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Learned helplessness decreases [3H]imipramine binding in rat cortex.

A D Sherman, F Petty

    Journal of Affective Disorders
    |February 1, 1984
    PubMed
    Summary
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    Learned helplessness in rats, an animal model of depression, showed decreased [3H]imipramine binding in the frontal neocortex. This suggests specific serotonin transporter changes in depression.

    Area of Science:

    • Neuroscience
    • Psychiatry
    • Pharmacology

    Background:

    • Learned helplessness is a behavioral model for depression.
    • Serotonin transporter (SERT) binding is a target for antidepressant drugs.
    • Previous studies suggest alterations in SERT in depression.

    Purpose of the Study:

    • To investigate changes in [3H]imipramine binding to the serotonin transporter (SERT) in the frontal neocortex of rats exhibiting learned helplessness.
    • To determine if these changes are specific to certain brain regions or related to affinity versus density of the transporter.

    Main Methods:

    • Rats were subjected to learned helplessness paradigms.
    • Radioligand binding assays using [3H]imipramine were performed on brain tissue (frontal neocortex, septum, hippocampus).

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  • Analysis focused on maximal binding (Bmax) and dissociation constant (Kd) to assess receptor density and affinity, respectively.

    • Main Results:

    • A significant decrease in maximal [3H]imipramine binding was observed in the frontal neocortex of rats with learned helplessness.
    • No significant changes in the affinity (Kd) of [3H]imipramine for the binding site were detected in the frontal neocortex.
    • No alterations in [3H]imipramine binding were found in the septum or hippocampus.

    Conclusions:

    • Learned helplessness is associated with a reduction in the density of serotonin transporters (SERT) in the rat frontal neocortex.
    • These findings in an animal model of depression mirror alterations observed in human depression and suicide.
    • The results support the role of frontal cortical SERT changes in the pathophysiology of depression.