Acute ketamine challenge increases resting state prefrontal-hippocampal connectivity in both humans and rats

Grimm, O.; Gass, Natalia; Weber‐Fahr, Wolfgang; Sartorius, Alexander; Schenker, Esther; Spedding, Michael; Risterucci, Céline; Schweiger, Janina I.; Böhringer, Andreas; Zang, Zhenxiang; Tost, Heike; Schwarz, Adam J.; Meyer‐Lindenberg, Andreas

doi:10.1007/s00213-015-4022-y

Cited by 84 publications

(75 citation statements)

References 85 publications

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“…[26] Immediately (minutes to hours) after administration of ketamine, the amplitude of BOLD signal fluctuations[29] and FC[23] was observed to increase , although the amplitude of task-evoked responses was reduced. [39] Chronic administration (greater than 24 hours) of ketamine focally reduced FC in selected RSNs.…”

Section: Discussionmentioning

confidence: 99%

N-methyl-D-aspartate receptor encephalitis mediates loss of intrinsic activity measured by functional MRI

et al. 2016

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Spontaneous brain activity is required for the development and maintenance of normal brain function. Many disease processes disrupt the organization of intrinsic brain activity but few pervasively reduce the amplitude of resting state blood oxygen level dependent (BOLD) fMRI fluctuations. We report the case of a female with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis, longitudinally studied during the course of her illness in order to determine the contribution of NMDAR signaling to spontaneous brain activity. Resting state BOLD fMRI was measured at the height of her illness and 18 weeks following discharge from hospital. Conventional resting state networks were defined using established methods. Correlation and covariance matrices were calculated by extracting the BOLD time-series from regions of interest and calculating either the correlation or covariance quantity. The intrinsic activity was compared between visits, and to expected activity from 45 similarly-aged healthy individuals. Near the height of the illness, the patient exhibited profound loss of consciousness, high-amplitude slowing of the electroencephalogram, and a severe reduction in the amplitude of spontaneous BOLD fMRI fluctuations. The patient’s neurological status and measures of intrinsic activity improved following treatment. We conclude that NMDAR-mediated signaling plays a critical role in the mechanisms that give rise to organized spontaneous brain activity. Loss of intrinsic activity is associated with profound disruptions of consciousness and cognition.

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Section: Discussionmentioning

confidence: 99%

N-methyl-D-aspartate receptor encephalitis mediates loss of intrinsic activity measured by functional MRI

et al. 2016

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“…In healthy subjects, functional connectivity between the rACC and mPFC increased acutely (95) and decreased 24 hours after ketamine infusion (96). Furthermore, using PET imaging methods, ketamine associated with increased glucose metabolism in the dorsal ACC (dACC) (97), altered glucose metabolism in PFC regions (97–99) in MDD, and increased glucose metabolism in the dACC and putamen in BD patients (100).…”

Section: Ketamine and Functional Neural Circuitry In Depressionmentioning

confidence: 99%

Glutamate and Gamma-Aminobutyric Acid Systems in the Pathophysiology of Major Depression and Antidepressant Response to Ketamine

Lener

Niciu

Ballard

et al. 2017

Biological Psychiatry

382

214

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In patients with major depressive disorder (MDD) or bipolar disorder (BD), abnormalities in excitatory and/or inhibitory neurotransmission and neuronal plasticity may lead to aberrant functional connectivity patterns within large brain networks. Network dysfunction in association with altered brain levels of glutamate (Glu) and gamma-aminobutyric acid (GABA) have been identified in both animal and human studies of depression. In addition, evidence of an antidepressant response to subanesthetic dose ketamine has led to a collection of studies that have examined neurochemical (e.g. glutamatergic and GABA-ergic) and functional imaging correlates associated with such an effect. Results from these studies suggest that an antidepressant response in association with ketamine occurs, in part, by reversing these neurochemical/physiological disturbances. Future studies in depression will require a combination of neuroimaging approaches from which more biologically homogeneous subgroups can be identified, particularly with respect to treatment response biomarkers of glutamatergic modulation.

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“…Another study by Grimm et al (2015) investigated ketamine-induced changes in functional connectivity specifically between the dlPFC and hippocampus. They found that acute ketamine administration increased dlPFC-hippocampus connectivity in both healthy human subjects and in rats.…”

Section: Pharmacological Imaging and The Behavioral Effects Of Ketaminementioning

confidence: 99%

Ketamine and pharmacological imaging: use of functional magnetic resonance imaging to evaluate mechanisms of action

Maltbie¹,

Kaundinya²,

Howell

2017

Behavioural Pharmacology

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Ketamine has been used as a pharmacological model for schizophrenia, as sub-anesthetic infusions have been shown to produce temporary schizophrenia-like symptoms in healthy humans. More recently, ketamine has emerged as a potential treatment for multiple psychiatric disorders, including treatment-resistant depression and suicidal ideation. However, the mechanisms underlying both the psychotomimetic and therapeutic effects of ketamine remain poorly understood. This review provides an overview of what is known of the neural mechanisms underlying the effects of ketamine and details what functional magnetic resonance imaging studies have revealed at a systems level focused on brain circuitry. Multiple analytic approaches show that ketamine produces robust and consistent effects at the whole-brain level. These effects are highly conserved across human and nonhuman primates, validating the use of nonhuman primate models for further investigations with ketamine. Regional analysis of brain functional connectivity suggests that the therapeutic potential of ketamine may be derived from a strengthening of executive control circuitry, making it an intriguing candidate for the treatment of drug abuse. There are still important questions about the mechanism of action and therapeutic potential of ketamine that can be addressed using appropriate functional neuroimaging techniques.

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Acute ketamine challenge increases resting state prefrontal-hippocampal connectivity in both humans and rats

Cited by 84 publications

References 85 publications

N-methyl-D-aspartate receptor encephalitis mediates loss of intrinsic activity measured by functional MRI

N-methyl-D-aspartate receptor encephalitis mediates loss of intrinsic activity measured by functional MRI

Glutamate and Gamma-Aminobutyric Acid Systems in the Pathophysiology of Major Depression and Antidepressant Response to Ketamine

Ketamine and pharmacological imaging: use of functional magnetic resonance imaging to evaluate mechanisms of action

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