Perception – Gain Control
Task Name
Description
Steady state
visual evoked
potentials to
magnocellular
vs.
parvocellular
biased
stimuli.
Magnocellular and
parvocellular visual pathway
function assessed using
steady-state visual evoked
potentials. This task that
takes ~ 15 min. The
magnocellular system
responds to low luminance
contrast and the parvocellular
system does not begin to
respond until contrast has
reached about 16%. In this
task, isolated checks are
modulated at low contrasts to
bias responding towards the
magnocellular visual pathway
and are modulated around a
high contrast "pedestal" to
bias responding towards the
parvocellular pathway.
Signal-to-noise ratio, which is
the amplitude of the response
corrected for noise, is
calculated for each contrast
and is the dependent
variable.
(Butler et al., 2001)
(Butler et al., 2005)
(Zemon & Gordon, 2006)
MANUSCRIPTS ON THE
WEBSITE:
Butler, P. D., Zemon, V.,
Schechter, I., Saperstein, A.
M., Hoptman, M. J., Lim, K.
O., et al. (2005). Early-stage
visual processing and cortical
amplification deficits in
schizophrenia. Arch Gen
Psychiatry, 62(5), 495-504.
Cognitive Construct
Validity
The magnocellular-biased
condition produces a steeply
rising increase in response to
low contrast stimuli which
reaches a saturation-level
once luminance contrast
reaches ~16% (Butler et al.,
2001; Butler et al., 2005;
Zemon & Gordon, 2006). This
leads to a characteristic Sshaped, non-linear contrast
gain control curve. The initial
steeply rising part of the
curve reflects substantial
amplification of low contrast
stimuli, permitting M-pathway
neurons to respond robustly
even at low contrasts. This
magnocellular-pathway
response is an example of
gain control because
response levels are optimized
within a limited dynamic
signaling range and the
sensory signal is amplified.
(Butler et al., 2001)
(Butler et al., 2005)
(Zemon & Gordon, 2006)
Neural Construct Validity
Reliability
The contrast response curves
obtained in human studies in
healthy controls (Butler et al.,
2001; Butler et al., 2005;
Zemon & Gordon, 2006)
(Fox, Sato, & Daw, 1990) to
magnocellular- and
parvocellular-biased stimuli
are very similar to what is
seen in single-cell recordings
in monkeys supporting the
concept that magnocellular
and parvocellular responses
are being examined. In
addition, visual pathways
within the brain use glutamate
as their primary
neurotransmitter and NMDA
appears to have a central role
in gain control. For instance,
NMDA receptors amplify
responses to isolated stimuli
as well as amplifying the
effects of lateral inhibition
(e.g., increase surround
antagonism of center
receptive field responses)
(Daw, Stein, & Fox, 1993)
(Kwon, Nelson, Toth, & Sur,
1992). Thus, an NMDA
deficit would result in
decreased amplification and
less lateral inhibition.
Microinufsion of NMDA
antagonists into cat lateral
geniculate nucleus or primary
visual cortex produced
shallower gain at low contrast
and a much lower plateau
indicating decreased signal
amplification in
electrophysiological studies
There has been
some work on test
retest reliability
(Butler et al.,
unpublished
observations).
Twenty participants
(10 controls and 10
schizophrenia
patients) have been
tested twice. The
correlation between
signal-to-noise ratios
(the dependent
measure which is a
measure of amplitude
corrected for noise)
obtained in first and
second test sessions
was significant (total
group: r=0.81,
p<0.0001; patients
alone: r=0.72, n=14,
p=0.004; controls
alone: r=0.88, n=6,
p=0.02).
Psychometric
Characteristics
The task does not
appear to have
practice effects. It is a
passive viewing task
in which
electrophysiological
responses are
obtained. The
responses do not
habituate even
following repeated
presentation of the
stimulus conditions. It
is not a learned task,
so that presentation
at multiple test dates
is not affected by
prior testing. There
do not appear to be
floor effects because
most people,
including patients,
give at least a small
response at low
contrast and a slightly
higher response as
contrast increases.
There is not a ceiling
effect because the
amplitude of the
electrophysiological
response does not
have a ceiling.
Animal Model
Stage of Research
Single cell recordings
from magnocellular
and parvocellular
neurons in monkey
lateral geniculate
nucleus (LGN) show
characteristic
electrophysiological
responses.
Magnocellular neurons
show steep increases
in responding at low
contrast and
saturation at higher
contrast. Parvocellular
neurons show a
shallow slope at low
contrast and a nonsaturating response.
The curves found in
the proposed task are
very similar to those
seen in monkey work.
Studies in cat LGN
show decreased slope
and decreased
plateau following
infusion of NMDA
antagonists (Daw et
al., 1993) (Kwon et al.,
1992) similar to what
is seen in
schizophrenia patients
in this task (Butler et al
2005).
There is evidence
that this specific task
elicits deficits in
schizophrenia.
We need to assess
psychometric
characteristics such
as test-retest
reliability, practice
effects, and
ceiling/floor effects
for this task.
We need to study
whether or not
performance on this
task changes in
response to
psychological or
pharmacological
intervention.
(Fox et al., 1990). Thus, the
magnocellular-biased task
may be assessing NMDAmediated signal amplification.
Indeed, schizophrenia
patients show curves very
similar to those seen
following infusion of NMDA
antagonists in animal studies.
Zemon, V., & Gordon, J.
(2006). Luminance-contrast
mechanisms in humans:
visual evoked potentials and
a nonlinear model. Vision
Res, 46(24), 4163-4180.
ContrastContrast
Effect (CCE)
Task
Gain control has been
successfully studied using the
Contrast-Contrast Effect
(CCE) task in which contrast
sensitivity for a ringed target
can be influenced by the
contrast of a circular surround
(Chubb, Sperling, & Solomon,
1989). In this task,
participants are asked to
match a variable contrast
patch to a central patch.
When the surround is highcontrast, the inner target is
perceived to be of lower
contrast than when the same
target is perceived without a
surround (Chubb et al., 1989;
Dakin, Carlin, & Hemsley,
2005).
MANUSCRIPTS ON THE
WEBSITE:
Dakin, S., Carlin, P., &
Hemsley, D. (2005). Weak
suppression of visual context
in chronic schizophrenia. Curr
Biol, 15(20), R822-824.
Zenger-Landolt, B., &
Heeger, D. J. (2003).
This task is ideal for
examining gain control in
schizophrenia because: 1)
reduced gain control, or
contextual modulation, would
be indicated by more
accurate contrast judgments
regarding the inner circle
compared to controls; and 2)
there is already evidence for
reduced spatial context
effects in vision in
schizophrenia (Must, Janka,
Benedek, & Keri, 2004;
Uhlhaas et al., 2006). An
important feature of this task
is that full psychometric
functions can be obtained for
subjects. From these,
separate indicators of
precision (the minimum size
of contrast differences that
are detectable, which is
indicated by the slope of the
function) and bias (reflecting
the amount of offset that is
needed between the target
and the surround to produce
a perceptual match) can be
obtained, allowing us to
examine discrimination
accuracy independent of
(Daw et al., 1993)
(Fox et al., 1990)
(Kwon et al., 1992)
Converging evidence from
psychophysics and fMRI
indicates that the contrastcontrast effect is linked to
gain control within primary
visual cortex (V1) (ZengerLandolt & Heeger, 2003).
Further evidence indicates
that the effect within V1 is
likely due to both activity
arising within V1 and to topdown feedback from higher,
object-processing areas to V1
(Lotto & Purves, 2001).
Because 90% of cells in V1
are subject to suppression
from neighboring cells, tasks
such as this that are known to
act on V1 neurons are ideal
methods for the study of gain
control.
(Zenger-Landolt & Heeger,
2003)
(Lotto & Purves, 2001)
This has not been
assessed.
An important feature
of this task is that full
psychometric
functions can be
obtained for subjects.
From these, separate
indicators of precision
(the minimum size of
contrast differences
that are detectable,
which is indicated by
the slope of the
function) and bias
(reflecting the amount
of offset that is
needed between the
target and the
surround to produce
a perceptual match)
can be obtained,
allowing us to
examine
discrimination
accuracy
independent of
response bias (as
with other signaldetection analyses).
This suggests the
absence of
floor/ceiling effects
Not Known
There is evidence
that this specific task
elicits deficits in
schizophrenia.
We need to assess
psychometric
characteristics such
as test-retest
reliability, practice
effects, and
ceiling/floor effects
for this task.
We need to study
whether or not
performance on this
task changes in
response to
psychological or
pharmacological
intervention.
Mismatch
Negativity
Response suppression in v1
agrees with psychophysics of
surround masking. J
Neurosci, 23(17), 6884-6893.
response bias (as with other
signal-detection analyses).
Mismatch negativity (MMN) is
an auditory event-related
potential (ERP) elicited in an
"oddball" task, in which a
sequence of repetitive
standard tones is interrupted
by a physically different
"deviant" tone that violates
expectancies created by the
standard. MMN can be
recorded and quantified using
standard ERP recording
systems (e.g. Neuroscan,
Biosemi, ANT). (Umbricht &
Krljes, 2005)
MMN indexes perception of
stimulus deviance at the level
of auditory cortex.
Generation of MMN depends
upon gain control (i.e. signal
amplification) of neurons
sensitive to stimulus
deviance. Presentation of
repetitive standards should,
under normal conditions, lead
to upward bias of the gain
process. In schizophrenia,
this bias mechanism appears
to be impaired.
MANUSCRIPTS ON THE
WEBSITE:
Javitt, D. C., Spencer, K. M.,
Thaker, G. K., Winterer, G., &
Hajos, M. (2008).
Neurophysiological
biomarkers for drug
development in
schizophrenia. Nat Rev Drug
Discov, 7(1), 68-83.
Pakarinen, S., Takegata, R.,
Rinne, T., Huotilainen, M., &
Naatanen, R. (2007).
Measurement of extensive
auditory discrimination
profiles using the mismatch
negativity (MMN) of the
auditory event-related
potential (ERP). Clin
Neurophysiol, 118(1), 177185.
(Uhlhaas et al., 2006)
(Must et al., 2004)
At the neural level, MMN
reflects current flow through
open, unblocked NMDA
receptors within auditory
cortex. Similar mechanisms
mediate gain control within
visual cortex, suggesting a
parallel phenomenon. MMN
generation can be
antagonized by administration
of NMDA agonists such as
PCP or ketamine in either
human or animal models
(Javitt, 2000; Javitt,
Steinschneider, Schroeder, &
Arezzo, 1996; Turetsky et al.,
2007; Umbricht et al., 2000).
MMN tracks auditory
perceptual performance
across a variety of
dimensions (Pakarinen,
Takegata, Rinne, Huotilainen,
& Naatanen, 2007).
Test-retest reliability
of mismatch
negativity for
duration, frequency
and intensity changes
(Hall et al., 2006;
Tervaniemi et al.,
1999).
Hall (average of 18
days): 0.34-0.66
ICCs
Tervaniemi (average
of 8.3 days):
Correlations between
0.41 and 0.78.
MMN is generated
preattentively in the
absence of a
behavioral task.
Floor effects depend
upon quality of EEG
recording and can be
minimized through
good
electrophysiological
technique. Testretest studies show
no significant
"learning" (i.e.
repetition effects see references on
test/retest reliability).
As MMN amplitude
increases with dF
and
standards/deviant
ratio, ceiling effect is
not relevant (Javitt,
Spencer, Thaker,
Winterer, & Hajos,
2008).
Homologues exist in
monkeys (Javitt et al.,
1996) (definitely) and
rodents
(probably)(Ehrlichman,
Maxwell, Majumdar, &
Siegel, 2008;
Umbricht, Vyssotki,
Latanov, Nitsch, &
Lipp, 2005).
There is evidence
that this specific task
elicits deficits in
schizophrenia.
Data already exists
on psychometric
characteristics of this
task, such as testretest reliability,
practice effects,
ceiling/floor effects.
There is evidence
that performance on
this task can improve
in response to
psychological or
pharmacological
interventions.
Prepulse
Inhibition of
Startle
Individuals are presented with
two auditory probes in
sequences. The P50
response to the second probe
is typically reduced in
individuals with intact sensory
gating.
It is not clear whether this
correlates with other
measures of inhibition.
(Swerdlow, Braff, Taaid, &
Geyer, 1994)
(Braff & Geyer, 1990)
(Cadenhead, Carasso,
Swerdlow, Geyer, & Braff,
1999)
There is a large literature on
the neural substrates of
Prepulse inhibition in animals,
and a large literature on
pharmacological effects.
There are now human
imaging studies (at least one)
looking at prepulse inhibition
in the scanner.
YES
We need to assess
psychometric
characteristics such
as test-retest
reliability, practice
effects, and
ceiling/floor effects
for this task.
(Joober, Zarate, Rouleau,
Skamene, & Boksa, 2002)
(Kumari, Antonova, & Geyer,
2008)
(Campbell et al., 2007)
(Kumari et al., 2007)
(Kumari et al., 2003)
MANUSCRIPTS ON THE
WEBSITE:
There is evidence
that this specific task
elicits deficits in
schizophrenia
(Swerdlow et al.,
2006).
This task has been
studies with
psychopharamcology
methods
Swerdlow, N. R., Light, G. A.,
Cadenhead, K. S., Sprock, J.,
Hsieh, M. H., & Braff, D. L.
(2006). Startle gating deficits
in a large cohort of patients
with schizophrenia:
relationship to medications,
symptoms, neurocognition,
and level of function. Arch
Gen Psychiatry, 63(12),
1325-1335.
Turetsky, B. I., Calkins, M. E.,
Light, G. A., Olincy, A.,
Radant, A. D., & Swerdlow,
N. R. (2007).
Neurophysiological
endophenotypes of
schizophrenia: the viability of
selected candidate measures.
Schizophr Bull, 33(1), 69-94.
Contrast
Sensitivity
This is a classic
psychophysical task that has
Contrast is an example of
gain control, which takes into
Gain control in the visual
system refers to processes
I am not aware of any
published data on
The task does not
have a ceiling effect,
There have been
numerous studies
There is evidence
that this specific task
been used for over 50 years
(Bodis-Wollner, 1972;
Movshon & Kiorpes, 1988;
Robson, 1966). There are
different variations on the
method. One method is use
of a two-alternative forced
choice design. In this design,
contrast sensitivity functions
can be obtained by
presenting sine-wave gratings
at several different spatial
frequencies from low to high
(e.g., 0.5 to 21
cycles/degree). Gratings are
presented on one half (either
the right or left side) of a
visual display, with the other
side having a uniform field.
Participants are asked to
state which side of the display
contains the grating. Contrast
is varied across trials using
an up-and-down transformed
response method to
determine contrast sensitivity
(e.g., the contrast at which
the side the grating is on is
correctly detected 79% of the
time).
MANUSCRIPTS ON THE
WEBSITE:
Butler, P. D., Zemon, V.,
Schechter, I., Saperstein, A.
M., Hoptman, M. J., Lim, K.
O., et al. (2005). Early-stage
visual processing and cortical
amplification deficits in
schizophrenia. Arch Gen
Psychiatry, 62(5), 495-504.
Keri, S., Antal, A., Szekeres,
G., Benedek, G., & Janka, Z.
(2002). Spatiotemporal visual
account spatial and temporal
context. Contrast sensitivity
varies with spatial context (as
well as with temporal context
(Robson, 1966). In addition,
gain control assists sensory
subsystems in increasing
contrast between adjacent
and successive stimuli.
that generally occur at early
stages of processing such as
at the level of the LGN or
primary visual cortex and
utilizes excitatory and
inhibitory lateral interactions
between neurons. Contrast
sensitivity can be assessed
and contrast sensitivity
curves obtained from
recordings of LGN neurons
as well as from neurons in
primary visual cortex
(Kiorpes, Tang, Hawken, &
Movshon, 2003). Contrast
sensitivity curves produce an
inverted U shaped function
with a peak in the mid-range
of spatial frequencies and falloff at lower and higher spatial
frequencies. The fall-off at
lower spatial frequencies is
mainly a function of inhibitory
lateral interactions between
center and surround whereas
fall-off at higher spatial
frequencies is more a
function of excitatory
interactions (Burbeck & Kelly,
1980).
test retest reliability.
In our laboratory, 29
people have been
tested twice and
there was a
significant correlation
between first and
second test time for
all spatial frequencies
(0.5 - 21c/degree)
examined (r=0.670.4, p=0.0001-0.02
for the different
spatial frequencies).
but, in theory, could
have a floor effect.
Higher contrast
sensitivity indicates
better performance.
Contrast sensitivity is
the inverse of
threshold so that a
high contrast
sensitivity of 100
corresponds to a low
threshold of 1%
contrast. There is no
theoretical limit on
how high contrast
sensitivity can go. A
contrast sensitivity of
500, for instance,
would correspond to
a threshold of 0.2%
contrast. On the
other hand, poor
performance leads to
low contrast
sensitivity and
corresponding high
thresholds. For
example, a contrast
sensitivity of 1 would
correspond to a
threshold of 100%
contrast. It is not
possible to go higher
than 100% contrast.
However, in practice,
unless there is a
serious visual
problem, people do
not need 100%
contrast to do this
task. I am not aware
of data on practice
effects, though this is
not a learned task so
that practice effects
should be minimal.
done in a variety of
species including
goldfish, cat, and
falcon (Movshon &
Kiorpes, 1988).
Contrast sensitivity
can be obtained in
macaques using
behavioral methods
(Movshon & Kiorpes,
1988).
elicits deficits in
schizophrenia (Butler
et al., 2005; Keri,
Antal, Szekeres,
Benedek, & Janka,
2002; Slaghuis,
1998).
We need to assess
psychometric
characteristics such
as test-retest
reliability, practice
effects, and
ceiling/floor effects
for this task.
We need to study
whether or not
performance on this
task changes in
response to
psychological or
pharmacological
intervention.
processing in schizophrenia.
J Neuropsychiatry Clin
Neurosci, 14(2), 190-196.
REFERENCES:
Bodis-Wollner, I. (1972). Contrast sensitivity and increment threshold. Perception, 1(1), 73-83.
Braff, D. L., & Geyer, M. A. (1990). Sensorimotor gating and schizophrenia. Human and animal model studies. Arch Gen Psychiatry, 47(2), 181-188.
Burbeck, C. A., & Kelly, D. H. (1980). Spatiotemporal characteristics of visual mechanisms: excitatory-inhibitory model. J Opt Soc Am, 70(9), 1121-1126.
Butler, P. D., Schechter, I., Zemon, V., Schwartz, S. G., Greenstein, V. C., Gordon, J., et al. (2001). Dysfunction of early-stage visual processing in schizophrenia. Am J Psychiatry, 158(7), 1126-1133.
Butler, P. D., Zemon, V., Schechter, I., Saperstein, A. M., Hoptman, M. J., Lim, K. O., et al. (2005). Early-stage visual processing and cortical amplification deficits in schizophrenia. Arch Gen Psychiatry, 62(5),
495-504.
Cadenhead, K. S., Carasso, B. S., Swerdlow, N. R., Geyer, M. A., & Braff, D. L. (1999). Prepulse inhibition and habituation of the startle response are stable neurobiological measures in a normal male population.
Biol Psychiatry, 45(3), 360-364.
Campbell, L. E., Hughes, M., Budd, T. W., Cooper, G., Fulham, W. R., Karayanidis, F., et al. (2007). Primary and secondary neural networks of auditory prepulse inhibition: a functional magnetic resonance
imaging study of sensorimotor gating of the human acoustic startle response. Eur J Neurosci, 26(8), 2327-2333.
Chubb, C., Sperling, G., & Solomon, J. A. (1989). Texture interactions determine perceived contrast. Proc Natl Acad Sci U S A, 86(23), 9631-9635.
Dakin, S., Carlin, P., & Hemsley, D. (2005). Weak suppression of visual context in chronic schizophrenia. Curr Biol, 15(20), R822-824.
Daw, N. W., Stein, P. S., & Fox, K. (1993). The role of NMDA receptors in information processing. Annu Rev Neurosci, 16, 207-222.
Ehrlichman, R. S., Maxwell, C. R., Majumdar, S., & Siegel, S. J. (2008). Deviance-elicited Changes in Event-related Potentials are Attenuated by Ketamine in Mice. J Cogn Neurosci.
Fox, K., Sato, H., & Daw, N. (1990). The effect of varying stimulus intensity on NMDA-receptor activity in cat visual cortex. Journal of Neurophysiology, 64, 1413-1428.
Hall, M. H., Schulze, K., Rijsdijk, F., Picchioni, M., Ettinger, U., Bramon, E., et al. (2006). Heritability and reliability of P300, P50 and duration mismatch negativity. Behav Genet, 36(6), 845-857.
Javitt, D. C. (2000). Intracortical mechanisms of mismatch negativity dysfunction in schizophrenia. Audiol Neurootol, 5(3-4), 207-215.
Javitt, D. C., Spencer, K. M., Thaker, G. K., Winterer, G., & Hajos, M. (2008). Neurophysiological biomarkers for drug development in schizophrenia. Nat Rev Drug Discov, 7(1), 68-83.
Javitt, D. C., Steinschneider, M., Schroeder, C. E., & Arezzo, J. C. (1996). Role of cortical N-methyl-D-aspartate receptors in auditory sensory memory and mismatch negativity generation: implications for
schizophrenia. Proc Natl Acad Sci U S A, 93(21), 11962-11967.
Joober, R., Zarate, J. M., Rouleau, G. A., Skamene, E., & Boksa, P. (2002). Provisional mapping of quantitative trait loci modulating the acoustic startle response and prepulse inhibition of acoustic startle.
Neuropsychopharmacology, 27(5), 765-781.
Keri, S., Antal, A., Szekeres, G., Benedek, G., & Janka, Z. (2002). Spatiotemporal visual processing in schizophrenia. J Neuropsychiatry Clin Neurosci, 14(2), 190-196.
Kiorpes, L., Tang, C., Hawken, M. J., & Movshon, J. A. (2003). Ideal observer analysis of the development of spatial contrast sensitivity in macaque monkeys. J Vis, 3(10), 630-641.
Kumari, V., Antonova, E., & Geyer, M. A. (2008). Prepulse inhibition and "psychosis-proneness" in healthy individuals: An fMRI study. Eur Psychiatry.
Kumari, V., Antonova, E., Geyer, M. A., Ffytche, D., Williams, S. C., & Sharma, T. (2007). A fMRI investigation of startle gating deficits in schizophrenia patients treated with typical or atypical antipsychotics. Int J
Neuropsychopharmacol, 10(4), 463-477.
Kumari, V., Gray, J. A., Geyer, M. A., ffytche, D., Soni, W., Mitterschiffthaler, M. T., et al. (2003). Neural correlates of tactile prepulse inhibition: a functional MRI study in normal and schizophrenic subjects.
Psychiatry Res, 122(2), 99-113.
Kwon, Y. H., Nelson, S. B., Toth, L. J., & Sur, M. (1992). Effect of stimulus contrast and size on NMDA receptor activity in cat lateral geniculate nucleus. J Neurophysiol, 68(1), 182-196.
Lotto, R. B., & Purves, D. (2001). An empirical explanation of the Chubb illusion. J Cogn Neurosci, 13(5), 547-555.
Movshon, J. A., & Kiorpes, L. (1988). Analysis of the development of spatial contrast sensitivity in monkey and human infants. J Opt Soc Am A, 5(12), 2166-2172.
Must, A., Janka, Z., Benedek, G., & Keri, S. (2004). Reduced facilitation effect of collinear flankers on contrast detection reveals impaired lateral connectivity in the visual cortex of schizophrenia patients. Neurosci
Lett, 357(2), 131-134.
Pakarinen, S., Takegata, R., Rinne, T., Huotilainen, M., & Naatanen, R. (2007). Measurement of extensive auditory discrimination profiles using the mismatch negativity (MMN) of the auditory event-related
potential (ERP). Clin Neurophysiol, 118(1), 177-185.
Robson, J. G. (1966). Spatial and temporal contrast-sensitivity functions of the visual system. Journal of the Optical Society of America, 56, 1141-1142.
Slaghuis, W. L. (1998). Contrast sensitivity for stationary and drifting spatial frequency gratings in positive- and negative-symptom schizophrenia. J Abnorm Psychol, 107(1), 49-62.
Swerdlow, N. R., Braff, D. L., Taaid, N., & Geyer, M. A. (1994). Assessing the validity of an animal model of deficient sensorimotor gating in schizophrenic patients. Arch Gen Psychiatry, 51(2), 139-154.
Swerdlow, N. R., Light, G. A., Cadenhead, K. S., Sprock, J., Hsieh, M. H., & Braff, D. L. (2006). Startle gating deficits in a large cohort of patients with schizophrenia: relationship to medications, symptoms,
neurocognition, and level of function. Arch Gen Psychiatry, 63(12), 1325-1335.
Tervaniemi, M., Lehtokoski, A., Sinkkonen, J., Virtanen, J., Ilmoniemi, R. J., & Naatanen, R. (1999). Test-retest reliability of mismatch negativity for duration, frequency and intensity changes. Clin Neurophysiol,
110(8), 1388-1393.
Turetsky, B. I., Calkins, M. E., Light, G. A., Olincy, A., Radant, A. D., & Swerdlow, N. R. (2007). Neurophysiological endophenotypes of schizophrenia: the viability of selected candidate measures. Schizophr Bull,
33(1), 69-94.
Uhlhaas, P. J., Linden, D. E., Singer, W., Haenschel, C., Lindner, M., Maurer, K., et al. (2006). Dysfunctional long-range coordination of neural activity during Gestalt perception in schizophrenia. J Neurosci,
26(31), 8168-8175.
Umbricht, D., & Krljes, S. (2005). Mismatch negativity in schizophrenia: a meta-analysis. Schizophr Res, 76(1), 1-23.
Umbricht, D., Schmid, L., Koller, R., Vollenweider, F. X., Hell, D., & Javitt, D. C. (2000). Ketamine-induced deficits in auditory and visual context-dependent processing in healthy volunteers: implications for
models of cognitive deficits in schizophrenia. Arch Gen Psychiatry, 57(12), 1139-1147.
Umbricht, D., Vyssotki, D., Latanov, A., Nitsch, R., & Lipp, H. P. (2005). Deviance-related electrophysiological activity in mice: is there mismatch negativity in mice? Clin Neurophysiol, 116(2), 353-363.
Zemon, V., & Gordon, J. (2006). Luminance-contrast mechanisms in humans: visual evoked potentials and a nonlinear model. Vision Res, 46(24), 4163-4180.
Zenger-Landolt, B., & Heeger, D. J. (2003). Response suppression in v1 agrees with psychophysics of surround masking. J Neurosci, 23(17), 6884-6893.