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Dopamine Induces a Slow Afterdepolarization in Lateral Amygdala Neurons

¹Department of Physiology, Kanazawa Medical University, Ishikawa; and ²Department of Integrative Brain Science, Kyoto University Graduate School of Medicine, Kyoto, Japan

Submitted 26 February 2007; accepted in final form 1 June 2007

The amygdala and dopaminergic innervation thereunto are considered to cooperatively regulate emotional states and behaviors. The present experiments examined effects of dopamine on lateral amygdala (LA) neuron excitability by whole cell recordings. Bath application of dopamine induced slow afterdepolarization (sADP). This sADP lasted for >5 s, and its magnitude varied in a concentration-dependent manner. Co-application of the D1 receptor antagonist SKF83566 reduced its amplitude. The D1 receptor agonist SKF38393, applied alone, induced sADP of a smaller amplitude. Induction of the full sADP required 5-HT₂ and noradrenalin ₁ receptor activation as well. D2 receptor activation or blockade did not affect sADP induction. The calcium channel blocker cadmium or intracellular calcium chelator bis-(o-aminophenoxy)-N,N,N',N' tetraacetic acid (BAPTA) blocked induction of the sADP, which was suggested to be triggered by calcium influx. Under voltage clamp, membrane conductance decreased at the peak of sADP current (I_sADP). I_sADP was suppressed by cesium included in pipettes. The I-V curve of the net I_sADP was shifted as the external concentration of potassium was raised, and the reversal potential was identical to that of potassium, suggesting that dopamine decreases potassium conductance to induce the sADP. The present sADP may serve as a positive-feedback regulator of excitability in LA neurons.

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