before starting the experimental
session, participants completed 5 practice trial pairs and had
questions answered to ensure that the task requirements were
Response times of less than 100 ms (anticipations), or greater
than 1000 ms (insufficient vigilance) [both less than 1%], were
excluded from reaction time analyses. The low incidence of
anticipations, along with the comparatively large probe-trial RT
values observed for the 1-Response tasks (Table 1), indicate
that, as instructed, participants largely waited to detect the
probe event before responding. Trials where a button-press
error had occurred, and probe trials that were preceded by a
prime-trial, button-press error, were also excluded.
Prime-Trial Data
Mean reaction times associated with prime-trial target presenta-
Copyright © 2012 SciRes. 669
Copyright © 2012 SciRes.
Table 1.
Mean probe-trial reaction times (ms) for ignored-repetition (IR), target-repeat (TR), distractor-prime control (CO) and target-prime control (CO) trials
as a function of response number (1, 4) and prime-trial event locations (central, peripheral).
1-Response 4-Response
Event Locations Central Task 1
Peripheral Task 2
Central Task 3
Task 4 (P[4-R])
Distractor Prime
Trial Type
Ignored-Repetition 303 (11.3) 316 (12.1) 488 (7.8)
468 (12.2)
Control 298 (10.7) 287 (7.2) 452 (10.1)
440 (9.5)
After-Effects (IR-CO)
(Error Rate Difference) 05 29* 36*
Target Prime
Target-Repeat 284 (9.3)
295 (10.2)
416 (5.4)
412 (6.9)
Control 286 (9.3) 279 (9.5) 452 (7.2)
434 (7.8)
After-Effects (TR-CO)
(Error Rate Difference) 02 16* 36*
Note: distractor-prime, when a distractor event only appears on the prime trial; target-prime, when only a target event appears on the prime trial; peripheral location =
visual angle 7˚; central location = visual angle 2.2˚; ( ) = standard error (ms); [ ] = button-press error (%); *p < 0.05.
tions were 367 ms (SE = 5.21), 366 ms (SE = 5.25), 457 ms (SE
= 5.53), and 438 ms (SE = 8.07) for Tasks 1 through 4, respec-
tively. Button-press error rates occurred 3.93% and 3.96% of
the Task 3 (C[4-R]) and Task 4 (P[4-R]) trials, respectively.
Incorrectly producing a manual response following distractor
prime-trials occurred at the following rates; 3.39%, 2.81%,
0.50%, and, 0.42% of the trials administered for Tasks 1
through 4, respectively.
Probe-Trial Data
A separate analysis of variance (ANOVA) was calculated
using mean subject reaction times or button-press error rates
(4-response tasks only) for distractor or target primes. Response
Number (1 vs 4: between-subjects), Event Location (central vs
peripheral) and Trial-type (ignored-repetition vs control, or
target-repeat vs control) served as the main factors for the la-
tency ANOVAs. Only the latter two factors were involved with
the error rate ANVOAs. ANOVA cell means are found in Ta-
ble 1.
Following a Distractor Prime
Reaction Times. Overall, reactions were significantly slower
for 4-response (462 ms) than for 1-response (301 ms) tasks, F(1,
58) = 176.09, p < 0.01, MSE = 17656), and for ignored-repeti-
tion (394 ms) than for control (370 ms) trials, the latter signify-
ing the presence of an inhibitory after-effect (24 ms), F(1, 58) =
112.51, p < 0.01, MSE = 618. Importantly, the three-way inter-
action was significant, F(1, 58) = 23.55, p < 0.01, MSE = 334.
Two, follow-up planned comparisons were calculated; one
using only the 4-response, the other using only the 1-response,
tasks. The 4-response tasks (Tasks 3 (C[4-R]) & 4 (P[4-R]) did
not yield a significant interaction, F(1, 29) = 2.24, p = 0.15,
MSE = 202, producing comparable inhibitory after-effect mag-
nitudes (Task 3 = 36 ms, SNP-central effect; Task 4 = 28 ms,
SNP-peripheral). For the 1-Response Tasks (1 and 2), a signi-
ficant Trial-type by Location interaction materialized, F(1, 29)
= 34.50, p < 0.01, MSE = 132. Newman-Keuls tests (p < 0.05)
revealed the expected presence of a significant IOR effect for
peripheral event locations (Task 2, P[1-R] = 29 ms) but, impor-
tantly, not for the central distractor locations (Task 1 C[1-R] =
05 ms).
Button-Press Error Rates (4-response Tasks). The ANOVA
using button-press error rates produced a significant Trial-type
main effect. Button-press error rates were reliably higher for
ignored-repetition (7.1%) than for control (4.0%) trials, F(1, 29)
= 11.26, p < 0.01, MSE = 0.003. No other significant effects
were obtained. This result has been reported before in SNP-
central tasks (e.g., Buckolz et al., 2008; Fitzgeorge & Buckolz,
2008; Guy & Buckolz, 2007) and is consistent with the view
that the SNP-central effect is the result execution resistance
(ER) imparted to the prime distractor response at the time of its
inhibition (Fitzgeorge et al., 2011). On some ignored-repetition
trials, ER, absent on control trials, successfully drives response
selection away from the former prime distractor response,
causing an error.
Following Target Primes
Reaction Times. An overall significant Trial-type main effect,
F(1, 58) = 24.21, p < 0.01, MSE= 288, was qualified by two
first order interactions; Trial-type by Response Number, F(1, 58)
= 66.68, p < 0.01, MSE = 288, and Trial-type by Location, F(1,
58) = 22.02, p < 0.01, MSE= 162. No other significant effects
were found.
A planned comparison using just the 1-response tasks
(C[1-R], P[1-R]) produced a significant interaction, F(1, 29) =
20.32, p < 0.01, MSE= 111. A Newman-Keuls test showed the
presence of a significant IOR effect for target-repeat trials (16
ms) only when peripheral event locations were used (P[1-R],
Task 2). A further planned comparison involving only the
4-response tasks (C[4-R], P[4-R]) produced a significant Trial-
type by Event Location interaction as well, F(1, 29) = 6.44, p <
0.02, MSE = 214. Along with Newman-Keuls tests, the analy-
ses revealed a significant facilitation effect for target-repeat
trials for both central (36 ms; C[4-R]) and peripheral (22 ms;
P[4-R]) event locations, being reliably smaller in the latter in-
stance. Interestingly, the reduced target-repeat effect size (22
ms), comparing Task 3 (C[4-R]) to Task 4 (P[4-R]), was about
equal to the orientation inhibition (16 ms, in the P[1-R] task)
presumably added to Task 4 due to its peripheral locations [i.e.,
36 ms – 16 ms = 20 ms). Seemingly, positive and negative la-
tency processing interacts to produce a net effect on target-
repeat reaction time in SNP-peripheral tasks (P[4-R]).
Button-Press Error Rates (4-Response Tasks). An ANOVA,
calculated as above, found only the Trial-type main factor to be
significant, F(1, 29) = 18.70, p < 0.01, MSE = 0.002. Button-
press error rates were larger for control (7.5%) than for target-
repeat (4.2%) trials for the 4-Response tasks. Response selec-
tion is less likely to deviate from the correct option if it includes
a repetition of the just-executed response, and the target-repeat
RT benefit was not achieved by trading off accuracy for speed.
The advantage of fully repeating the previous trial is faster and
less error prone response production.
The perceptual processing of centrally delivered events does
not generate orienting response urges (i.e., inhibition vectors)
or orientation inhibition that cause inhibitory after-effects.
No inhibitory after-effects were produced when either target
or distractor prime-trial events were presented at central loca-
tions in a 1-response task (i.e., Task 1, Table 1). Hence, central
distractor or target occupied locations are not associated with
inhibition (the pre-requisite for after-effect production), either
because the location generated an orienting response urge (i.e.,
inhibition vector) with its attendant orientation inhibition, or
because the position itself was inhibited. Thus, the SNP-central
effect, both here (Task 3, C[4-R]), and in much prior SNP re-
search (e.g., Buckolz et al., 2004, 2008; Guy et al., 2004;
Fitzgeorge & Buckolz, 2008; Neill et al., 1994), has not been
produced by orientation or location inhibition associated with
the processing of the centrally delivered prime events. This
finding reinforces prior work showing that the SNP-central
effect is produced entirely as a result of response inhibition
(e.g., Guy et al., 2006; Edgar, 2011) and supports the view that
the IOR (being produced by orientation inhibition) and the
SNP-central phenomenon have distinct causes.
Before accepting this conclusion, we need to address a pos-
sible procedural limitation; namely, that the absence of inhibit-
tory after-effects in Task 1 (C[1-R]) occurred because the loca-
tion discrimination pre-requisite for this after-effect production
failed to occur, since it was not required to perform the 1-
Response task (Note—the use of catch trials would not remedy
this concern). One step in this regard is to note that location
discrimination seems to take place automatically for centrally
positioned events (Fitzgeorge et al., 2011) [and, incidentally,
for peripherally delivered events as well, Mulckhuyse & Theeu-
wes, 2010]. Fitzgeorge et al. demonstrated that inhibitory af-
ter-effects in an SNP-central task were highly comparable both
for non-masked, and for successfully masked, distractor primes.
Since masked distractor prime processing is held to be auto-
matic (Mulckhuyse & Theeuwes; Sumner, 2007), the compara-
ble after-effects found by Fitzgeorge et al. suggest that non
masked distractor primes are also automatically processed,
including, of course, location discrimination.
Even if one accepts that location discrimination occurs
automatically, there is still a need to address the caution that
“automatic does not mean inevitable”. Hence, location discri-
mination cannot be assumed to have occurred in Task 1 (C[1-R])
on this account. Our general response to this caution is that
available experimental evidence indicates that it is not inevita-
bly true, and that a delineation of those aspects of automated
processing that are changeable, and those which are not, is still
ongoing. Nonetheless, even at this preliminary stage, we do not
believe that the caution applies to concerns about whether
automatic location discrimination occurred in Task 1 (C[1-R])
To begin with, simply rendering aspects of automatic pro-
cessing unnecessary (i.e., location discrimination) is not suffi-
cient to prevent this processing. This is evident in the produc-
tion of Simon effects (obtained with central locations: Hommel,
1993; Proctor & Lu, 1994; Wang & Proctor, 1996) and in the
inhibitory after-effects produced at prime distractor locations in
identity negative priming tasks (Connelly & Hasher, 1993). So,
although rendered unnecessary in Task 1 (C[1-R]) here, auto-
matic location discrimination would not have been prevented
on this account.
Furthermore, when automatic processing outcomes (i.e., lo-
cation discrimination) go beyond simply being unnecessary and,
instead, are deemed to be entirely unwanted, individuals still
seem incapable of stopping the automatic processing. A simple
illustration of this occurs when individuals are instructed to
ignore prime-trial distractor objects in SNP-central tasks (i.e.,
and so prevent their processing). They seem unwilling or un-
able to do this, as distractor-occupied locations yield significant
inhibitory after-effects (i.e., location discrimination had to have
occurred for this to happen). A more sophisticated example of
the difficulty in preventing unwanted automatic processing was
provided by Fitzgeorge and Buckolz (2008), and by Fitzgeorge
(2009). They showed that the SNP-central effect was elimi-
nated when distractor free probe trials were likely (75%) and, in
fact, materialized. However, when a distractor unexpectedly
appeared with the probe target, the SNP effect was restored.
Clearly, the lack of a SNP-central effect on distractor-free
probe trials was not caused because the automatic processing
needed to produce the ingredients necessary for this effect had
been prevented. Rather, the absence of the SNP-central effect
was logically the result of retrieval blocks, preventing access to
the stored after-effect producing information (Edgar, 2011;
Fitzgeorge et al; 2011). This access denial was circumvented by
a separate retrieval route (Fitzgeorge) activated by the probe
distractor object.
Evidently, then, some aspects of automatic processing resist
prevention. Speculating as to what these might be more broadly,
these might include the basic processing operations needed to
produce (spatial) inhibitory after-effects as highlighted by
Fitzgeorge et al. (2011); including location discrimination, the
idea that a stimulus event will retrieve its related response if
one exists, and the automatic self-inhibition of unintended re-
sponse activations in direct access systems (Schlaghecken,
Rowley, Sembi, Simmons, & Whitcomb, 2007).
In contrast, some automatic processing features are likely
Copyright © 2012 SciRes. 671
subject to modulation. These have contributed to the caution
that “automatic does not mean inevitable”. For example,
O’Connor and Neill (2010) have shown that the stimulus-re-
sponse (S-R) mapping rule utilized by the automatic processing
of a masked distractor prime can be altered; in their case, the
rule mimicked the S-R mapping utilized by the same event
when it was visible on the probe trial. In a similar but not iden-
tical vein, when a masked prime event predicted the probe re-
sponse, this contingency was somehow discovered [Bodner &
Mulji, 2010; Perry, 2011] and then used to automatically acti-
vate the forecast output. It seems that while a familiar stimulus
will inevitably contact its associated response during automatic
processing, there is some flexibility as to which response that
will be. Note, too, that while response associations underwent
change during automatic processing, inhibitory after-effects
nonetheless persisted (O’Connor & Neill).
In sum, the caution that “automatic does not mean inevita-
ble” does not appear to undermine the current view that loca-
tion discrimination occurred automatically in our Task 1
(C[1-R]), nor our main conclusion that central event locations
do not generate inhibitory after-effects. We, nonetheless, car-
ried out a pilot study that more directly tested whether the lack
of inhibitory after-effects in Task 1 (C[1-R]) was due to the
absence of location discrimination in that condition (Appendix
We induced location discrimination in Task 1 in spite of its
1-Response component by requiring participants (n = 20) to
verbally report the location of the prime event after responding
to the probe trial. This report requirement does not eliminate
either the IOR (Fitzgeorge & Buckolz, 2009) or SNP-central
effects (Guy et al., 2007). Subjects accurately reported the posi-
tion of the prime event about 97% of the time and so had un-
dertaken location differentiation. If the absence of location
discrimination had caused the lack of an inhibitory after-effect
in Task 1 ([1-R]), we should now observe these after-effects.
This did not occur. The lack of location discrimination in Task
1 did not cause the absence of inhibitory after-effects. More-
over, the pilot study results reinforce the position that distrac-
tor-occupied central locations do not produce inhibitory after-
Accordingly, the SNP-central effect is unrelated to orienta-
tion inhibition arising out of the processing of central distrac-
tor-occupied locations. Hence, SNP-central and IOR are dis-
tinct phenomena.
Before proceeding, we note that Possami (1986) found that
centrally positioned distractor events did produce inhibitory
after-effects. Unlike the work referred to earlier, which used
only (pure) central locations, Possami delivered distracter
events at both central and peripheral locations, intermixed in a
trial series. Possibly, inhibitory processing may differ for pure
and intermixed designs in a way that could explain why Pos-
sami found inhibitory after-effects with his central distractor
locations (Buckolz, Kajaste, Lok, Cameron, & Khan, 2011).
For the moment, it seems that Possami’s results may not repre-
sent a contradiction to research indicating that distractor-occu-
pied central locations do not generate inhibitory after-effects
(pure design).
What after-effects are produced when orientation inhibition
and response inhibition operate together (SNP-peripheral task,
When both orientation and response inhibition types possibly
functioned together on an ignored-repetition trial in Task 4
(P[4-R]), the inhibitory after-effect produced (28 ms) was
equivalent in size to that which each inhibition type produced
on its own; i.e., orientation inhibition (29 ms, Task 2 [P(1-R)])
and response inhibition (36 ms, Task 3 [C(4-R)]). With this size
equivalence, it is not possible to say whether the orientation and
response inhibition types are processed in parallel, or whether
one overrides the other. In either case, while we can expect
equivalent SNP values from the SNP-central and SNP-peri-
pheral procedures; maintaining this SNP task distinction may
still be important. This is because the two SNP task types may
respond differently to the same experimental manipulation,
given that one task includes orientation inhibition (SNP-peri-
pheral), while the other does not. Below is a recent demonstra-
tion of this possibility.
When the prime trial contains both a target and a distractor,
the predictable absence of a probe-trial distractor eliminates the
SNP effect with the SNP-central procedure (Buckolz, Bouloug-
ouris, & Khan, 2002; Fitzgeorge & Buckolz, 2008; Guy et al.,
2004; Tipper et al., 1990) but not with the SNP-peripheral de-
sign Chao (2009). These apparently discordant results are read-
ily explained when one is mindful of the SNP-central vs.
SNP-peripheral distinction. Chao simply demonstrated what
has been known for some time; namely, that orientation inhibi-
tion and the IOR effect survive certain distractor-free (probe)
trials (e.g., Posner & Cohen, 1984), even when a response is
made on the prime trial (e.g., Coward et al., 2004).
There is further data here indicating that orientation inhibit-
tion operates within SNP-peripheral designs, justifying the
SNP-central vs SNP-peripheral task distinction. When orienta-
tion inhibition (ve impact) was added to the facilitation proc-
essing (+ve impact) observed on target-repeat trials (see Task 3,
C[4-R]), an interaction effect was observed. As we noted earlier,
the magnitude of the target-repeat after-effect was the net result
of these negative and positive forces. Two implications follow
from this finding. One, it shows that orientation inhibition op-
erates in SNP-peripheral tasks. The other is more remote. It
argues against the current practice of using target-repeat facili-
tation or null effects to signal the absence of orientation inhibi-
tion (e.g., Chao, 2009; Christie & Klein, 2001). Here, we found
target-repeat facilitation in the SNP-peripheral task spite of the
involvement of orientation inhibition.
Overall, it is evident that the SNP-central task ought to be
distinguished from the IOR and SNP-peripheral tasks, as should
the latter two.
What about the view that the IOR effect includes a re-
sponse-inhibition component: Coward et al. (2004)?
Coward et al. (2004) proposed that the IOR effect included a
response inhibition contribution in addition to that made by
orientation inhibition. They suggested that the distractor-occu-
pied location on the prime trial forms a bond with the manual
response it activated, a response that is subsequently inhibited
(i.e., activation suppressed to prevent execution). When the
probe target later appears at the former distractor location (i.e.,
distractor-target trial), it not only invokes orientation inhibition,
it also triggers a recall of the recent response inhibition of the
now required manual response (but see Welsh & Pratt, 2006).
In any event, time is required to set aside this recollection and
so adds to IOR size. Coward et al. then pointed out that manual
response inhibition would be avoided when subjects responded
to a target on the prime. Thus, a probe target appearing at the
same prime location (i.e., target-repeat or target-target trials)
would experience orientation inhibition but not response inhibi-
Copyright © 2012 SciRes.
tion. Consistent with this reasoning, Coward et al. found IOR to
be significantly smaller for target-target than for distractor-
target locations. We replicated this result (i.e., IOR was smaller
for target-target [16] ms) than for distractor-target [29 ms] =
trials) in Task 2, but not for Task 1. Possibly, central and pe-
ripheral event location processing differ in another way; the
latter, but not the former, causes a response inhibition IOR
Centrally-positioned, distractor-occupied locations do not
cause inhibitory after-effects, showing, among other things, that
such locations do not invoke “orientation inhibition”, held to
primarily or exclusively cause the inhibition-of-return (IOR)
phenomenon (e.g., Posner & Cohen, 1984). Accordingly, the
production of spatial negative priming effect observed with
central distractor events (SNP-central) has a cause that is dis-
tinct from that of the IOR effect, a cause thought to result from
the inhibitory after-effects resulting from the inhibition of the
prime-trial distractor response (Guy et al., 2006; Edgar, 2011).
Bodner, G. E., & Mulji, R. (2010). Prime proportion affects masked
priming of fixed and free-choice responses. Experimental Psychol-
ogy, 67, 360-366.
Buckolz, E., Avramidis, C., & Fitzgeorge, L. (2008). Prime-trial de-
mands and their impact on distractor processing in a spatial negative
priming task. Psychological Research, 72, 235-248.
Buckolz, E., Boulougouris, A., & Khan, M. (2002). The influence of
probe-trial selection requirements on the location negative priming
effect. Canadian Journal of Experimental Psycho l og y, 56, 2774-283.
Buckolz, E., Goldfarb, A., & Khan, M. (2004). The use of a distrac-
tor-assigned response slows later responding in a location negative
priming task. Perception & Psychophysics, 66, 837-845.
Buckolz, E., Kajaste, B., Lok, M., Edgar, C., & Khan, M. (2011). Do
centrally presented stimulations cause orientation inhibition? Pre-
sented to the North American Society for Psychology of Sport and
Physical Activity. Burlington, Vermont.
Chao, H. F. (2009). Revisiting the role of probe distracters in negative
priming: Location negative priming is observed when probe distrac-
ters are consistently absent. Attention, Perception, & Psychophysics,
71, 1072-1082. doi:10.3758/APP.71.5.1072
Christie, J., & Klein, R. (2001). Negative priming for spatial location?
Canadian Journal of Experimental Psychology, 55, 24-38.
Connelly, S. L., & Hasher, L. (1993). Aging and the inhibition of spa-
tial location. Journal of Experimental Psychology: Human Percep-
tion and Performance, 19, 1238-1250.
Corneil, B. D., Munoz, D. P., Chapman, B. B., Admans, T., & Cushing,
S. L. (2007). Neuromuscular consequences of reflexive covert ori-
enting. Nature Neurosc i e n c e , 155, 13-15.
Coward, R. S., Poliakoff, E., O’Boyle, D. J., & Lowe, C. L. (2004). The
contribution of non-ocular response inhibition to visual inhibition of
return. Experimental Brain Research, 155, 124-128.
Edgar, C. (2011). Preventing response-based inhibition processing re-
trieval: SNP disengagement. Masters Thesis, London: The University
of Western Ontario.
Fitzgeorge, L. (2009). Cognitive inhibition: Inhibitory after-effects.
Doctoral Thesis, London: The University of Western Ontario.
Fitzgeorge, L., & Buckolz, E. (2008). Spatial negative priming modula-
tion: The influence of probe-trial target cueing, distractor presence
and an intervening response. European Journal of Cognitive Psy-
chology, 20, 994-1026. doi:10.1080/09541440701686250
Fitzgeorge, L., & Buckolz, E. (2009). Automatic versus volitional ori-
enting and the production of the inhibition-of-return effect. Canadian
Journal of Experimental Psychol og y, 63, 94-102.
Fitzgeorge, L., Buckolz, E., & Khan, M. (2011). Recently inhibited
responses are avoided for both masked and non-masked primes in a
spatial negative priming task. Attention, Perception, & Psychophys-
ics, 73, 1435-1452. doi:10.3758/s1341-011-0125-7
Guy, S., & Buckolz, E. (2007). The locus and modulation of the loca-
tion negative priming effect. Psychological Research, 71, 178-191.
Guy, S., Buckolz, E., & Fitzgeorge, L. (2007). Disengaging the location
negative priming effect: The influence of an intervening response.
European Journal of Cognitive Psychology, 19, 789-812.
Guy, S., Buckolz, E., & Khan, M. (2006). The locus of location repeti-
tion latency effects. Canadian Journal of Experimental Psychology,
60, 307-318. doi:10.1037/cjep2006028
Guy, S., Buckolz, E., & Pratt, J. (2004). The influence of distractor-
only prime trials on the location negative priming mechanism. Ex-
perimental Psychology, 51, 4-14. doi:10.1027/1618-3169.51.1.4
Hommel, B. (1993). The role of attention for the Simon effect. Psycho-
logical Research, 55, 208-222. doi:10.1007/BF00419608
Klein, R., Christie, J., & Morris, E. P. (2005). Vector averaging of
inhibition of return. Psychonomic Bulletin & Review, 12, 295-300.
Lupianez, J., Klein, R., & Bartolomeo, P. (2006). Inhibition of return:
Twenty years after. Cognitive Neuropsychology, 23, 1003-1014.
Milliken, B., Tipper, S. P., Houghton, G., & Lupianez, J. (2000). At-
tending, ignoring, and repetition: On the relation between negative
priming and inhibition of return. Perception & Psychophysics, 62,
1289-1296. doi:10.3758/BF03212130
Mulckhuyse, M., & Theeuwes, J. (2010). Unconscious attentional ori-
enting to exogenous cues: A review of the literature. Acta Psy-
chologica, 134, 200-309. doi:10.1016/j.actpsy.2010.03.002
Neill, W. T., Terry, K. M., & Valdes, L. A. (1994). Negative priming
without probe selection. Psychonomic Bulletin and Review, 1, 119-
121. doi:10.3758/BF03200767
O’Connor, P. A., & Neill, W. T. (2010). Does subliminal priming of
free response choices depend on taskset or automatic response acti-
vation? Conscious nes s a n d Cognition, 20, 280-287.
Perry, J. (2011). An investigation of masked priming mechanisms in
binary classification tasks. Ph.D. Thesis, London: The University of
Western Ontario.
Posner, M. I., & Cohen, Y. (1984). Components of visual orienting. In
H. Bouma, & D. G. Bouwhuis (Eds.), Attention and performance X
(pp. 531-556). Hillsdale, NJ: Lawrence Earlbaum Assoc.
Posner, M. I., Rafal, R. D., Choate, L. S., & Vaughan, J. (1985). Inhibi-
tion of return: Neural basis and function. Cognitive Neuropsychology,
2, 211-228. doi:10.1080/02643298508252866
Proctor, R. W., & Lu, C.-H. (1994). Referential coding and atten-
tion-shifting accounts of the Simon effect. Psychological Research,
56, 185-195. doi:10.1007/BF00419706
Possami, C.-A. (1986). Relationship between inhibition and facilitation
following a visual cue. Acta Psychologica, 61, 243-258.
Rafal, R., Calabresi, P., Brennan, C., & Sciolto, T. (1989). Saccade
preparation inhibits reorienting to recently attended locations. Jour-
nal of Experimental Psychology: Human Perception and Perform-
ance, 15, 673-685. doi:10.1037/0096-1523.15.4.673
Rafal, R., Davies, J., & Lauder, J. (2006). Inhibitory tagging at subse-
quently fixated locations: Generation of “inhibition of return” with-
out saccade inhibition. Visual Cognition, 13, 308-323.
Schlaghecken, F., Rowley, L., Sembi, S., Simmons, R., & Whitcomb, D.
(2007). The negative compatibility effect: A case for self-inhibition.
Copyright © 2012 SciRes. 673
Copyright © 2012 SciRes.
Advances in Cognitive Psychology, 3, 227-240.
Sumner, P. (2007). Negative and positive masked-priming—Implica-
tions for motor inhibition. Advances in Cognitive Psychology, 3, 317-
326. doi:10.2478/v10053-008-0033-0
Tassinari, G., Aglioti, S., Chelazzi, L., Marzi, C. A., & Berlucchi, G.
(1987). Distribution in the visual field of he cost of voluntarily allo-
cated attention and the inhibitory after-effects of covert orienting.
Neuropsychologia, 25, 55-71.
Tipper, S. P., Brehaut, J. C., & Driver, J. (1990). Selection of moving
and static objects for control of spatially directed action. Journal of
Experimental Psychology: Human Perception & Performance, 16,
492-504. doi:10.1037/0096-1523.16.3.492
Tipper, S. P., Weaver, B., Cameron, S., Brehaut, J., & Bastedo, J.
(1991). Inhibitory mechanisms of attention in identification and lo-
calization tasks; Time course and disruption. Journal of Experimen-
tal Psychology: Learning, Memory, and Cognition, 17, 681-692.
Verhaeghen, P., & De Meersman, L. (1998). Aging and the negative
priming effect: A meta-analysis. Psychology an d Aging, 13, 435-444.
Wang, H., & Proctor, R. W. (1996). Stimulus-response compatibility as
a function of stimulus code and response modality. Journal of Ex-
perimental Psychology: Human Perception and Performance, 22,
1201-1217. doi:10.1037/0096-1523.22.5.1201
Welsh, T. N., & Pratt, J. (2006). Inhibition of return in cue-target and
target-target tasks. Experimental Brain Research, 174, 167-175.
Appendix A
An ANOVA was calculated using mean within-subject probe
reactions following distractor primes. Trial-type and Location
(inside, outside) served as the main factors. Neither of the main
effects, nor their interaction, F(1, 19) = 1.61, p = 0.220, MSE =
235, proved to be significant. The ANOVA carried out follow-
ing target prime trials indicated that the target-repeat facilitation
effect was not significant, F(1, 19) = 2.46, p = 0.13, MSE = 796,
while inside probe targets were responded to significantly
slower (378 ms) than were the outside locations (371 ms). The
interaction was non-significant, F < 1. The reported location of
the prime event was correct 97% of the time, verifying that
location discrimination took place. Hence, the absence of in-
hibitory after-effects here, and in Task 1 (C[1-R]) of the main
experiment, cannot be attributed to the lack of location dis-
crimination, since this absence occurs when location discrimi-
nation has occurred.
Table A1.
Pilot data reaction times (ms) using the Task 1 (central locations,
1-response) of the main experiment, along with a requirement to ver-
bally report prime event location.
Prime Type
Distractor Target
Trial-Types Ignored- Target-
RepetitionControl NP Repeat ControlTR
Inside 399 (17)407 (21) 08 373 (15) 383 (19)10
Outside 411 (20)410 (28) 01 366 (16) 376 (18)10
SNP = spatial negative priming effect; TR = target-repeat effect; ( ) = standard