Davide Rivolta
I am a psychologist with interest in cognitive neuroscience, neuropsychology, cognitive psychology, psychiatry and psychotherapy. My main areas of research involve (i) the cognitive and neural correlates of face perception, both in normal subjects and in people with congenital prosopagnosia, and (ii) the neurophysiology of psychiatric disorders, such as schizophrenia.
I completed my Ph.D. at the Macquarie Centre for Cognitive Science (MACCS), Macquarie University, Sydney, Australia. There, I conducted behavioural and neuroimaging investigations on typical and atypical (i.e., prosopagnosia) face processing. I then worked at the Department of Neurophysiology of the Max Planck Institute for Brain Research, in Frankfurt, Germany. Here, using MEG, I investigated neural oscillations in psychiatric populations and in human pharmacological models (i.e., ketamine) of psychosis. I have been Senior lecturer in Psychology at the University of East London where I conducted research on the neurophysiological (tDCS, EEG) bases of face, body and object processing. I am currently Associate professor at the University of Bari Aldo Moro; here I focus on the neurophysiological bases of cognition.
Supervisors: Max Coltheart, Mark A Williams, Romina Palermo, Peter J Uhlhaas, Wolf Singer, Michael A Nitsche, and Michael Wibral
Address: London, England, United Kingdom
I completed my Ph.D. at the Macquarie Centre for Cognitive Science (MACCS), Macquarie University, Sydney, Australia. There, I conducted behavioural and neuroimaging investigations on typical and atypical (i.e., prosopagnosia) face processing. I then worked at the Department of Neurophysiology of the Max Planck Institute for Brain Research, in Frankfurt, Germany. Here, using MEG, I investigated neural oscillations in psychiatric populations and in human pharmacological models (i.e., ketamine) of psychosis. I have been Senior lecturer in Psychology at the University of East London where I conducted research on the neurophysiological (tDCS, EEG) bases of face, body and object processing. I am currently Associate professor at the University of Bari Aldo Moro; here I focus on the neurophysiological bases of cognition.
Supervisors: Max Coltheart, Mark A Williams, Romina Palermo, Peter J Uhlhaas, Wolf Singer, Michael A Nitsche, and Michael Wibral
Address: London, England, United Kingdom
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Papers by Davide Rivolta
(NMDA-R) has been prominently implicated in the pathophysiology
of schizophrenia (ScZ). The current study
tested the effects of ketamine, a dissociative anesthetic and
NMDA-R antagonist, on resting-state activity recorded
with magnetoencephalography (MEG) in healthy volunteers.
In a single-blind cross-over design, each participant
(n = 12) received, on 2 different sessions, a subanesthetic
dose of S-ketamine (0.006 mg/Kg) and saline injection.
MEG-data were analyzed at sensor- and source-level in the
beta (13–30 Hz) and gamma (30–90 Hz) frequency ranges.
In addition, connectivity analysis at source-level was performed
using transfer entropy (TE). Ketamine increased
gamma-power while beta-band activity was decreased.
Specifically, elevated 30–90 Hz activity was pronounced
in subcortical (thalamus and hippocampus) and cortical
(frontal and temporal cortex) regions, whilst reductions in
beta-band power were localized to the precuneus, cerebellum,
anterior cingulate, temporal and visual cortex. TE
analysis demonstrated increased information transfer in a
thalamo-cortical network after ketamine administration.
The findings are consistent with the pronounced dysregulation
of high-frequency oscillations following the inhibition
of NMDA-R in animal models of ScZ as well as with
evidence from electroencephalogram-data in ScZ-patients
and increased functional connectivity during early illness
stages. Moreover, our data highlight the potential contribution
of thalamo-cortical connectivity patterns towards
ketamine-induced neuronal dysregulation, which may be
relevant for the understanding of ScZ as a disorder of disinhibition
of neural circuits.
(NMDA-R) has been prominently implicated in the pathophysiology
of schizophrenia (ScZ). The current study
tested the effects of ketamine, a dissociative anesthetic and
NMDA-R antagonist, on resting-state activity recorded
with magnetoencephalography (MEG) in healthy volunteers.
In a single-blind cross-over design, each participant
(n = 12) received, on 2 different sessions, a subanesthetic
dose of S-ketamine (0.006 mg/Kg) and saline injection.
MEG-data were analyzed at sensor- and source-level in the
beta (13–30 Hz) and gamma (30–90 Hz) frequency ranges.
In addition, connectivity analysis at source-level was performed
using transfer entropy (TE). Ketamine increased
gamma-power while beta-band activity was decreased.
Specifically, elevated 30–90 Hz activity was pronounced
in subcortical (thalamus and hippocampus) and cortical
(frontal and temporal cortex) regions, whilst reductions in
beta-band power were localized to the precuneus, cerebellum,
anterior cingulate, temporal and visual cortex. TE
analysis demonstrated increased information transfer in a
thalamo-cortical network after ketamine administration.
The findings are consistent with the pronounced dysregulation
of high-frequency oscillations following the inhibition
of NMDA-R in animal models of ScZ as well as with
evidence from electroencephalogram-data in ScZ-patients
and increased functional connectivity during early illness
stages. Moreover, our data highlight the potential contribution
of thalamo-cortical connectivity patterns towards
ketamine-induced neuronal dysregulation, which may be
relevant for the understanding of ScZ as a disorder of disinhibition
of neural circuits.