 |
 Previous Article | Next Article 
The Journal of Neuroscience, June 1, 2002, 22(11):4563-4567
Defining the Neural Mechanisms of Probabilistic Reversal Learning
Using Event-Related Functional Magnetic Resonance Imaging
Roshan
Cools1,
Luke
Clark1,
Adrian M.
Owen2, and
Trevor W.
Robbins1
1 Department of Experimental Psychology, University of
Cambridge, Cambridge CB2 3EB, United Kingdom, and
2 Medical Research Council Cognition and Brain
Sciences Unit, Cambridge CB2 2EF, United Kingdom
 |
ABSTRACT |
Event-related functional magnetic resonance imaging was used to
measure blood oxygenation level-dependent responses in 13 young healthy
human volunteers during performance of a probabilistic reversal-learning task. The task allowed the separate investigation of
the relearning of stimulus-reward associations and the reception of
negative feedback. Significant signal change in the right ventrolateral prefrontal cortex was demonstrated on trials when subjects stopped responding to the previously relevant stimulus and shifted responding to the newly relevant stimulus. Significant signal change in the region
of the ventral striatum was also observed on such reversal errors, from
a region of interest analysis. The ventrolateral prefrontal cortex and
ventral striatum were not significantly activated by the other,
preceding reversal errors, or when subjects received negative feedback
for correct responses. Moreover, the response on the final reversal
error, before shifting, was not modulated by the number of preceding
reversal errors, indicating that error-related activity does not simply
accumulate in this network. The signal change in this ventral
frontostriatal circuit is therefore associated with reversal learning
and is uncontaminated by negative feedback. Overall, these data concur
with findings in rodents and nonhuman primates of reversal-learning
deficits after damage to ventral frontostriatal circuitry, and also
support recent clinical findings using this task.
Key words:
reversal shifting; brain imaging; ventrolateral PFC; VS; probabilistic learning; inhibitory control
| |
INTRODUCTION |
Reversal learning involves the
adaptation of behavior according to changes in stimulus-reward
contingencies, a capacity relevant to socio-emotional behavior (Rolls,
1999 ). It is exemplified by visual discrimination tasks where subjects
must learn to respond according to the opposite, previously irrelevant,
stimulus-reward pairing. Reversal learning is disrupted after lesions
of the ventral prefrontal cortex (PFC) and ventral striatum (VS) in
nonhuman primates (Divac et al., 1967; Iversen and Mishkin, 1970; Dias et al., 1996). However, evidence of the same system being involved in
reversal performance in humans is limited to two studies in patients
with nonselective ventral PFC damage (Rolls et al., 1994; Rahman
et al., 1999). In the current study, event-related functional magnetic
resonance imaging (fMRI) was used, enabling the identification of
neural mechanisms associated with reversal learning in the intact human
brain, with the further aim of dissecting the components and temporal
dynamics of this process.
Previous neuroimaging studies have associated the ventral PFC and VS
with a variety of functions related indirectly to reversal learning,
including unconditioned (Zald and Pardo, 1997) and conditioned (Delgado
et al., 2000; Knutson et al., 2001; O'Doherty et al., 2001) reward
processing and low-level inhibitory control (Garavan et al., 1999;
Konishi et al., 1999). A recent positron emission tomography
investigation using a blocked design failed to identify blood-flow
changes in the PFC during reversal learning, although changes were
observed in the ventral caudate nucleus (Rogers et al., 2000). However,
in blocked designs a signal may be attenuated through the averaging of
activity over an extended period. Methodological developments in fMRI
have enabled the identification of neural responses to single events,
and event-related fMRI is perfectly suited to investigating reversal
learning, where critical errors occur against a background of correct responses.
The aim of the current study was to explore the involvement of ventral
frontostriatal regions in reversal learning. The event-related approach
offers the additional advantage of being able to examine, for the first
time, the temporal dynamics of neural activity during the reversal
phase in humans. "Final" reversal errors followed directly by
shifting were modeled separately from other preceding reversal errors,
not directly leading to changes of behavior (Fig. 1). The use of a difficult, probabilistic
task, where negative feedback was given to correct responses on a
minority of trials, encouraged perseverative behavior after contingency
reversals. Separate investigation of probabilistic errors, final
reversal errors, and preceding reversal errors enabled independent
assessment of the neural correlates of reversal learning and negative
feedback. We predicted specific signal changes in a ventral
frontostriatal network during final reversal errors (directly leading
to changes in behavior) but not during probabilistic errors or
preceding reversal errors.
View larger version (30K):
[in this window]
[in a new window]
|
Figure 1.
The probabilistic reversal-learning task. An
example of several consecutive trials in the probabilistic
reversal-learning task is shown (running from bottom to
top). On each trial, subjects are presented with two
abstract visual patterns. Using trial-and-error feedback, subjects must
discover which of the two patterns is correct (here indicated by a
small arrowhead on top of the pattern to improve
legibility). Feedback (a green smiley face or red
sad face) is presented as soon as the subject has chosen
one of the patterns by a left or right button press.
|
|
An important rationale for the current study was based on recent
findings that performance on a probabilistic reversal-learning task was
impaired by dopaminergic medication in patients with mild Parkinson's
disease (Swainson et al., 2000; Cools et al., 2001). This detrimental
effect of dopamine was hypothesized to be a result of "overdosing"
a ventral frontostriatal circuit (Swainson et al., 2000; Cools et al.,
2001), given neuroanatomical evidence for a relative preservation of
the VS in the early stages of the disease (Kish et al., 1988).
Confirmation of ventral frontostriatal involvement in reversal learning
would considerably strengthen this "overdose" hypothesis.
| |
MATERIALS AND METHODS |
Subjects. Fourteen right-handed, young, healthy
volunteers participated in this study. One subject was unable to
perform satisfactorily on the task and was therefore excluded from the
analysis. All remaining 13 subjects (5 males, 8 females; mean
age, 25.9; SD, 3.82; range, 22-37) gave informed consent, which was
approved by the local Research Ethics Committee.
Experimental design. Each subject was scanned performing the
behavioral task in three successive 9 min sessions. Before entering the
scanner, subjects performed a 30 trial training session. This was a
simple probabilistic discrimination task (i.e., without reversal
stages) designed to introduce the subject to the concept of a
probabilistic error without the need to reverse responding. On each go,
the same two patterns were presented. One of the patterns was correct
and the other pattern was wrong, and subjects had to choose the correct
pattern on each go. During the task, the rule changed intermittently so
that the other pattern was usually correct. Subjects were instructed to
only start choosing the other pattern when they were sure that the rule
had changed.
The task was programmed in Microsoft (Seattle, WA) Visual Basic
6.0 and stimuli were presented on a computer display projected onto a
mirror in the MRI scanner. Different stimuli were used in each of the
three task blocks (and training stage), and the order of presentation
of the blocks was counter-balanced across subjects. Each block
consisted of 10 discrimination stages, and therefore, 9 reversal
stages. Reversal of the stimulus-reward contingency occurred after
between 10 and 15 correct responses (including probabilistic errors).
The number of probabilistic errors between each reversal varied from 0 to 4. To prevent subjects from adopting a strategy such as always
reversing after two consecutive errors, probabilistic negative feedback
was given on two consecutive trials once during each task block. Each
block lasted ~8.5 min depending on level of performance. The two
stimuli in each block were abstract colored patterns presented
simultaneously in the left and right visual fields (location
randomized) (Fig. 1). Responses were made using the left or right
button on a button box positioned on the stomach of the subject. On
each individual trial, the stimuli were presented for 2000 msec within
which the response had to be made (or else a "too late" message was
presented). Feedback, consisting of a green smiley face for correct
responses or a red sad face for incorrect responses, was presented
immediately after the response (Fig. 1). The feedback faces were
presented centrally, between the 2 stimuli, for 500 msec during which
the stimuli also remained on the screen. After feedback, the stimuli
were removed and the face was replaced by a fixation cross for a
variable interval so that the overall interstimulus interval was 3253 msec, enabling precise desynchronization from the repetition time (TR)
(of 3000 msec) and sufficient sampling across the hemodynamic response function.
Imaging acquisition. Imaging data were collected using a
Bruker Medspec scanner (S300; Bruker, Ettlingen, Germany) operating at
3 tesla. A total of 180 T2*-weighted echo-planar images (EPIs), depicting blood oxygenation level-dependent contrast, were acquired in
each session (TR, 3 sec; echo time, 27 msec). A total of 21 slices (each of 4 mm thickness; interslice gap, 5 mm; matrix size, 64 × 64; bandwidth, 100 kHz; axial oblique acquisition
orientation) per image were acquired. The first seven EPIs in each
session were discarded to avoid T1 equilibrium effects. We were unable to collect data from the orbitofrontal and ventromedial PFC because of susceptibility artifacts in nasal sinuses leading to signal dropout.
Imaging analysis. Data analysis was performed using SPM 99 (Statistical Parametric Mapping; Wellcome Department of Cognitive Neurology, London, UK). Preprocessing procedures included slice acquisition time correction, reorientation, within-subject realignment, geometric undistortion using fieldmaps (Cusack et al., 2001), spatial
normalization using EPI masking (to exclude areas susceptible to signal
dropout from nonlinear warping) to the standard Montreal Neurological
Institute EPI template, and spatial smoothing using a Gaussian kernel
(8 mm full-width at half-maximum). Time series were high-pass filtered.
A canonical hemodynamic response function was used as a covariate in a
general linear model and a parameter estimate was generated for each
voxel for each event type. The parameter estimate, derived from the
mean least squares fit of the model to the data, reflects the strength
of covariance between the data and the canonical response function for
a given condition. Individuals' contrast images, derived from
pair-wise contrasts between parameter estimates for different events,
were taken to a second-level group analysis in which t
values were calculated for each voxel treating intersubject variability
as a random effect. The t values were transformed to unit
normal Z distribution to create a statistical parametric map
for each of the planned contrasts (described below).
The hemodynamic response function was modeled to the onset of the
responses, which co-occurred with the presentation of the feedback. The
following events were modeled (Fig. 1): (1) correct responses,
co-occurring with positive feedback, as a baseline; (2) probabilistic
errors, on which negative feedback was given to correct responses
(trials on which subjects reversed after a probabilistic error were not
included in the model); (3) final reversal errors, resulting in the
subject shifting their responding; and (4) the other preceding reversal
errors, following a contingency reversal but preceding the final
reversal errors. The final reversal errors (co-occurring with the last
negative feedback) were chosen as critical events of interest (i.e.,
reflecting reversal learning) because activation of a reversal network
was assumed to follow this last negative feedback. Error trials that
could not be classified as probabilistic errors or reversal errors
(so-called "spontaneous" errors) were not included in the model.
The following contrasts were assessed: (1) final reversal errors minus
correct responses, (2) other preceding reversal errors minus correct
responses, (3) probabilistic errors minus correct responses, (4) final
reversal errors minus other preceding reversal errors, and (5) final
reversal errors minus probabilistic errors. In addition, we assessed
whether the final reversal errors were parametrically modulated by the
number of reversal errors directly preceding them. We predicted
significant signal change in the ventral frontostriatal brain regions
in contrasts 1, 4, and 5 but not in contrasts 2 or 3. All contrasts
were initially thresholded at p < 0.05, corrected for
multiple comparisons. Strong predictions about the involvement of the
VS in reversal learning (see the introductory remarks) justified
application of small volume corrections using a sphere around the VS.
This a priori defined region of interest (ROI) was a sphere centered on
x, y, z = +/ 10, 8, 4 with a radius of 8 mm (i.e., the smoothing kernel). These
coordinates represent the center of the nucleus accumbens as defined
using the Talairach atlas, and are very close to ventral striatal foci specified in previous fMRI studies (Delgado et al., 2000; Breiter et
al., 2001; Knutson et al., 2001). These coordinates were unaltered by
conversion from Talairach to Montreal Neurological Institute (MNI)
space using an algorithm by M. Brett (Medical Research Council Cognition and Brain Sciences Unit, Cambridge, UK) (available at www.mrc-cbu.cam.ac.uk/imaging).
Finally, ROI analyses were performed on the less powerful contrasts 4 and 5, which did not include baseline correct responses but were
predicted to generate ventrolateral PFC signal change. A region in the
ventrolateral PFC was defined on the basis of previous functional
neuroimaging studies. Specifically, the ventral PFC has been activated
repeatedly in studies of working memory (Owen, 1997), and on the basis
of these studies coordinates have been reported that define the
approximate functional extent of this neuroanatomical region
(stereotaxic coordinates x = +/26 to
x = +/50, y = +16 to
y = +24, and z = 9 to
z = 8) (Owen et al., 1999). The only fMRI study
specifically looking at reversal learning did not scan below the
anterior commissure-posterior commissure (AC-PC) axis (Nagahama et
al., 2001). The above-described statistical model was then reapplied to
the average signal within the ROI, using the MarsBar tool (M. Brett,
personal communication; see
www.mrc-cbu.cam.ac.uk/imaging/marsbar.html).
| |
RESULTS |
Behavioral data
All 13 subjects included in the analysis performed well on the
task. On average, subjects made 2.6 (SD, 0.51) perseverative reversal
errors after reversal of stimulus-reward contingencies. Over the task
as a whole, subjects made on average (SD) 320.7 (4.4) correct
responses, 48.4 (2.7) probabilistic errors, 43.4 (13.9) preceding
reversal errors, and 27 (0) final reversal errors.
Imaging data
Significant effects observed in whole-brain analyses are displayed
in Table 1.
Comparison of the final reversal errors with the baseline correct
responses (contrast 1; see Materials and Methods) revealed significant
signal change in the right ventrolateral PFC (Table 1 and Fig.
2). The effect in the left ventrolateral
PFC was present but did not reach significance (coordinates
x, y, z = 32, 24, 4;
T = 6.8). Other significant effects in this contrast
were observed in medial frontal cortex (Brodmann area 8) and right parietal cortex (Table 1). Small volume corrections, restricting the
search volume to a sphere around the ventral striatum (see Materials
and Methods) revealed significant signal changes in that region
bilaterally (coordinates x, y, z = 10, 2, 2; T = 6.3; p < 0.003;
and coordinates x, y, z = 14, 2, 6; T = 4.3; p = 0.03).
View larger version (66K):
[in this window]
[in a new window]
|
Figure 2.
Signal changes in ventral frontostriatal circuitry
during the critical final reversal errors. Signal changes in the
bilateral ventrolateral PFC and ventral striatum, identified by the
contrast, final reversal errors minus correct responses, are
superimposed on the MNI template brain (individual brain considered
most typical of the 305 brains used to define the MNI standard). See
Results and Table 1 for statistical values. In all three axial slices,
the z-coordinate represents the position of the slice
relative to the anterior commissure-posterior commissure axis (dorsal,
positive).
|
|
An ROI analysis, restricting the search volume to an independently
defined area in the ventrolateral PFC (see Materials and Methods),
revealed that signal change in the right ROI during the final reversal
error was also significantly greater than that observed during the
preceding reversal errors (contrast 4; T = 2.79;
p = 0.016) and during the probabilistic errors
(contrast 5; T = 2.84; p = 0.014).
Significant effects in the ventrolateral PFC and VS were absent when
the other preceding reversal errors were contrasted with the baseline
correct responses (contrast 2) and when the probabilistic errors were
contrasted with the baseline correct responses (contrast 3). Moreover,
there was no significant parametric effect at the final reversal errors
as a function of the number of preceding reversal errors, even when the
search volume was restricted to the ventrolateral PFC using an ROI analysis.
| |
DISCUSSION |
The present results demonstrate recruitment of a ventral
frontostriatal system in a task of probabilistic reversal learning. Detailed analyses showed that this significant signal change, observed
in the right ventrolateral PFC and in the region of the VS, occurred
specifically during the final reversal error, at which point subjects
stopped responding to a previously relevant pattern and reversed
responding to a newly relevant pattern.
These data are consistent with our predictions and concur with primate
and rodent lesion studies showing that damage to the ventral PFC
(Iversen and Mishkin, 1970; Jones and Mishkin, 1972; Dias et al., 1996)
and VS (Divac et al., 1967; Taghzouti et al., 1985; Annett et al.,
1989; Stern and Passingham, 1995) disrupts reversal learning. For
example, Stern and Passingham (1995) have shown that lesions of the
nucleus accumbens in monkeys lead to deficits on tasks of spatial (but
not object or motor) reversal learning, while leaving acquisition
performance intact. In rats, dopamine (6-OHDA) and ibotenic acid
lesions of the nucleus accumbens have led to both acquisition and
reversal-learning impairments in a spatial T-maze and a Morris water
maze (Taghzouti et al., 1985; Annett et al., 1989), suggesting a role
for the nucleus accumbens in the relearning of new location-reward
associations, rather than in stopping old responses (Annett et al.,
1989). The current study indicates that the VS, at least in humans, is
also implicated in the reversal or the relearning of object-reward associations. In contrast, human brain-imaging studies have emphasized a role for the right lateral ventral PFC in behavioral inhibition (or
stopping) using, for example, go-nogo tasks (Garavan et al., 1999;
Konishi et al., 1999). It is possible that the observed signal change
in the ventrolateral PFC, also lateralized to the right hemisphere,
reflects behavioral inhibition, whereas the signal change in the VS
reflects the learning of new associations. However, our study was not
designed to functionally dissociate learning from stopping; this could
be addressed in future event-related brain-imaging studies.
The use of an event-related technique enabled the separate
investigation of distinct error trial types that loaded differentially on reversal shifting and simple negative feedback. The signal change in
the ventrolateral PFC and VS was significantly greater at the final
reversal error compared with baseline correct responses. A region of
interest analysis revealed that signal change in the right
ventrolateral PFC was also significantly greater during the final
reversal error than during all other error trial types. Moreover, the
absence of a parametric effect suggests that the effects at the final
reversal error were not modulated by the number of preceding reversal
errors. This indicates that the focus was not the result of gradual
accumulation of activity caused by the preceding errors, although given
power considerations such conclusions cannot be considered to be
definitive. Finally, these areas were not significantly activated
during the preceding reversal errors or probabilistic errors when
compared with baseline correct responses. Although it is not possible
conceptually to doubly dissociate reversal learning from negative
feedback, these results suggest that the effect during the final
reversal error in the ventrolateral PFC is primarily attributable to
reversal learning and cannot be explained by an effect of negative feedback.
These findings are broadly consistent with those observed in a recent
event-related fMRI study of high-level attentional set shifting (Monchi
et al., 2001). Monchi et al. (2001) demonstrated signal change in an
area in the ventrolateral PFC, at coordinates very similar to the
current focus, in response to negative feedback, signaling a shift of
set. However, in that study it was not possible to isolate the shifting
component from the negative-feedback component. Thus, the current study
extends their results by showing that the effect in the ventrolateral
PFC is uncontaminated by negative feedback. The present data also
indicate that shifting of lower-level stimulus-reward associations, as
opposed to shifting of a higher-level attentional set, is sufficient to
activate the ventrolateral PFC.
Two additional neuroimaging studies have used reversal-learning tasks
with event-related fMRI. Nagahama et al. (2001) did not scan brain
areas below the horizontal plane through the AC-PC axis (Talairach
coordinate z = 0). This precluded conclusions about the
role of the VS and ventral PFC in reversal learning. Instead, they
emphasized a role for a (more dorsal) posteroventral PFC area in
shifting, which was not replicated in the current study. However, the
focus in this posteroventral area was later clarified by Monchi et al.
(2001) to be nonspecifically activated [i.e., to respond during both
negative feedback (triggering set shifting) and positive feedback
(triggering set maintenance)]. The relevant contrasts (subtracting
positive-feedback trials from negative-feedback trials) in the current
study were not designed to address this question of nonspecific
feedback. A second event-related fMRI study, using a probabilistic
reversal-learning paradigm to assess orbitofrontal neural responses to
reward and punishment (O'Doherty et al., 2001), revealed signal change
in the right ventrolateral PFC during reception of negative feedback.
This signal change was interpreted to reflect punishment. However, it
was not possible in that study to exclude the contribution of reversal
learning. In fact, our results show that this ventrolateral PFC effect
more likely reflects reversal learning. In addition, O'Doherty et al.
(2001) observed signal change in the medial orbitofrontal cortex that
correlated with the magnitude of reward, and observed signal change in
the lateral orbitofrontal cortex that correlated with the magnitude of
punishment. Because of susceptibility artifacts, we were unable to
image these latter brain regions and are therefore unable to draw
conclusions on orbitofrontal effects during trials on which negative
feedback was received without consequences for behavior (as on
probabilistic errors and preceding reversal errors).
The orbitofrontal cortex is connected to the nucleus accumbens of the
ventral striatum in a segregated frontostriatal "loop" (Alexander
et al., 1986; Groenewegen et al., 1997). Functional evidence implicates
the orbitofrontal cortex, in interaction with the amygdala, in
unconditioned (and conditioned) reward processing (Delgado et al.,
2000; Breiter et al., 2001; Knutson et al., 2001; O'Doherty et al.,
2001). In contrast, the ventrolateral PFC is connected to the ventral
putamen, a structure implicated in motor function. The integrative role
of the ventral striatum has been suggested to be the funnelling of
motivational information from the "limbic" system to the motor
system (Mogenson, 1987), thereby mediating the effects of
stimulus-reward mechanisms on goal-directed behavior (Robbins et al.,
1989; Schultz et al., 1992). Thus, whereas the orbitofrontal cortex may
be important for the "low-level" representation of reward or
punishment values (O'Doherty et al., 2001), the more lateral PFC may
play a role in the adaptation of behavior in response to changes in
such reward or punishment values. Our finding that the ventrolateral
PFC is critically involved in reversal learning, uncontaminated by the
reception of negative feedback per se, is consistent with this proposed
hierarchy within corticostriatal systems.
Finally, our results provide a clear interpretation of recent data
demonstrating that administration of dopaminergic medication to
patients with mild Parkinson's disease has a detrimental effect on
probabilistic reversal learning (Swainson et al., 2000; Cools et al.,
2001). Recent studies have shown that, in early Parkinson's disease,
dopamine depletion is restricted to the putamen and the dorsal caudate
nucleus, only later progressing to more ventral parts of the striatum
and the mesocorticolimbic system (Kish et al., 1988; Agid et al.,
1993). It was hypothesized that administration of
L-3,4-dihydroxyphenylalanine (L-DOPA) doses,
necessary to remediate the dopamine depletion in the dorsal striatum
and its connections to the dorsolateral PFC, may detrimentally overdose
relatively intact brain regions, such as the VS and its connections to
the ventral PFC (Gotham et al., 1988; Cools et al., 2001). The current data, showing involvement of the ventral PFC and VS in probabilistic reversal learning, considerably strengthen the possibility that dopaminergic agents can indeed overdose a relatively intact ventral frontostriatal system. This work highlights the potential of combining pharmacological and functional imaging approaches to understand the
underlying neural substrates of cognitive functions in both basic and
clinical settings.
| |
FOOTNOTES |
Received Jan. 14, 2002; revised March 12, 2002; accepted March 12, 2002.
This work was supported by a Wellcome Trust Programme grant (T.W.R.)
and completed within a Medical Research Council Company-operative Group
in Brain, Behavior, and Neuropsychiatry. R.C. holds the C. D. Marsden Parkinson's Disease Society Studentship. We thank Paul
Fletcher and Matthew Brett for helpful discussion and Victoria Liversidge, Ruth Bisbrown-Chippendale, and Tim Donovan from the Wolfson
Brain Imaging Centre (Cambridge, UK) for radiographic assistance with
this study.
Correspondence should be addressed to Trevor W. Robbins, Department of
Experimental Psychology, University of Cambridge, Downing Street,
Cambridge CB2 3EB, UK.E-mailtwr2{at}cus.cam.ac.uk.
| |
REFERENCES |
-
Agid Y,
Ruberg M,
Javoy-Agid,
Hirsch E,
Raisman-Vozari R,
Vyas S,
Faucheux B,
Michel P,
Kastner A,
Blanchard V,
Damier P,
Villares J,
Zhang P
(1993)
Are dopaminergic neurons selectively vulnerable to Parkinson's disease?
Adv Neurol
60:148-164[Medline].
-
Alexander G,
DeLong M,
Stuck P
(1986)
Parallel organisation of functionally segregated circuits linking basal ganglia and cortex.
Annu Rev Neurosci
9:357-381[Web of Science][Medline].
-
Annett L,
McGregor A,
Robbins T
(1989)
The effects of ibotenic acid lesions of the nucleus accumbens on spatial learning and extinction in the rat.
Behav Brain Res
31:231-242[Web of Science][Medline].
-
Breiter H,
Aharon I,
Kahneman D,
Dale A,
Shizgal P
(2001)
Functional imaging of neural response to expectancy and experience of monetary gains and losses.
Neuron
30:619-639[Web of Science][Medline].
-
Cools R,
Barker R,
Sahakian B,
Robbins T
(2001)
Enhanced or impaired cognitive function in Parkinson's disease as a function of dopaminergic medication and task demands.
Cereb Cortex
11:1136-1143[Abstract/Free Full Text].
-
Cusack R,
Papadakis N,
Martin K,
Brett M
(2001)
A new robust 3D phase-unwrapping algorithm applied to fMRI field maps for the undistortion of EPIs.
NeuroImage
13:103.
-
Delgado MR,
Nystrom LE,
Fissell C,
Noll DC,
Fiez JA
(2000)
Tracking the hemodynamic responses to reward and punishment in the striatum.
J Neurophysiol
84:3072-3077[Abstract/Free Full Text].
-
Dias R,
Robbins TW,
Roberts AC
(1996)
Dissociation in prefrontal cortex of affective and attentional shifts.
Nature
380:69-72[Medline].
-
Divac I,
Rosvold HE,
Szwarcbart MK
(1967)
Behavioral effects of selective ablation of the caudate nucleus.
J Comp Physiol Psychol
63:184-190[Web of Science][Medline].
-
Garavan H,
Ross T,
Stein E
(1999)
Right hemispheric dominance of inhibitory control: an event-related functional MRI study.
Proc Natl Acad Sci USA
96:8301-8306[Abstract/Free Full Text].
-
Gotham AM,
Brown RG,
Marsden CD
(1988)
"Frontal" cognitive function in patients with Parkinson's disease "on" and "off" levodopa.
Brain
111:299-321[Abstract/Free Full Text].
-
Groenewegen H,
Wright C,
Uylings H
(1997)
The anatomical relationships of the prefrontal cortex with limbic structures and the basal ganglia.
J Psychopharmacol
11:99-106[Abstract/Free Full Text].
-
Iversen S,
Mishkin M
(1970)
Perseverative interference in monkeys following selective lesions of the inferior prefrontal convexity.
Exp Brain Res
11:376-386[Web of Science][Medline].
-
Jones B,
Mishkin M
(1972)
Limbic lesions and the problem of stimulus-reinforcement associations.
Exp Neurol
36:362-377[Web of Science][Medline].
-
Kish S,
Shannak K,
Hornykiewicz O
(1988)
Uneven patterns of dopamine loss in the striatum of patients with idiopathic Parkinson's disease.
N Engl J Med
318:876-880[Abstract].
-
Knutson B,
Adams C,
Fong G,
Hommer D
(2001)
Anticipation of increasing monetary reward selectively recruits nucleus accumbens.
J Neurosci
21:1-5[Web of Science][Medline].
-
Konishi S,
Nakajima K,
Uchida I,
Kikyo H,
Kameyama M,
Miyashita Y
(1999)
Common inhibitory mechanisms in human inferior prefrontal cortex revealed by event-related functional MRI.
Brain
122:981-991[Abstract/Free Full Text].
-
Mogenson G
(1987)
Limbic-motor integration.
Prog Psychobiol Physiol Psychol
12:117-169.
-
Monchi O,
Petrides M,
Petre V,
Worsley K,
Dagher A
(2001)
Wisconsin Card Sorting revisited: distinct neural circuits participating in different stages of the task identified by event-related functional magnetic resonance imaging.
J Neurosci
21:7733-7741[Abstract/Free Full Text].
-
Nagahama Y,
Okada T,
Katsumi Y,
Hayashi T,
Yamauchi H,
Oyanagi C,
Konishi J,
Fukuyama H,
Shibasaki H
(2001)
Dissociable mechanisms of attentional control within the human prefrontal cortex.
Cereb Cortex
11:85-92[Abstract/Free Full Text].
-
O'Doherty J,
Kringelbach M,
Rolls E,
Hornak J,
Andrews C
(2001)
Abstract reward and punishment representations in the human orbitofrontal cortex.
Nat Neurosci
4:95-102[Web of Science][Medline].
-
Owen AM
(1997)
The functional organization of working memory processes within human lateral frontal cortex: the contribution of functional neuroimaging.
Eur J Neurosci
9:1329-1339[Web of Science][Medline].
-
Owen AM,
Herrod NJ,
Menon DK,
Clark JC,
Downey SPMJ,
Carpenter A,
Minhas PS,
Turkheimer FE,
Williams EJ,
Robbins TW,
Sahakian BJ,
Petrides M,
Pickard D
(1999)
Redefining the functional organization of working memory processes within human lateral prefrontal cortex.
Eur J Neurosci
11:567-574[Web of Science][Medline].
-
Rahman S,
Sahakian B,
Hodges J,
Rogers R,
Robbins T
(1999)
Specific cognitive deficits in mild frontal variant frontotemporal dementia.
Brain
122:670-673.
-
Robbins T,
Cador M,
Taylor J,
Everitt B
(1989)
Limbic-striatal interactions in reward-related processes.
Neurosci Biobehav Rev
13:155-162[Web of Science][Medline].
-
Rogers RD,
Andrews TC,
Grasby PM,
Brooks DJ,
Robbins TW
(2000)
Contrasting cortical and subcortical activations produced by attentional-set shifting and reversal learning in humans.
J Cogn Neurosci
12:142-162[Web of Science][Medline].
-
Rolls ET
(1999)
The functions of the orbitofrontal cortex.
Neurocase
5:301-312[Web of Science].
-
Rolls ET,
Hornak J,
Wade D,
McGrath J
(1994)
Emotion-related learning in patients with social and emotional changes associated with frontal lobe damage.
J Neurol Neurosurg Psychiatry
57:1518-1524[Abstract/Free Full Text].
-
Schultz W,
Apicella P,
Scarnati E,
Ljungberg T
(1992)
Neuronal activity in monkey ventral striatum related to the expectation of reward.
J Neurosci
12:4595-4610[Abstract].
-
Stern C,
Passingham R
(1995)
The nucleus accumbens in monkeys (Macaca fascicularis).
Exp Brain Res
106:239-247[Web of Science][Medline].
-
Swainson R,
Rogers RD,
Sahakian BJ,
Summers BA,
Polkey CE,
Robbins TW
(2000)
Probabilistic learning and reversal deficits in patients with Parkinson's disease or frontal or temporal lobe lesions: possible adverse effects of dopaminergic medication.
Neuropsychologia
38:596-612[Web of Science][Medline].
-
Taghzouti K,
Louilot A,
Herman J,
Le Moal M,
Simon H
(1985)
Alternation behaviour, spatial discrimination, and reversal disturbances following 6-hydroxydopamine lesions in the nucleus accumbens of the rat.
Behav Neural Biol
44:354-363[Web of Science][Medline].
-
Zald D,
Pardo J
(1997)
Emotion, olfaction, and the human amygdala: amygdala activation during aversive olfactory stimulation.
Proc Natl Acad Sci USA
94:4119-4124[Abstract/Free Full Text].
Copyright © 2002 Society for Neuroscience 0270-6474/02/22114563-05$05.00/0
This article has been cited by other articles:
|
|
|
|
 
S. B. R. E. Brown and K. R. Ridderinkhof
Aging and the neuroeconomics of decision making: A review
Cogn Affect Behav Neurosci,
December 1, 2009;
9(4):
365 - 379.
[Abstract]
[PDF]
|
|
|
|
|
|
|
D. G. Ghahremani, J. Monterosso, J. D. Jentsch, R. M. Bilder, and R. A. Poldrack
Neural Components Underlying Behavioral Flexibility in Human Reversal Learning
Cereb Cortex,
November 13, 2009;
(2009)
bhp247v1.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. K. Krugel, G. Biele, P. N. C. Mohr, S.-C. Li, and H. R. Heekeren
Genetic variation in dopaminergic neuromodulation influences the ability to rapidly and flexibly adapt decisions
PNAS,
October 20, 2009;
106(42):
17951 - 17956.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. G. V. Mitchell, Q. Luo, S. B. Avny, T. Kasprzycki, K. Gupta, G. Chen, E. C. Finger, and R. J. R. Blair
Adapting to Dynamic Stimulus-Response Values: Differential Contributions of Inferior Frontal, Dorsomedial, and Dorsolateral Regions of Prefrontal Cortex to Decision Making
J. Neurosci.,
September 2, 2009;
29(35):
10827 - 10834.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Tachibana, K. Suzuki, E. Mori, N. Miura, R. Kawashima, K. Horie, S. Sato, J. Tanji, and H. Mushiake
Neural Activity in the Human Brain Signals Logical Rule Identification
J Neurophysiol,
September 1, 2009;
102(3):
1526 - 1537.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Jocham, J. Neumann, T. A. Klein, C. Danielmeier, and M. Ullsperger
Adaptive Coding of Action Values in the Human Rostral Cingulate Zone
J. Neurosci.,
June 10, 2009;
29(23):
7489 - 7496.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. X Cohen, N. Axmacher, D. Lenartz, C. E. Elger, V. Sturm, and T. E. Schlaepfer
Nuclei Accumbens Phase Synchrony Predicts Decision-Making Reversals Following Negative Feedback
J. Neurosci.,
June 10, 2009;
29(23):
7591 - 7598.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Elliott, Z. Agnew, and J.F.W. Deakin
Hedonic and Informational Functions of the Human Orbitofrontal Cortex
Cereb Cortex,
May 12, 2009;
(2009)
bhp092v1.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. D. Walsh and M. L. Phillips
Interacting Outcome Retrieval, Anticipation, and Feedback Processes in the Human Brain
Cereb Cortex,
May 8, 2009;
(2009)
bhp098v1.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. S. Lawrence, F. Jollant, O. O'Daly, F. Zelaya, and M. L. Phillips
Distinct Roles of Prefrontal Cortical Subregions in the Iowa Gambling Task
Cereb Cortex,
May 1, 2009;
19(5):
1134 - 1143.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Jocham, T. A. Klein, J. Neumann, D. Y. von Cramon, M. Reuter, and M. Ullsperger
Dopamine DRD2 Polymorphism Alters Reversal Learning and Associated Neural Activity
J. Neurosci.,
March 25, 2009;
29(12):
3695 - 3704.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Kazama and J. Bachevalier
Selective Aspiration or Neurotoxic Lesions of Orbital Frontal Areas 11 and 13 Spared Monkeys' Performance on the Object Discrimination Reversal Task
J. Neurosci.,
March 4, 2009;
29(9):
2794 - 2804.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Glascher, A. N. Hampton, and J. P. O'Doherty
Determining a Role for Ventromedial Prefrontal Cortex in Encoding Action-Based Value Signals During Reward-Related Decision Making
Cereb Cortex,
February 1, 2009;
19(2):
483 - 495.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. Passamonti, J. B. Rowe, C. Schwarzbauer, M. P. Ewbank, E. von dem Hagen, and A. J. Calder
Personality Predicts the Brain's Response to Viewing Appetizing Foods: The Neural Basis of a Risk Factor for Overeating
J. Neurosci.,
January 7, 2009;
29(1):
43 - 51.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. D. Ragland, R. Cools, M. Frank, D. A. Pizzagalli, A. Preston, C. Ranganath, and A. D. Wagner
CNTRICS Final Task Selection: Long-Term Memory
Schizophr Bull,
January 1, 2009;
35(1):
197 - 212.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. M. Barch, T. S. Braver, C. S. Carter, R. A. Poldrack, and T. W. Robbins
CNTRICS Final Task Selection: Executive Control
Schizophr Bull,
January 1, 2009;
35(1):
115 - 135.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Schiller, I. Levy, Y. Niv, J. E. LeDoux, and E. A. Phelps
From Fear to Safety and Back: Reversal of Fear in the Human Brain
J. Neurosci.,
November 5, 2008;
28(45):
11517 - 11525.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Xue, D. G. Ghahremani, and R. A. Poldrack
Neural Substrates for Reversing Stimulus-Outcome and Stimulus-Response Associations
J. Neurosci.,
October 29, 2008;
28(44):
11196 - 11204.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. F. Clarke, T. W. Robbins, and A. C. Roberts
Lesions of the Medial Striatum in Monkeys Produce Perseverative Impairments during Reversal Learning Similar to Those Produced by Lesions of the Orbitofrontal Cortex
J. Neurosci.,
October 22, 2008;
28(43):
10972 - 10982.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. J.R Beveridge, K. E Gill, C. A Hanlon, and L. J Porrino
Parallel studies of cocaine-related neural and cognitive impairment in humans and monkeys
Phil Trans R Soc B,
October 12, 2008;
363(1507):
3257 - 3266.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. M. Gold, J. A. Waltz, K. J. Prentice, S. E. Morris, and E. A. Heerey
Reward Processing in Schizophrenia: A Deficit in the Representation of Value
Schizophr Bull,
September 1, 2008;
34(5):
835 - 847.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. K. Murray, F. Cheng, L. Clark, J. H. Barnett, A. D. Blackwell, P. C. Fletcher, T. W. Robbins, E. T. Bullmore, and P. B. Jones
Reinforcement and Reversal Learning in First-Episode Psychosis
Schizophr Bull,
September 1, 2008;
34(5):
848 - 855.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R.J.R Blair
The amygdala and ventromedial prefrontal cortex: functional contributions and dysfunction in psychopathy
Phil Trans R Soc B,
August 12, 2008;
363(1503):
2557 - 2565.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. B. Rowe, L. Hughes, B. C. P. Ghosh, D. Eckstein, C. H. Williams-Gray, S. Fallon, R. A. Barker, and A. M. Owen
Parkinson's disease and dopaminergic therapy--differential effects on movement, reward and cognition
Brain,
August 1, 2008;
131(8):
2094 - 2105.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. M. Dodds, U. Muller, L. Clark, A. van Loon, R. Cools, and T. W. Robbins
Methylphenidate Has Differential Effects on Blood Oxygenation Level-Dependent Signal Related to Cognitive Subprocesses of Reversal Learning
J. Neurosci.,
June 4, 2008;
28(23):
5976 - 5982.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. X. COHEN
Neurocomputational mechanisms of reinforcement-guided learning in humans: A review
Cogn Affect Behav Neurosci,
June 1, 2008;
8(2):
113 - 125.
[Abstract]
[PDF]
|
|
|
|
|
|
|
E. C. Finger, A. A. Marsh, D. G. Mitchell, M. E. Reid, C. Sims, S. Budhani, D. S. Kosson, G. Chen, K. E. Towbin, E. Leibenluft, et al.
Abnormal Ventromedial Prefrontal Cortex Function in Children With Psychopathic Traits During Reversal Learning
Arch Gen Psychiatry,
May 1, 2008;
65(5):
586 - 594.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Valerius, A. Lumpp, A.-K. Kuelz, T. Freyer, and U. Voderholzer
Reversal Learning as a Neuropsychological Indicator for the Neuropathology of Obsessive Compulsive Disorder? A Behavioral Study
J Neuropsychiatry Clin Neurosci,
May 1, 2008;
20(2):
210 - 218.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. M. McIntosh, H. C. Whalley, J. McKirdy, J. Hall, J. E. D. Sussmann, P. Shankar, E. C. Johnstone, and S. M. Lawrie
Prefrontal Function and Activation in Bipolar Disorder and Schizophrenia
Am J Psychiatry,
March 1, 2008;
165(3):
378 - 384.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. Bellebaum, B. Koch, M. Schwarz, and I. Daum
Focal basal ganglia lesions are associated with impairments in reward-based reversal learning
Brain,
March 1, 2008;
131(3):
829 - 841.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. H. Williams-Gray, A. Hampshire, R. A. Barker, and A. M. Owen
Attentional control in Parkinson's disease is dependent on COMT val158met genotype
Brain,
February 1, 2008;
131(2):
397 - 408.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. J. Hallam, N. D. Silverberg, A. K. LaMarre, I. R. A. Mackenzie, and H. H. Feldman
Clinical Presentation of Prodromal Frontotemporal Dementia
American Journal of Alzheimer's Disease and Other Dementias,
January 1, 2008;
22(6):
456 - 467.
[Abstract]
[PDF]
|
|
|
|
|
|
|
T. A. Klein, J. Neumann, M. Reuter, J. Hennig, D. Y. von Cramon, and M. Ullsperger
Genetically Determined Differences in Learning from Errors
Science,
December 7, 2007;
318(5856):
1642 - 1645.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Wingen, K.P.C. Kuypers, and J.G. Ramaekers
Selective verbal and spatial memory impairment after 5-HT1A and 5-HT2A receptor blockade in healthy volunteers pre-treated with an SSRI
J Psychopharmacol,
July 1, 2007;
21(5):
477 - 485.
[Abstract]
[PDF]
|
|
|
|
|
|
|
T.W Robbins
Shifting and stopping: fronto-striatal substrates, neurochemical modulation and clinical implications
Phil Trans R Soc B,
May 29, 2007;
362(1481):
917 - 932.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
X. Liu, D. K. Powell, H. Wang, B. T. Gold, C. R. Corbly, and J. E. Joseph
Functional Dissociation in Frontal and Striatal Areas for Processing of Positive and Negative Reward Information
J. Neurosci.,
April 25, 2007;
27(17):
4587 - 4597.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. N. Hampton and J. P. O'Doherty
Decoding the neural substrates of reward-related decision making with functional MRI
PNAS,
January 23, 2007;
104(4):
1377 - 1382.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Hampshire and A. M. Owen
Fractionating Attentional Control Using Event-Related fMRI
Cereb Cortex,
December 1, 2006;
16(12):
1679 - 1689.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. L. Remijnse, M. M. A. Nielen, A. J. L. M. van Balkom, D. C. Cath, P. van Oppen, H. B. M. Uylings, and D. J. Veltman
Reduced orbitofrontal-striatal activity on a reversal learning task in obsessive-compulsive disorder.
Arch Gen Psychiatry,
November 1, 2006;
63(11):
1225 - 1236.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. I. Hooker, L. T. Germine, R. T. Knight, and M. D'Esposito
Amygdala response to facial expressions reflects emotional learning.
J. Neurosci.,
August 30, 2006;
26(35):
8915 - 8922.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. N. Hampton, P. Bossaerts, and J. P. O'Doherty
The Role of the Ventromedial Prefrontal Cortex in Abstract State-Based Inference during Decision Making in Humans.
J. Neurosci.,
August 9, 2006;
26(32):
8360 - 8367.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. A. Crone, C. Wendelken, S. E. Donohue, and S. A. Bunge
Neural Evidence for Dissociable Components of Task-switching
Cereb Cortex,
April 1, 2006;
16(4):
475 - 486.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Gorrindo, R.J.R. Blair, S. Budhani, D. P. Dickstein, D. S. Pine, and E. Leibenluft
Deficits on a Probabilistic Response-Reversal Task in Patients With Pediatric Bipolar Disorder
Am J Psychiatry,
October 1, 2005;
162(10):
1975 - 1977.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. D. Barber and C. S. Carter
Cognitive Control Involved in Overcoming Prepotent Response Tendencies and Switching Between Tasks
Cereb Cortex,
July 1, 2005;
15(7):
899 - 912.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. A. Seger and C. M. Cincotta
The Roles of the Caudate Nucleus in Human Classification Learning
J. Neurosci.,
March 16, 2005;
25(11):
2941 - 2951.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. E. Longworth, S. E. Keenan, R. A. Barker, W. D. Marslen-Wilson, and L. K. Tyler
The basal ganglia and rule-governed language use: evidence from vascular and degenerative conditions
Brain,
March 1, 2005;
128(3):
584 - 596.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Y Nagahama, T Okina, N Suzuki, H Nabatame, and M Matsuda
The cerebral correlates of different types of perseveration in the Wisconsin Card Sorting Test
J. Neurol. Neurosurg. Psychiatry,
February 1, 2005;
76(2):
169 - 175.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Deco and E. T. Rolls
Synaptic and Spiking Dynamics underlying Reward Reversal in the Orbitofrontal Cortex
Cereb Cortex,
January 1, 2005;
15(1):
15 - 30.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. R. Ridderinkhof, M. Ullsperger, E. A. Crone, and S. Nieuwenhuis
The Role of the Medial Frontal Cortex in Cognitive Control
Science,
October 15, 2004;
306(5695):
443 - 447.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. C. Turner, M. R.F. Aitken, D. R. Shanks, B. J. Sahakian, T. W. Robbins, C. Schwarzbauer, and P. C. Fletcher
The Role of the Lateral Frontal Cortex in Causal Associative Learning: Exploring Preventative and Super-learning
Cereb Cortex,
August 1, 2004;
14(8):
872 - 880.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. R. Aron, S. Monsell, B. J. Sahakian, and T. W. Robbins
A componential analysis of task-switching deficits associated with lesions of left and right frontal cortex
Brain,
July 1, 2004;
127(7):
1561 - 1573.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Cools, L. Clark, and T. W. Robbins
Differential Responses in Human Striatum and Prefrontal Cortex to Changes in Object and Rule Relevance
J. Neurosci.,
February 4, 2004;
24(5):
1129 - 1135.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Pears, J. A. Parkinson, L. Hopewell, B. J. Everitt, and A. C. Roberts
Lesions of the Orbitofrontal but not Medial Prefrontal Cortex Disrupt Conditioned Reinforcement in Primates
J. Neurosci.,
December 3, 2003;
23(35):
11189 - 11201.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. O'Doherty, H. Critchley, R. Deichmann, and R. J. Dolan
Dissociating Valence of Outcome from Behavioral Control in Human Orbital and Ventral Prefrontal Cortices
J. Neurosci.,
August 27, 2003;
23(21):
7931 - 7939.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. K. Fellows and M. J. Farah
Ventromedial frontal cortex mediates affective shifting in humans: evidence from a reversal learning paradigm
Brain,
August 1, 2003;
126(8):
1830 - 1837.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
TOP
ABSTRACT
INTRODUCTION
