Increased hemodynamic response in the hippocampus, thalamus and prefrontal cortex during abnormal sensory gating in schizophrenia

Tregellas, Jason R.; Davalos, Deana B.; Rojas, Donald C.; Waldo, Merilyne; Gibson, Linzi; Wylie, Korey P.; Du, Yiping P.; Freedman, Robert

doi:10.1016/j.schres.2006.12.033

Cited by 130 publications

(115 citation statements)

References 37 publications

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“…That is, activation in such a network should increase with increasing P50 suppression. An indirect approach to this issue used a comparison between the fMRI-BOLD response to nine click repetitions, separated by 500 ms, with that to a single click, in a group of schizophrenic patients as well as in controls (Tregellas et al, 2007). EEG P50 suppression was reduced in the patients but, contrary to expectations, the BOLD response in a network consisting of dorsolateral prefrontal cortex, hippocampus, and thalamus, was increased.…”

Section: Box 4 Human Electrophysiology As Indices Of a 'Unified Brainmentioning

confidence: 97%

How Human Electrophysiology Informs Psychopharmacology: from Bottom-up Driven Processing to Top-Down Control

Kenemans

Kähkönen

2010

Neuropsychopharmacol

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This review surveys human event-related brain potential (ERP) and event-related magnetic field (ERF) approaches to psychopharmacology and psychopathology, and the way in which they complement behavioral studies and other neuroimaging modalities. The major paradigms involving ERP/ERF are P50 suppression, loudness-dependent auditory evoked potential (LDAEP), mismatch negativity (MMN), P300, mental chronometry, inhibitory control, and conflict processing (eg, error-related negativity (ERN)). Together these paradigms cover a range of more bottom-up driven to more top-down controlled processes. A number of relationships between the major neurotransmitter systems and electrocortical mechanisms are highlighted. These include the role of dopamine in conflict processing, and perceptual processing vs motor preparation; the role of serotonin in P50 suppression, LDAEP, and MMN; glutamate/NMDA and MMN; and the role of acetylcholine in P300 generation and memory-related processes. A preliminary taxonomy for these relationships is provided, which should be helpful in attuning possible new treatments or new applications of existing treatments to various disorders.

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Section: Box 4 Human Electrophysiology As Indices Of a 'Unified Brainmentioning

confidence: 97%

How Human Electrophysiology Informs Psychopharmacology: from Bottom-up Driven Processing to Top-Down Control

Kenemans

Kähkönen

2010

Neuropsychopharmacol

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“…Indeed, there are several reports on enhanced activity of brain areas involved in the pathophysiology of schizophrenia under conditions of limited cognitive load. For example, one study found greater activation in the hippocampus, thalamus, and dorsolateral prefrontal cortex in patients with schizophrenia during the sensory gating task and in response to urban noise (Tregellas et al, 2007(Tregellas et al, , 2009, whereas another group reported on the elevated hippocampal and amygdala activity during the passive viewing of human faces (Holt et al, 2006). However, when the behavioral performance sets additional demands on these networks, activity will increase further, and such an above-physiological increase will now be accompanied by abnormally high or lost synchronization, phenomena also observed after short-term application of sufficiently high doses of PCP-like drugs (Sebban et al, 2002;Pinault, 2008).…”

Section: Mglu2/3 Receptor Agonistsmentioning

confidence: 99%

Glutamatergic (N-Methyl-d-aspartate Receptor) Hypofrontality in Schizophrenia: Too Little Juice or a Miswired Brain?

Marek

Behl²,

Bespalov³

et al. 2009

Mol Pharmacol

139

115

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Dopamine D2 receptor blockade has been an obligate mechanism of action present in all medications that effectively treat positive symptoms of schizophrenia (e.g., delusions and hallucinations) and have been approved by regulatory agencies since the 1950s. Blockade of 5-hydroxytrypatmine 2A receptors plays a contributory role in the actions of the second generation of antipsychotic drugs, the so-called atypical antipsychotics. Nevertheless, substantial unmet medical needs remain for the treatment of negative symptoms and cognitive dysfunction. Recognition that dissociative anesthetics block the N-methyl-D-aspartate (NMDA) receptor channel has inspired a search for glutamatergic therapeutic mechanisms because ketamine and phencyclidine are known to induce psychotic-like symptoms in healthy volunteers and exacerbate the symptoms of patients with schizophrenia. Current pathophysiological theories of schizophrenia emphasize that hypofunction of NMDA receptors at critical sites in local circuits modulate the function of a given brain region or control projections from one region to another (e.g., hippocampal-cortical or thalamocortical projections). The demonstration that a metabotropic glutamate 2/3 (mGlu2/3) receptor agonist prodrug decreased both positive and negative symptoms of schizophrenia raised hopes that glutamatergic mechanisms may provide therapeutic advantages. In addition to discussing the activation of mGlu2 receptors with mGlu2/3 receptor agonists or mGlu2 receptor positive allosteric modulators (PAMs), we discuss other methods that may potentially modulate circuits with hypofunctional NMDA receptors such as glycine transporter inhibitors and mGlu5 receptor PAMs. The hope is that by modulating glutamatergic neurotransmission, the dysfunctional circuitry of the schizophrenic brain (both local circuits and long-loop pathways) will be improved. Dopamine and serotonin, as opposed to emerging interest in glutamate, played a dominant role during the formative years of modern psychopharmacology when thinking about the pathophysiology and treatment of schizophrenia. Models derived from studying the behavioral effects of amphetamine and serotonergic hallucinogens were emphasized (Table 1). The seminal observations by Arvid Carlsson and his colleagues in the late early 1960s that first postulated functional dopamine receptor blockade as a necessary therapeutic action by the phenothiazine and butyrophenone structural classes set the stage for our current mechanistic understanding of all antipsychotic drugs currently used today (Carlsson and Lindqvist, 1963). The emergence of in vitro receptor binding and positron emission topography receptor occupancy studies in healthy volunteers and patients identified dopamine D2 receptor Article, publication date, and citation information can be found at

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“…P50 sensory gating is thought to reflect a complex interaction of inhibitory neurocircuits located primarily in the hippocampus, dorsolateral prefrontal cortex, and thalamus 16 . Thus, alterations in P50 sensory gating in infants may suggest altered development in these regions of the brain.…”

Section: Discussionmentioning

confidence: 99%

P50 Sensory Gating in Infants

Ross

Hunter

Groth

et al. 2013

JoVE

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Attentional deficits are common in a variety of neuropsychiatric disorders including attention deficit-hyperactivity disorder, autism, bipolar mood disorder, and schizophrenia. There has been increasing interest in the neurodevelopmental components of these attentional deficits; neurodevelopmental meaning that while the deficits become clinically prominent in childhood or adulthood, the deficits are the results of problems in brain development that begin in infancy or even prenatally. Despite this interest, there are few methods for assessing attention very early in infancy. This report focuses on one method, infant auditory P50 sensory gating.Attention has several components. One of the earliest components of attention, termed sensory gating, allows the brain to tune out repetitive, noninformative sensory information. Auditory P50 sensory gating refers to one task designed to measure sensory gating using changes in EEG. When identical auditory stimuli are presented 500 ms apart, the evoked response (change in the EEG associated with the processing of the click) to the second stimulus is generally reduced relative to the response to the first stimulus (i.e. the response is "gated"). When response to the second stimulus is not reduced, this is considered a poor sensory gating, is reflective of impaired cerebral inhibition, and is correlated with attentional deficits.Because the auditory P50 sensory gating task is passive, it is of potential utility in the study of young infants and may provide a window into the developmental time course of attentional deficits in a variety of neuropsychiatric disorders. The goal of this presentation is to describe the methodology for assessing infant auditory P50 sensory gating, a methodology adapted from those used in studies of adult populations.

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Increased hemodynamic response in the hippocampus, thalamus and prefrontal cortex during abnormal sensory gating in schizophrenia

Cited by 130 publications

References 37 publications

How Human Electrophysiology Informs Psychopharmacology: from Bottom-up Driven Processing to Top-Down Control

How Human Electrophysiology Informs Psychopharmacology: from Bottom-up Driven Processing to Top-Down Control

Glutamatergic (N-Methyl-d-aspartate Receptor) Hypofrontality in Schizophrenia: Too Little Juice or a Miswired Brain?

P50 Sensory Gating in Infants

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