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1 Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA; Center for Neural Basis of Cognition, Pittsburgh, PA, USA
2 Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA
3 Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA; Psychiatry and Psychology, University of Pittsburgh, Pittsburgh, PA, USA
* To whom correspondence should be addressed. E-mail: kroener{at}musc.edu.
The amygdala plays a role in affective behaviors, which are modulated by the dopamine (DA) innervation of the basolateral amygdala complex (BLA). While in vivo
studies indicate that activation of DA receptors alters BLA neuronal activity, it is unclear whether DA exerts direct effects upon BLA neurons, or whether it acts via indirect effects upon 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 
-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 post-synaptic currents recorded in projection neurons without changing release of GABA. These data demonstrate that DA exerts direct effects upon 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.
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