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Catecholamines released from cerebral cortex in the cat; decrease during sensory stimulation

T A Reader, J De Champlain, H Jasper

    Brain Research
    |July 23, 1976
    PubMed
    Summary
    This summary is machine-generated.

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    This study investigated catecholamine (CA) release in the cat cortex. Sensory stimulation significantly reduced norepinephrine (NE) and dopamine (DA) release, suggesting acetylcholine (ACh) may regulate CA release.

    Area of Science:

    • Neuroscience
    • Neurochemistry

    Background:

    • Catecholamines (CA) like norepinephrine (NE) and dopamine (DA) play crucial roles in the cerebral cortex.
    • Understanding the regulation of CA release is vital for comprehending cortical function.

    Purpose of the Study:

    • To determine the functional role of catecholamine (CA) nerve terminals in the cerebral cortex.
    • To measure the release of endogenous NE and DA from the visual and somatosensory cortex of cats under various conditions.

    Main Methods:

    • Utilized a sensitive radiometric enzymatic assay involving catechol-O-methyltransferase (COMT) and a [3H]-methyl donor to quantify CA release.
    • Measured CA concentrations in superfusates from feline visual and somatosensory cortex.
    • Employed intermittent sensory stimulation (visual and somatic) and drug perfusion (nicotine, atropine) to investigate regulatory mechanisms.

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    Main Results:

    • Basal release rates for NE and DA were measured in the visual cortex (NE: 20.09 pg/min/sq.cm; DA: 34.01 pg/min/sq.cm).
    • Intermittent visual stimulation significantly reduced NE release by ~42% and DA release by ~64% in the visual cortex.
    • Sensory stimulation non-specifically decreased CA release in both visual and somatosensory cortical areas.
    • Perfusion with nicotine or atropine markedly increased CA release.

    Conclusions:

    • Sensory stimulation leads to a significant reduction in catecholamine release in the cerebral cortex.
    • Acetylcholine (ACh) is proposed to regulate CA release at presynaptic CA terminals in the cortex, similar to its role in the periphery.
    • The observed effects of nicotine and atropine support the hypothesis of ACh-mediated regulation of CA release.