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J Neurophysiol 93: 1598-1610, 2005. First published November 10, 2004; doi:10.1152/jn.00843.2004
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Dopamine Modulates Excitability of Basolateral Amygdala Neurons In Vitro

Sven Kröner1,3,*, J. Amiel Rosenkranz1,*, Anthony A. Grace1,2 and German Barrionuevo1,3

1Departments of Neuroscience and 2Psychiatry and Psychology, University of Pittsburgh; and 3Center for Neural Basis of Cognition, Pittsburgh, Pennsylvania

Submitted 17 August 2004; accepted in final form 3 November 2004

The amygdala plays a role in affective behaviors, which are modulated by the dopamine (DA) innervation of the basolateral amygdala complex (BLA). Although in vivo studies indicate that activation of DA receptors alters BLA neuronal activity, it is unclear whether DA exerts direct effects on BLA neurons or whether it acts via indirect effects on BLA afferents. Using whole cell patch-clamp recordings in rat brain slices, we investigated the site and mechanisms through which DA regulates the excitability of BLA neurons. Dopamine enhanced the excitability of BLA projection neurons in response to somatic current injections via a postsynaptic effect. Dopamine D1 receptor activation increased excitability and evoked firing, whereas D2 receptor activation increased input resistance. Current- and voltage-clamp experiments in projection neurons showed that D1 receptor activation enhanced excitability by modulating a 4-aminopyridine- and {alpha}-dendrotoxin-sensitive, slowly inactivating K+ current. Furthermore, DA and D1 receptor activation increased evoked firing in fast-spiking BLA interneurons. Consistent with a postsynaptic modulation of interneuron excitability, DA also increased the frequency of spontaneous inhibitory postsynaptic currents recorded in projection neurons without changing release of GABA. These data demonstrate that DA exerts direct effects on BLA projection neurons and indirect actions via modulation of interneurons that may work in concert to enhance the neuronal response to large, suprathreshold inputs, while suppressing weaker inputs.

Present address and address for reprint requests and other correspondence: S. Kröner, Dept. of Physiology, Medical University of South Carolina, 173 Ashley Ave., 403 BSB, Charleston, SC 29425 (E-mail: kroener{at}musc.edu)




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