Abstract
The recent identification of the trace amine associated receptor 1 (TAAR1) provides an opportunity to dissociate the effects of trace amines on the dopamine transporter from receptor‐mediated effects. In order to separate both effects on a physiological level, a Taar1‐deficient mouse line was generated.Taar1‐deficient mice displayed increased sensitivity to amphetamine as revealed by enhanced amphetamine‐triggered increases in locomotor activity and augmented striatal release of dopamine as compared to wild‐type animals. Under baseline conditions, locomotion as well as extracellular striatal dopamine levels were similar between Taar1 knock‐out and wild‐type mice. Electrophysiological recordings revealed an elevated spontaneous firing rate of dopaminergic neurons in the ventral tegmental area of Taar1 knock‐out mice. The endogenous TAAR1 agonist p‐tyramine specifically decreased the spike frequency of these neurons in wild‐type but not in Taar1 knock‐out mice, consistent with the prominent expression of Taar1 in the ventral tegmental area.Taken together, the data reveal TAAR1 as regulator of dopaminergic neurotransmission.
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