Effect of dopamine receptor stimulation on voltage-dependent fast-inactivating Na+ currents in medial prefrontal cortex (mPFC) pyramidal neurons in adult rats
TL;DRAbstract
Impaired working memory is a common feature of neuropsychiatric disorders. It is dependent on control of the medial prefrontal cortex (mPFC) neurons by dopamine. The purpose of this study was to test the effects of a D1/5-type dopamine receptor agonist (SKF 38393, 10 microM) on the membrane potential and on voltage-dependent fast-inactivating Na+ currents in mPFC pyramidal neurons obtained from adult (9-week-old) rats. Treatment of the pyramidal neurons with SKF 38393 did not affect the membrane potential recorded with the perforated-patch method. When recordings were performed in cellattached configuration, the application of SKF 38393 did not change the Na+ current amplitude and shifted the currentvoltage relationship of the Na+ currents towards hyperpolarisation, thus resulting in an increase of the current amplitudes in response to suprathreshold depolarisations. Pretreatment of the cells with a D1/5 receptor antagonist (SCH 23390, 10 microM) abolished the effect of the D1/5-type r
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Impaired working memory is a common feature of neuropsychiatric disorders. It is dependent on control of the medial prefrontal cortex (mPFC) neurons by dopamine. The purpose of this study was to test the effects of a D1/5-type dopamine receptor agonist (SKF 38393, 10 microM) on the membrane potential and on voltage-dependent fast-inactivating Na+ currents in mPFC pyramidal neurons obtained from adult (9-week-old) rats. Treatment of the pyramidal neurons with SKF 38393 did not affect the membrane potential recorded with the perforated-patch method. When recordings were performed in cellattached configuration, the application of SKF 38393 did not change the Na+ current amplitude and shifted the currentvoltage relationship of the Na+ currents towards hyperpolarisation, thus resulting in an increase of the current amplitudes in response to suprathreshold depolarisations. Pretreatment of the cells with a D1/5 receptor antagonist (SCH 23390, 10 microM) abolished the effect of the D1/5-type r
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