Inhibition of the cortex using transcranial magnetic stimulation in psychiatric populations: current and future directions

Radhu, Natasha; Ravindran, Lakshmi N.; Levinson, Andrea; Daskalakis, Zafiris J.

doi:10.1503/jpn.120003

Cited by 24 publications

(25 citation statements)

References 121 publications

(146 reference statements)

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“…The ICF originates from excitatory postsynaptic potentials (PSPs) mainly mediated by glutamatargic NMDA receptors [37]. Their latency is about 10 ms, consistent with the time course of intracortical facilitation [38]. Pharmacological studies support such observation, as NMDA receptor antagonists (i.e.…”

Section: Discussionmentioning

confidence: 87%

Association of anxiety with intracortical inhibition and descending pain modulation in chronic myofascial pain syndrome

et al. 2014

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BackgroundThis study aimed to answer three questions related to chronic myofascial pain syndrome (MPS): 1) Is the motor cortex excitability, as assessed by transcranial magnetic stimulation parameters (TMS), related to state-trait anxiety? 2) Does anxiety modulate corticospinal excitability changes after evoked pain by Quantitative Sensory Testing (QST)? 3) Does the state-trait anxiety predict the response to pain evoked by QST if simultaneously receiving a heterotopic stimulus [Conditional Pain Modulation (CPM)]? We included females with chronic MPS (n = 47) and healthy controls (n = 11), aged 19 to 65 years. Motor cortex excitability was assessed by TMS, and anxiety was assessed based on the State-Trait Anxiety Inventory. The disability related to pain (DRP) was assessed by the Profile of Chronic Pain scale for the Brazilian population (B:PCP:S), and the psychophysical pain measurements were measured by the QST and CPM.ResultsIn patients, trait-anxiety was positively correlated to intracortical facilitation (ICF) at baseline and after QST evoked pain (β = 0.05 and β = 0.04, respectively) and negatively correlated to the cortical silent period (CSP) (β = -1.17 and β = -1.23, respectively) (P <0.05 for all comparisons). After QST evoked pain, the DRP was positively correlated to ICF (β = 0.02) (P < 0.05). Pain scores during CPM were positively correlated with trait-anxiety when it was concurrently with high DRP (β = 0.39; P = 0.02). Controls’ cortical excitability remained unchanged after QST.ConclusionsThese findings suggest that, in chronic MPS, the imbalance between excitatory and inhibitory descending systems of the corticospinal tract is associated with higher trait-anxiety concurrent with higher DRP.

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Section: Discussionmentioning

confidence: 87%

Association of anxiety with intracortical inhibition and descending pain modulation in chronic myofascial pain syndrome

et al. 2014

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“…It is instructive to contrast rTMS with medication treatments for depression because it is delivered at a very different level of biologic organization, applied to defined cortical neuroanatomic targets. Interestingly, in stimulated cortex, rTMS has effects on GABAergic neurotransmission and cortical excitability that are analogous to those of ketamine, with the effects of stimulation spreading rapidly to alter activity in multiple limbic structures, including the bilateral middle prefrontal cortex (PFC), right orbital frontal cortex, left hippocampus, and dorsomedial nucleus of the thalamus …”

Section: Antidepressant Treatments May Exert Similar Actions At Diffementioning

confidence: 99%

“…12 It is instructive to contrast rTMS with medication treatments for depression because it is delivered at a very different level of biologic organization, applied to defined cortical neuroanatomic targets. Interestingly, in stimulated cortex, rTMS has effects on GABAergic neurotransmission and cortical excitability that are analogous to those of ketamine, 13 with the effects of stimulation spreading rapidly to alter activity in multiple limbic structures, including the bilateral middle prefrontal cortex (PFC), right orbital frontal cortex, left hippocampus, and dorsomedial nucleus of the thalamus. 14 Although the MOA of antidepressant treatments has not been fully elucidated, these varied treatments all lead to increased neuroplasticity, 1,15 and recent theories have suggested that enhanced plasticity represents a common MOA of aminergic and glutamatergic antidepressants, as well as of neuromodulatory treatments such as rTMS.…”

Section: Antidepressant Treatments May Exert Similar Actions At Diffementioning

confidence: 99%

Rhythms and blues: modulation of oscillatory synchrony and the mechanism of action of antidepressant treatments

Leuchter

Hunter

Krantz

et al. 2015

Annals of the New York Academy of Sciences

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Treatments for major depressive disorder (MDD) act at different hierarchical levels of biological complexity, ranging from the individual synapse to the brain as a whole. Theories of antidepressant medication action traditionally have focused on the level of cell-to-cell interaction and synaptic neurotransmission. However, recent evidence suggests that modulation of synchronized electrical activity in neuronal networks is a common effect of antidepressant treatments, including not only medications, but also neuromodulatory treatments such as repetitive transcranial magnetic stimulation. Synchronization of oscillatory network activity in particular frequency bands has been proposed to underlie neurodevelopmental and learning processes, and also may be important in the mechanism of action of antidepressant treatments. Here, we review current research on the relationship between neuroplasticity and oscillatory synchrony, which suggests that oscillatory synchrony may help mediate neuroplastic changes related to neurodevelopment, learning, and memory, as well as medication and neuromodulatory treatment for MDD. We hypothesize that medication and neuromodulation treatments may have related effects on the rate and pattern of neuronal firing, and that these effects underlie antidepressant efficacy. Elucidating the mechanisms through which oscillatory synchrony may be related to neuroplasticity could lead to enhanced treatment strategies for MDD.

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“…The AIS is innervated by a specialized subtype of GABAergic interneuron, the chandelier cell, which is thought to be one of the interneuron types that are dysfunctional in SCZ cerebral cortex as evidenced by molecular alterations both on the pre- and postsynaptic site of the AIS (Pierri et al, 1999; Volk et al, 2002; Woo et al, 1998). Importantly, these postmortem studies, together with related work in preclinical model systems, paved the way for clinical trials and novel treatment approaches aimed at alleviating GABAergic deficits at the AIS and other key nodes of the cortical inhibitory system (Geffen et al, 2012; Lett et al, 2013; Lewis et al, 2008; Radhu et al, 2012; Rowland et al, 2013; Rudolph and Mohler, 2014; Stan and Lewis, 2012). For example to test the concept that reduced GABA signalling from chandelier cells to pyramidal neurons contribute to working memory dysfunction via parvalbumin-positive GABA neurons, a benzodiazepine-like compound, MK-0777, a selective agonist of GABA A α-2 and α-3 subunits, was tested in clinical trials.…”

Section: Gabaergic Dysfunction In Schizophrenia – a Brief Chronologymentioning

confidence: 99%

Transcriptional regulation of GAD1 GABA synthesis gene in the prefrontal cortex of subjects with schizophrenia

Mitchell

Jiang

Peter

et al. 2015

Schizophrenia Research

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Expression of GAD1 GABA synthesis enzyme is highly regulated by neuronal activity and reaches mature levels in prefrontal cortex not before adolescence. A significant portion of cases diagnosed with schizophrenia show deficits in GAD1 RNA and protein levels in multiple areas of adult cerebral cortex, possibly reflecting molecular or cellular defects in subtypes of GABAergic interneurons essential for network synchronization and cognition. Here, we review 20 years of progress towards a better understanding of disease-related regulation of GAD1 gene expression. For example, deficits in cortical GAD1 RNA in some cases of schizophrenia are associated with changes in the epigenetic architecture of the promoter, affecting DNA methylation patterns and nucleosomal histone modifications. These localized chromatin defects at the 5′end of GAD1 are superimposed by disordered locus-specific chromosomal conformations, including weakening of long-range promoter-enhancer loopings and physical disconnection of GAD1 core promoter sequences from cis-regulatory elements positioned 50 kilobases further upstream. Studies on the 3-dimensional architecture of the GAD1 locus in neurons, including developmentally regulated higher order chromatin compromised by the disease process, together with exploration of locus-specific epigenetic interventions in animal models, could pave the way for future treatments of psychosis and schizophrenia.

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Inhibition of the cortex using transcranial magnetic stimulation in psychiatric populations: current and future directions

Cited by 24 publications

References 121 publications

Association of anxiety with intracortical inhibition and descending pain modulation in chronic myofascial pain syndrome

Association of anxiety with intracortical inhibition and descending pain modulation in chronic myofascial pain syndrome

Rhythms and blues: modulation of oscillatory synchrony and the mechanism of action of antidepressant treatments

Transcriptional regulation of GAD1 GABA synthesis gene in the prefrontal cortex of subjects with schizophrenia

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