 |
||||
|
||||
|
||||
|
||||
The Journal of Neuroscience, August 13, 2003, 23(19):7407-7411
Previous Article | Next Article
BRIEF COMMUNICATION
Abnormal Neural Synchrony in Schizophrenia
Kevin M. Spencer, Paul G. Nestor, Margaret A. Niznikiewicz, Dean F. Salisbury, Martha E. Shenton, andRobert W. McCarley Department of Psychiatry, Harvard Medical School/Veterans Affairs Boston Healthcare System, Brockton, Massachusetts 02301
Abstract
Top
Abstract
Introduction
Schizophrenia has been conceptualized as a failure of cognitive integration, and abnormalities in neural circuitry (particularly inhibitory interneurons) have been proposed as a basis for this disorder. We used measures of phase locking and phase coherence in the scalp-recorded electroencephalogram to examine the synchronization of neural circuits in schizophrenia. Compared with matched control subjects, schizophrenia patients demonstrated: (1) absence of the posterior component of the early visual gamma band response to Gestalt stimuli; (2) abnormalities in the topography, latency, and frequency of the anterior component of this response; (3) delayed onset of phase coherence changes; and (4) the pattern of anterior-posterior coherence increases in response to Gestalt stimuli found in controls was replaced by a pattern of interhemispheric coherence decreases in patients. These findings support the hypothesis that schizophrenia is associated with impaired neural circuitry demonstrated as a failure of gamma band synchronization, especially in the 40 Hz range.
Key words: schizophrenia; gamma band EEG; phase synchrony; wavelet analysis; visual perception; inhibitory interneurons
Introduction
As early as 1911, Bleuler had described schizophrenia as a "splitting of the psychic functions" (Bleuler, 1950/1911), in which various aspects of thought and personality were disintegrated. In the modern era, it has been proposed that the cognitive and affective impairments associated with schizophrenia may be related to a failure to integrate the activity of local and distributed neural circuits (Friston and Frith, 1995
Phase locking is a highly sensitive measure of neural synchronization in the EEG (Tallon-Baudry and Bertrand, 1999
We used phase locking and phase coherence to examine whether high-frequency neural synchronization associated with the perception of visual Gestalts is abnormal in schizophrenia patients. Previous studies of healthy individuals have reported enhancements of gamma band power (Tallon-Baudry and Bertrand, 1999
View larger version (26K):
[in this window]
[in a new window]
Figure 1. Illusory square discrimination task. A, Stimuli. The ratio of inducer radius to length of square was 0.2. B, Behavioral performance data (bars indicate SE). C, VEPs at electrode site PO6. D, Relationship between the Square minus No-Square RT (x-axis) and occipital phase-locking (y-axis) effects. The greater the RT savings, the larger the phase-locking effects for NC but not SZ.
Materials and Methods
Participants. Inclusion criteria for patients and controls included: (1) age between 18 and 50 years; (2) right handed; (3) no history of electroconvulsive treatment; (4) no history of neurological illness; (5) no history of alcohol or drug dependence, or abuse within the last year, or long duration (>1 year) of past abuse; (6) no present medication for medical disorders that would have deleterious EEG, neurological, and/or cognitive functioning consequences; (7) verbal intelligence quotient above 75; (8) no alcohol use in the 24 hr before testing; and (9) an ability and desire to cooperate with our experimental procedures as demonstrated by giving informed consent (following Harvard Medical School and Veterans Affairs Boston Healthcare System guidelines).Fourteen schizophrenia patients [diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (American Psychiatric Association, 1994
50%). The final sample for the SZ group consisted of 12 chronic medicated male patients (mean ± SD; age, 45 ± 9.2 years; illness duration, 21 ± 5.1 years). The NC group consisted of 12 healthy males (age, 47 ± 5.7 years) matched with the SZ group on the basis of age (F(1,22) = 0.311; NS) and parental socioeconomic status. Five patients were receiving conventional neuroleptics, six patients received atypical antipsychotics, and one patient received both types. Mean equivalent chlorpromazine dosage was 519 ± 539 mg.
Stimuli and experimental procedures. Subjects fixated a central cross and responded with a button press according to whether an illusory square (Fig. 1 A) was present or absent (response hands counterbalanced across subjects). Stimuli remained on the monitor until 300 msec after a response had been made. If no response had been made by 2000 msec after stimulus onset, the trial was ended, and the next trial began (1000 msec intertrial interval). Subjects performed a practice block and two experimental blocks, each consisting of 45 trials per condition.
Electrophysiological recording and processing. The EEG was recorded (0.01-100 Hz; 500 Hz digitization) with tin electrodes at 16 scalp sites (F3/Fz/F4, C3/Cz/C4, P3/Pz/P4, O1/Oz/O2, P7/P8, PO5/PO6) and the right mastoid, referenced to the left mastoid. The vertical electrooculogram (EOG) was recorded at Fp1, and the horizontal EOG was recorded at the outer canthi of the eyes. Electrode impedances were <5 k
. Error and no-response trials were excluded from analyses. Independent component analysis (Makeig et al., 1996
Data analysis. The complex Morlet wavelet transform (six-cycle length) (Torrence and Compo, 1998
The occipital component of the visual evoked gamma band response was measured as the average phase-locking value within the 80 -120 msec and 31-44 Hz ranges. Analysis of the fronto-central component was based on peak values at midline and right hemisphere sites where it was maximal, with latency and frequency ranges selected to avoid overlap with the visual-evoked potentials (VEPs). The latency range was 80 -160 msec for both groups and conditions, except for NC subjects in the Square condition, in which it was 80 -110 msec. Frequency ranges for both groups were 34 -58 (Square) and 28 -58 Hz (No-Square).
For phase coherence analyses of the Square and No-Square conditions, values were compared with the mean prestimulus baseline in two-tailed paired t tests at each time-frequency element (0 -300 msec period) for each group. In the Square versus No-Square comparison, t tests were computed between values for the respective conditions. Significance values were corrected for the number of frequency bins (n = 4; Fig. 3), resulting in a statistical criterion of p = 0.0125 (t = ± 2.98). A temporal threshold was applied to the statistical maps such that any period of coherence change above the t threshold had to be at least one cycle in duration at that particular frequency. Coherence changes were summed within each frequency bin across four time bins (Fig. 4).
View larger version (37K):
[in this window]
[in a new window]
Figure 3. Phase coherence results. The distributions of the number of coherence changes (increases and decreases) are plotted across frequency bins in each stimulus condition and the Square minus No-Square comparison. Note the different y-axis scales for each row of plots.
View larger version (55K):
[in this window]
[in a new window]
Figure 4. Phase coherence changes in the 37-44 Hz frequency bin plotted in space and time. Circles indicate electrode positions, with frontal sites at top and occipital sites at bottom. Red lines mark coherence increases between electrode sites, and blue lines mark coherence decreases.
VEP amplitudes were measured at sites O1/O2, P7/P8, and PO5/PO6. Latency ranges for the P1 were 76 -126 msec (NC) and 78 -138 msec (SZ), and for the N1, 126 -212 msec (NC) and 138 -212 msec (SZ).
Phase locking and VEP amplitude were statistically analyzed using ANOVA with the design group (SZ/NC) X stimulus (Square/No-Square) X site (relevant electrode sites). Effects on group level coherence changes were analyzed using the
2 goodness-of-fit test, comparing the distributions of coherence changes across frequency bins.
Results
Behavioral performance
NC and SZ subjects had similar median reaction time (RT) and error rate patterns (Fig. 1B). In general, subjects made more errors (F(1,22) = 4.99; p < 0.05) and had shorter RTs (F(1,22) = 9.92; p < 0.01) on Square than No-Square trials. This shorter RT for Squares also was present within the SZ group (F(1,11) = 7.61; p < 0.05) but not within the NC group (F(1,11) = 2.32; NS). Whereas the SZ patients' low overall error rate (3.9%) indicated that they did not have any particular difficulties with the task, they did make more errors (F(1,22) = 5.97; p < 0.05) and had longer RTs (F(1,22) = 9.06; p < 0.01) than the NC group.VEPs
The most notable group difference in the VEPs (Fig. 1C) was that the P1 component was larger in amplitude for NC than SZ subjects across stimulus conditions (F(1,22) = 6.22; p < 0.05). There was a trend for N1 component amplitude to be larger in the NC than the SZ group (F(1,22) = 3.11; p = 0.09), and across all subjects, the N1 was significantly larger for Square than No-Square stimuli (F(1,22) = 8.66; p < 0.01).Phase-locking data
For both the NC and SZ groups, visual stimuli evoked an early phase-locking response in the 24-48 Hz range that began as early as 80 msec and did not overlap with the low-frequency VEP at frontal, central, and occipital sites (Fig. 2A). Previous studies have differentiated this early evoked gamma band response into anterior and posterior components (Tallon-Baudry et al., 1997
View larger version (97K):
[in this window]
[in a new window]
Figure 2. Group average time-frequency maps of phase locking. A, Midline frontal (Fz), central (Cz), and occipital (Oz) sites. The early evoked gamma band response (circled in yellow) can be distinguished from the low-frequency VEP. B, Square minus No-Square difference map at the left occipital site (O1).
The most striking difference between the SZ and NC groups was in the occipital component of the response (group X stimulus; F(1,22) = 7.29; p < 0.05). In the NC group data, Square stimuli evoked this response maximally at the left occipital site, but there was no response to the No-Square stimuli (F(1,11) = 10.2; p < 0.01). For the SZ subjects, however, neither stimulus evoked the response (F(1,11) = 0.515; NS). These group differences are highlighted in Figure 2B. To try to determine the functional significance of the occipital phase-locking response, we computed nonparametric Spearman's
correlation coefficients between the Square minus No-Square differences in phase synchrony and RT across subjects in the NC group. This correlation was negative and statistically significant (
The fronto-central component of the early evoked gamma band response was abnormal in topography, latency, and frequency for the SZ group. Whereas for both groups this response was larger for No-Square than Square stimuli (NC: F(1,11) = 5.70; p < 0.05; SZ: F(1,11) = 5.19; p < 0.05), it was larger at central than frontal electrode sites for SZ (group X site; F(1,22) = 10.0; p < 0.01; SZ: F(1,11) = 24.5; p < 0.001) but not NC subjects (F(1,11) = 0.00695; NS). The latency of the fronto-central response to Square stimuli was longer for SZ than NC subjects (116.9 vs 99.2 msec; group X stimulus; F(1,22) = 5.66; p < 0.05; group: F(1,22) = 24.1; p < 0.0001), but there was no difference for No-Square stimuli (117.3 vs 119.1 msec; F(1,22) = 0.046; NS). Last, the frequency of the response to No-Square stimuli was lower for SZ than NC subjects at central sites (35.3 vs 42.4 Hz; group X stimulus X site; F(1,22) = 5.08; p < 0.05; group: F(1,22) = 4.45; p < 0.05), but there was no difference for Square stimuli (44.4 vs 41.5 Hz; F(1,22) = 1.04; NS).
In summary, the early evoked gamma band response differed between the SZ and NC groups in several ways, being absent for the occipital component and abnormal in topography, latency, and frequency for the fronto-central component. These results support the hypothesis that gamma band synchronization is abnormal in schizophrenia. The different patterns observed for the VEPs and phase-locking responses indicate that the latter are not artifacts of the low-frequency VEPs.
To test for potential confounds with medication, we computed Spearman's
Phase coherence data
Next, we examined phase coherence, which is indicative of coupling between distant brain regions (Varela et al., 2001Three main differences between the groups were observed (Fig. 3). First, the NC group had more coherence increases than the SZ group overall (249 vs 91) and in both the Square (
The spatio-temporal distributions of coherence changes in the 37-44 Hz bin (Fig. 4) revealed several patterns. For the NC group, coherence changes began in the 0 -75 msec interval and were concentrated in the 75-150 msec interval, coinciding with the early evoked gamma band response, and showed a roughly similar pattern of anterior-posterior coherence increases in the Square and No-Square conditions. Consequently, there were few differences in coherence in the Square minus No-Square comparison. For the SZ group, the onset of coherence changes was delayed, not beginning until after 75 msec. In the Square condition, the number of coherence changes (mainly decreases) was largest in the 225-300 msec interval and involved mostly interhemispheric interactions between posterior sites. In contrast, in the No-Square condition, the coherence changes were predominantly anterior-posterior increases in the 75-150 and 150 -225 msec intervals, more in agreement in latency and directionality with those in the NC data. In the Square minus No-Square comparison, the SZ subjects displayed a consistent pattern of interhemispheric coherence decreases between posterior sites across the 0-300 msec period, in contrast to the NC group. The electrodes most often involved in these coherence decreases were P7 and P8, which lie over posterior temporal visual areas. Thus, phase coherence changes generally had a delayed onset for SZ compared with NC subjects and differed maximally between the groups in the Square condition, in which the SZ pattern consisted of coherence decreases between posterior sites, contrasting with the NC pattern of coherence increases along the anterior-posterior axis.
These results demonstrate that long-range neural synchronization in the upper beta and gamma bands of the EEG is impaired in schizophrenia, particularly in the 40 Hz range. As in the phase-locking data, the illusory square stimuli were especially associated with a lack of coherence. It should be noted that while possible effects of volume conduction cannot be ruled out from these data, the calculation of phase coherence relative to the prestimulus baseline reduces such a confound by eliminating any overall level of coherence. Also, volume conduction would be expected to bias the spatial distribution of coherence patterns to adjacent electrodes, but this pattern was not observed (cf. Rodriguez et al., 1999
Discussion
We found that schizophrenia was associated with abnormal phase-locking and phase coherence responses to visual stimuli in a Gestalt perception task, supporting the hypothesis that abnormal neural circuit function may be an underlying cause of schizophrenia. The patients' phase-locking and coherence patterns were particularly abnormal in the Square condition, in which the perception of the illusory object presumably engages feature-binding mechanisms that rely on neural synchrony (Engel et al., 2001Earlier studies have documented SZ abnormalities in measures of gamma band power or amplitude in the EEG (Kwon et al., 1999
Several recent studies have demonstrated that a critical neural substrate of high-frequency oscillatory activity in the cortex lies in interactions between inhibitory interneurons, mediated both by GABAA synapses and gap junctions (Whittington et al., 2000
The phase coherence data are consistent with a growing body of functional (Fletcher et al., 1999
Footnotes
Received Mar. 10, 2003; revised Jun. 23, 2003; accepted Jun. 24, 2003.This study was supported by National Institute of Mental Health Grant 40799 to R.W.M., Fellowship 13022 to K.M.S., and Training Grant 016259. The Wavelet software was provided by C. Torrence and G. Compo (available at http://paos.colorado.edu/research/wavelets/).
Correspondence should be addressed to Dr. Robert W. McCarley, Harvard Medical School/Veterans Affairs Boston Healthcare System, Psychiatry 116A, 940 Belmont Street, Brockton, MA 02301. E-mail: robert_mccarley{at}hms.harvard.edu.
Copyright © 2003 Society for Neuroscience 0270-6474/03/237407-05$15.00/0
References
Benes FM (2000) Emerging principles of altered neural circuitry in schizophrenia. Brain Res Rev 31: 251-269.[Medline]
Bleuler E (1950/1911) Dementia praecox or the group of schizophrenias. New York: International UP.
American Psychiatric Association (1994) Diagnostic and statistical manual of mental disorders, Ed 4. Washington, DC: American Psychiatric Association.
Engel AK, Fries P, Singer W (2001) Dynamic predictions: oscillations and synchrony in top-down processing. Nat Rev Neurosci 2: 704-716.[ISI][Medline]
Fletcher P, McKenna PJ, Friston KJ, Frith CD, Dolan RJ (1999) Abnormal cingulate modulation of fronto-temporal connectivity in schizophrenia. NeuroImage 9: 337-342.[ISI][Medline]
Friston KJ, Frith CD (1995) Schizophrenia: a disconnection syndrome? Clin Neurosci 3: 89-97.[ISI][Medline]
Gordon E, Williams L, Haig AR, Wright J, Meares RA (2001) Symptom profile and "gamma" processing in schizophrenia. Cogn Neuropsychiatry 6: 7-19.
Green MF, Mintz J, Salveson D, Nuechterlein KH, Breitmeyer B, Light GA, Braff DL (2003) Visual masking as a probe for abnormal gamma range activity in schizophrenia. Biol Psychiatry 53: 1113-1119.[ISI][Medline]
Grunze HC, Rainnie DG, Hasselmo ME, Barkai E, Hearn EF, McCarley RW, Greene RW (1996) NMDA-dependent modulation of CA1 local circuit inhibition. J Neurosci 16: 2034-2043.
[Abstract/Free Full Text] Haig AR, Gordon E, De Pascalis V, Meares RA, Bahramali H, Harris A (2000) Gamma activity in schizophrenia: evidence of impaired network binding? Clin Neurophysiol 111: 1461-1468.[ISI][Medline]
Herrmann CS, Mecklinger A, Pfiefer E (1999) Gamma responses and ERPs in a visual classification task. Clin Neurophysiol 110: 636-642.[ISI][Medline]
Javitt DC, Zukin SR (1991) Recent advances in the phencyclidine model of schizophrenia. Am J Psychiatry 48: 1301-1308.
Kay SR, Fiszbein A, Opler LA (1987) The positive and negative syndrome scale (PANSS) for schizophrenia. Schizophr Bull 13: 261-276.
Kissler J, Muller MM, Fehr T, Rockstroh B, Elbert T (2000) MEG gamma band activity in schizophrenia patients and healthy subjects in a mental arithmetic task and at rest. Clin Neurophysiol 111: 2079-2087.[Medline]
Kubicki M, Westin C-F, Maier SE, Frumin M, Nestor PG, Salisbury DF, Kikinis R, Jolesz FA, McCarley RW, Shenton ME (2002) Uncinate fasciculus findings in schizophrenia: a magnetic resonance diffusion tensor imaging study. Am J Psychiatry 159: 813-820.
[Abstract/Free Full Text] Kwon JS, O'Donnell BF, Wallenstein GV, Greene RW, Hirayasu Y, Nestor PG, Hasselmo ME, Potts GF, Shenton ME, McCarley RW (1999) Gamma frequency-range abnormalities to auditory stimulation in schizophrenia. Arch Gen Psychiatry 56: 1001-1005.
[Abstract/Free Full Text] Lachaux J-P, Rodriguez E, Martinerie J, Varela FJ (1999) Measuring phase synchrony in brain signals. Hum Brain Mapp 8: 194-208.[ISI][Medline]
Lewis DA, Gonzalez-Burgos G (2000) Intrinsic excitatory connections in the prefrontal cortex and the pathophysiology of schizophrenia. Brain Res Bull 52: 309-317.[ISI][Medline]
Makeig S, Bell AJ, Jung T-P, Sejnowski TJ (1996) Independent component analysis of electroencephalographic data. Adv Neural Inf Process Syst 8: 145-151.
McBain CJ, Fisahn A (2001) Interneurons unbound. Nat Rev Neurosci 2: 11-23.[ISI][Medline]
Meyer-Lindenberg A, Poline J-B, Kohn PD, Holt JS, Egan MF, Weinberger DR, Berman KF (2001) Evidence for abnormal cortical functional connectivity during working memory in schizophrenia. Am J Psychiatry 158: 1809-1817.
[Abstract/Free Full Text] Rodriguez E, George N, Lachaux J-P, Martinerie J, Renault B, Varela FJ (1999) Perception's shadow: long-distance synchronization of human brain activity. Nature 397: 430-433.[Medline]
Selemon LD, Goldman-Rakic PS (1999) The reduced neuropil hypothesis: a circuit based model of schizophrenia. Biol Psychiatry 45: 17-25.[ISI][Medline]
Tallon-Baudry C, Bertrand O (1999) Oscillatory gamma activity in humans and its role in object representation. Trends Cogn Sci 3: 151-162.[ISI][Medline]
Tallon-Baudry C, Bertrand O, Wienbruch C, Ross B, Pantev C (1997) Combined EEG and MEG recordings of visual 40 Hz responses to illusory triangles in man. NeuroReport 8: 1103-1107.[ISI][Medline]
Torrence C, Compo GP (1998) A practical guide to wavelet analysis. Bull Am Meteor Soc 79: 61-78.
Tsai G, Coyle JT (2002) Glutamatergic mechanisms in schizophrenia. Annu Rev Pharmacol Toxicol 42: 165-179.[ISI][Medline]
Varela FJ, Lachaux J-P, Rodriguez E, Martinerie J (2001) The brainweb: phase synchronization and large-scale integration. Nat Rev Neurosci 2: 229-239.[ISI][Medline]
Volk DW, Pierri JN, Fritschy J-M, Auh S, Sampson AR, Lewis DA (2002) Reciprocal alterations in pre- and postsynaptic inhibitory markers at chandelier cell inputs to pyramidal neurons in schizophrenia. Cereb Cortex 12: 1063-1070.
[Abstract/Free Full Text] Whittington M, Faulkner HJ, Doheny HC, Traub RD (2000) Neuronal fast oscillations as a target site for psychoactive drugs. Pharmacol Ther 86: 171-190.[ISI][Medline]
This article has been cited by other articles:
A. K. Roopun, M. O. Cunningham, C. Racca, K. Alter, R. D. Traub, and M. A. Whittington
Region-Specific Changes in Gamma and Beta2 Rhythms in NMDA Receptor Dysfunction Models of Schizophrenia
Schizophr Bull, September 1, 2008; 34(5): 962 - 973.
[Abstract] [Full Text] [PDF]
P. J. Uhlhaas, C. Haenschel, D. Nikolic, and W. Singer
The Role of Oscillations and Synchrony in Cortical Networks and Their Putative Relevance for the Pathophysiology of Schizophrenia
Schizophr Bull, September 1, 2008; 34(5): 927 - 943.
[Abstract] [Full Text] [PDF]
G. Gonzalez-Burgos and D. A. Lewis
GABA Neurons and the Mechanisms of Network Oscillations: Implications for Understanding Cortical Dysfunction in Schizophrenia
Schizophr Bull, September 1, 2008; 34(5): 944 - 961.
[Abstract] [Full Text] [PDF]
B. J. Roach and D. H. Mathalon
Event-Related EEG Time-Frequency Analysis: An Overview of Measures and An Analysis of Early Gamma Band Phase Locking in Schizophrenia
Schizophr Bull, September 1, 2008; 34(5): 907 - 926.
[Abstract] [Full Text] [PDF]
F. Ferrarelli, M. Massimini, M. J. Peterson, B. A. Riedner, M. Lazar, M. J. Murphy, R. Huber, M. Rosanova, A. L. Alexander, N. Kalin, et al.
Reduced Evoked Gamma Oscillations in the Frontal Cortex in Schizophrenia Patients: A TMS/EEG Study
Am J Psychiatry, August 1, 2008; 165(8): 996 - 1005.
[Abstract] [Full Text] [PDF]
M. V. Puig, M. Ushimaru, and Y. Kawaguchi
Two distinct activity patterns of fast-spiking interneurons during neocortical UP states
PNAS, June 17, 2008; 105(24): 8428 - 8433.
[Abstract] [Full Text] [PDF]
S. Hirano, Y. Hirano, T. Maekawa, C. Obayashi, N. Oribe, T. Kuroki, S. Kanba, and T. Onitsuka
Abnormal Neural Oscillatory Activity to Speech Sounds in Schizophrenia: A Magnetoencephalography Study
J. Neurosci., May 7, 2008; 28(19): 4897 - 4903.
[Abstract] [Full Text] [PDF]
C. I. Moore and R. Cao
The Hemo-Neural Hypothesis: On The Role of Blood Flow in Information Processing
J Neurophysiol, May 1, 2008; 99(5): 2035 - 2047.
[Abstract] [Full Text] [PDF]
D. Vierling-Claassen, P. Siekmeier, S. Stufflebeam, and N. Kopell
Modeling GABA Alterations in Schizophrenia: A Link Between Impaired Inhibition and Altered Gamma and Beta Range Auditory Entrainment
J Neurophysiol, May 1, 2008; 99(5): 2656 - 2671.
[Abstract] [Full Text] [PDF]
T. Hashimoto, H. H. Bazmi, K. Mirnics, Q. Wu, A. R. Sampson, and D. A. Lewis
Conserved Regional Patterns of GABA-Related Transcript Expression in the Neocortex of Subjects With Schizophrenia
Am J Psychiatry, April 1, 2008; 165(4): 479 - 489.
[Abstract] [Full Text] [PDF]
T. W. Wilson, O. O. Hernandez, R. M. Asherin, P. D. Teale, M. L. Reite, and D. C. Rojas
Cortical Gamma Generators Suggest Abnormal Auditory Circuitry in Early-Onset Psychosis
Cereb Cortex, February 1, 2008; 18(2): 371 - 378.
[Abstract] [Full Text] [PDF]
P. L. Tierney, A. M. Thierry, J. Glowinski, J. M. Deniau, and Y. Gioanni
Dopamine Modulates Temporal Dynamics of Feedforward Inhibition in Rat Prefrontal Cortex In Vivo
Cereb Cortex, January 24, 2008; (2008) bhm252v1.
[Abstract] [Full Text] [PDF]
C. Haenschel, R. A. Bittner, F. Haertling, A. Rotarska-Jagiela, K. Maurer, W. Singer, and D. E. J. Linden
Contribution of Impaired Early-Stage Visual Processing to Working Memory Dysfunction in Adolescents With Schizophrenia: A Study With Event-Related Potentials and Functional Magnetic Resonance Imaging
Arch Gen Psychiatry, November 1, 2007; 64(11): 1229 - 1240.
[Abstract] [Full Text] [PDF]
O. van der Stelt and A. Belger
Application of Electroencephalography to the Study of Cognitive and Brain Functions in Schizophrenia
Schizophr Bull, July 1, 2007; 33(4): 955 - 970.
[Abstract] [Full Text] [PDF]
T. Demiralp, C. S. Herrmann, M. E. Erdal, T. Ergenoglu, Y. H. Keskin, M. Ergen, and H. Beydagi
DRD4 and DAT1 Polymorphisms Modulate Human Gamma Band Responses
Cereb Cortex, May 1, 2007; 17(5): 1007 - 1019.
[Abstract] [Full Text] [PDF]
S. Kroner, L. S. Krimer, D. A. Lewis, and G. Barrionuevo
Dopamine Increases Inhibition in the Monkey Dorsolateral Prefrontal Cortex through Cell Type-Specific Modulation of Interneurons
Cereb Cortex, May 1, 2007; 17(5): 1020 - 1032.
[Abstract] [Full Text] [PDF]
J. M. Ford, B. J. Roach, W. O. Faustman, and D. H. Mathalon
Synch Before You Speak: Auditory Hallucinations in Schizophrenia
Am J Psychiatry, March 1, 2007; 164(3): 458 - 466.
[Abstract] [Full Text] [PDF]
W.-J. Gao
Acute Clozapine Suppresses Synchronized Pyramidal Synaptic Network Activity by Increasing Inhibition in the Ferret Prefrontal Cortex
J Neurophysiol, February 1, 2007; 97(2): 1196 - 1208.
[Abstract] [Full Text] [PDF]
L. Menzies, C. Ooi, S. Kamath, J. Suckling, P. McKenna, P. Fletcher, E. Bullmore, and C. Stephenson
Effects of {gamma}-Aminobutyric Acid-Modulating Drugs on Working Memory and Brain Function in Patients With Schizophrenia
Arch Gen Psychiatry, February 1, 2007; 64(2): 156 - 167.
[Abstract] [Full Text] [PDF]
P. D. Butler, A. Martinez, J. J. Foxe, D. Kim, V. Zemon, G. Silipo, J. Mahoney, M. Shpaner, M. Jalbrzikowski, and D. C. Javitt
Subcortical visual dysfunction in schizophrenia drives secondary cortical impairments
Brain, February 1, 2007; 130(2): 417 - 430.
[Abstract] [Full Text] [PDF]
P. J. Uhlhaas and A. L. Mishara
Perceptual Anomalies in Schizophrenia: Integrating Phenomenology and Cognitive Neuroscience
Schizophr Bull, January 1, 2007; 33(1): 142 - 156.
[Abstract] [Full Text] [PDF]
R. Y. Cho, R. O. Konecky, and C. S. Carter
Impairments in frontal cortical {gamma} synchrony and cognitive control in schizophrenia
PNAS, December 26, 2006; 103(52): 19878 - 19883.
[Abstract] [Full Text] [PDF]
A. Del Cul, S. Dehaene, and M. Leboyer
Preserved Subliminal Processing and Impaired Conscious Access in Schizophrenia
Arch Gen Psychiatry, December 1, 2006; 63(12): 1313 - 1323.
[Abstract] [Full Text] [PDF]
S. Yeap, S. P. Kelly, P. Sehatpour, E. Magno, D. C. Javitt, H. Garavan, J. H. Thakore, and J. J. Foxe
Early Visual Sensory Deficits as Endophenotypes for Schizophrenia: High-Density Electrical Mapping in Clinically Unaffected First-Degree Relatives.
Arch Gen Psychiatry, November 1, 2006; 63(11): 1180 - 1188.
[Abstract] [Full Text] [PDF]
P. D. Skosnik, G. P. Krishnan, E. E. Aydt, H. A. Kuhlenshmidt, and B. F. O'Donnell
Psychophysiological Evidence of Altered Neural Synchronization in Cannabis Use: Relationship to Schizotypy
Am J Psychiatry, October 1, 2006; 163(10): 1798 - 1805.
[Abstract] [Full Text] [PDF]
