In rodents, acute pramipexole treatment decreases the mean firing rate and burst firing activity (possibly reflecting tonic and phasic firing, respectively) of dopaminergic neurons in the ventral tegmental area by acting on D2-autoreceptors and inhibiting presynaptic dopamine release (figure 3A). However, chronic pramipexole administration normalises tonic firing and the number of bursts per minute, but the number of neurons exhibiting burst activity following chronic pramipexole treatment is lower than after acute administration, suggesting lower phasic activity. This normalisation is related to desen- sitisation of D2-autoreceptors. After chronic pramipexole treatment, the firing rate of noradrenergic locus coeruleus activity also normalised, but burst activity remained low.28 By contrast, chronic pramipexole treatment increased the spontaneous firing rate and burst activity of serotonergic dorsal raphe neurons.28