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Effects of restraint and haloperidol on sensory gating in the midbrain of awake rats.

Effects of restraint and haloperidol on sensory gating in the midbrain of awake rats. Research Abstract Details 

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  • Effects of restraint and haloperidol on sensory gating in the midbrain of awake rats. Abstract Text:

    k k anstromK K Anstrom,h c cromwellH C Cromwell,d j woodwardD J Woodward,

    Deficits in sensory processing have been reported to be associated with an array of neuropsychiatric disorders including schizophrenia. Auditory sensory gating paradigms have been routinely used to test the integrity of inhibitory circuits hypothesized to filter sensory information. Abnormal dopaminergic neurotransmission has been implicated in the expression of schizophrenic symptoms. The aim of this study was to determine if inhibitory gating in response to paired auditory stimuli would occur in putative dopaminergic and non-dopaminergic midbrain neurons. A further goal of this study was to determine if restraint, a classic model of stress known to increase extracellular dopamine levels, and systemic haloperidol injections affected inhibitory mechanisms involved in sensory gating. Neural activity in the rat midbrain was recorded across paired auditory stimuli (first auditory stimulus (S1) and second auditory stimulus (S2)) under resting conditions, during restraint and after systemic haloperidol injections. Under resting conditions, a subset of putative GABA neurons showed fast, gated, short latency responses while putative dopamine neurons showed long, slow responses that were inhibitory and ungated. During restraint, gated responses in putative GABAergic neurons were decreased (increased S2/S1 or ratio of test to conditioning (T/C)) by reducing the response amplitude to S1. Systemic haloperidol decreased the T/C ratio by preferentially increasing response amplitude to S1. The results from this study suggest that individual neurons encode discrete components of the auditory sensory gating paradigm, that phasic midbrain GABAergic responses to S1 may trigger subsequent inhibitory filtering processes, and that these GABAergic responses are sensitive to restraint and systemic haloperidol.

    Effects of restraint and haloperidol on sensory gating in the midbrain of awake rats. Publishing Authors By Initials

    kk anstromKK Anstrom,hc cromwellHC Cromwell,dj woodwardDJ Woodward,

    For similar organic chemicals: carboxylic acids: acids, acyclic: butyric acids: aminobutyric acids: gamma-aminobutyric acid research abstracts see: organic chemicals: carboxylic acids: acids, acyclic: butyric acids: aminobutyric acids: gamma-aminobutyric acid research

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    MEDLINE DATE:

    Effects of restraint and haloperidol on sensory gating in the midbrain of awake rats. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Neuroscience

    VOLUME: 146

    Page Numbers: 515-24

    Journal Abbreviation:

    ISSN: 0306-4522

    DAY: 23

    MONTH: 03

    YEAR: 2007

    Effects of restraint and haloperidol on sensory gating in the midbrain of awake rats. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 7605074

    Effects of restraint and haloperidol on sensory gating in the midbrain of awake rats. Keywords Mesh Terms:

    KEYWORDS: gamma-Aminobutyric Acid

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Effects of restraint and haloperidol on sensory gating in the midbrain of awake rats. Information

    Substance Name: Tyrosine 3-Monooxygenase

    Registry Number: EC 1.14.16.2

    Grant and Affiliation Information for Effects of restraint and haloperidol on sensory gating in the midbrain of awake rats.

    AFFILIATION: Department of Physiology and Pharmacology, Wake Forest University Baptist Medical Center, Medical Center Boulevard, Winston-Salem, NC 27157, USA. kanstrom@wfubmc.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NINDS

    GRANT: NS19608

    ACRONYM: NS

    MEDLINETA: Neuroscience

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