Dopamine inhibits GABA(A) currents in ventral tegmental area dopamine neurons via activation of presynaptic G-protein coupled inwardly-rectifying potassium channels

Neuroscience
Avner Michaeli, Rami Yaka

Abstract

Dopamine (DA) neurons in the ventral tegmental area (VTA) constitute the origin of major dopaminergic neural pathways associated with essential functions including reward, motivation and cognition. Hence, regulation of VTA DA neurons' excitability is of important significance. Like other neurons, the activity level of VTA DA neurons is considerably determined by excitatory and inhibitory synaptic inputs. Here we show that DA itself, the most available modulator in the VTA, causes an inhibition of GABA receptor type A (GABA(A)R)-mediated evoked-IPSC (eIPSC) recorded from rat VTA DA neurons. The DA-induced inhibition was accomplished by activation of DA receptors, known to inhibit adenylyl cyclase activity (D2-like receptors), and was absent when these receptors were blocked. Moreover, blocking of either GABA receptor type B (GABA(B)R) or G-protein coupled inwardly-rectifying potassium (GIRK) channels was also found to effectively prevent the DA-induced inhibition of GABA(A)R eIPSC. In addition, we found that DA changes the values of both paired-pulse ratio (PPR) and coefficient of variation (CV) of GABA(A)R eIPSC amplitude, similar to the changes obtained by lowering the extracellular calcium concentration. Taken together, we pr...Continue Reading

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