Neuroscience Letters 383 (2005) 63–67 Striatal dopamine during sensorial stimulations: A[ 18 F]FDOPA PET study in human and cats Wadad Hassoun a , Stephane Thobois b,c , Nathalie Ginovart c , Luis Garcia-Larrea c , Marion Le Cavorsin a , Stephane Guillouet c , Frederic Bonnefoi c , Nicolas Costes c , Frank Lavenne c , Jean Pierre Martin d , Emmanuel Broussolle b , Vincent Leviel a,∗ a PhysiologieIntegrativeCellulaireetMol´ eculaire,CNRSUMR5123,8rueR.Dubois,LaDoua,43B d du11nov1943,69622Villeurbanne,France b Hˆ opitalNeurologiqueP.WertheimerandINSERMU534,59B d Pinel,69003Lyon,France c CERMEP,59B d Pinel,69003Lyon,France d HopitalDesgenettes,DptIRM,108BdPinel,69003Lyon,France Received 29 October 2004; received in revised form 25 February 2005; accepted 28 March 2005 Abstract Sensory stimulations of the forelimb in cats are known to increase dopamine release in the ipsilateral striatum and to decrease it in the homologous contralateral structure. Using positron emission tomography in both humans and cats, the present study shows that such sensory stimulations greatly reduce [ 18 F]FDOPA accumulation ipsilateral to the stimulation (by 40.4% and 26.4% in the human caudate and putamen, respectively, and by 33.3% in the cat striatum). This decrease in striatal [ 18 F]FDOPA uptake suggests a reduced DA storage resulting from the increased amine release. No change was observed in the contralateral striatum in neither human or cat suggesting, in contrast, that [ 18 F]FDOPA accumulation is not facilitated by decreased DA release. These results support the hypothesis that sensory stimulations activate a non-synaptic mode of dopamine release. © 2005 Elsevier Ireland Ltd. All rights reserved. Keywords: Basal ganglia; Dopamine; Dopamine synthesis; Positron emission tomography; [ 18 F]FDOPA It has been demonstrated that sensory stimulations of the forepaw in cats induce a long-lasting increase in dopamine (DA) release in the ipsilateral Caudate–Putamen complex. The opposite effect was observed in the contralateral struc- tures [6,21,22]. These stimulus-induced alterations in DA re- lease were originally measured as the efflux of [ 3 H]DA during a local superfusion with [ 3 H]tyrosine (the metabolic precur- sor of DA) through a push pull canula acutely implanted in the cat striatum. Although the physiological significance of this effect is still not fully understood, its biochemical mechanism was demonstrated to be mediated through a thalamo-cortico- striatal loop regulating DA in striatal terminals through local glutamate (GLU) afferents [1,20]. Indeed, local GLU afferents are well known to modu- late DA release. This was extensively studied and referenced ∗ Corresponding author. Tel.: +33 4 72 91 34 45; fax: +33 4 72 91 34 61. E-mailaddress: leviel@lyon.inserm.fr (V. Leviel). in several reports [1,6,8,12,18–20]. A recent study using positron emission tomography (PET) and [ 11 C]raclopride, a DA D2-receptor antagonist, was undertaken to reveal this phenomenon in human. This study was paralleled in cat as a reference model. It was observed that sensory stimulations of the forelimb did not change striatal [ 11 C]raclopride bind- ing in neither species [25]. The lack of post-synaptic effect of stimulation-induced DA overflow suggested that sensory stimulations may activate a tonic rather than phasic mode of DA release. These two different modes of DA release have been firstly proposed [9,12] and were also directly observed in vivo [24]. Specifically, phasic DA release is spike-dependent, occurs intrasynaptically, at high concentrations and is rapidly inactivated by reuptake. In contrast, tonic DA release is spike- independent, occurs extrasynaptically, at low concentrations and is regulated by corticostriatal glutamatergic afferents. An effect of forelimb stimulations on tonic rather than phasic DA release would involve too small changes in endogenous DA 0304-3940/$ – see front matter © 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.neulet.2005.03.067