Behavioral and pharmacological modulation of ventral tegmental dendritic dopamine release

Abstract

The mesocorticolimbic dopamine (DA) system is thought to comprise part of a neural substrate participating in behavioral reinforcement. While much emphasis has been placed on mesolimbic terminal field activity, the existence of somatodendritic DA release has also been established. In the present study, the release of endogenous DA from the ventral tegmental DA cell body region of freely moving rats was measured, using in vivo chronoamperometry after presentation of several environmental stimuli. While presentation of a 9-s moderately intense light stimulus did not significantly modify DA release, palatable food presentation (FD), 3 min of social interaction (SI) with another male rat and a 3-min tail-pinch (TP) produced an increase in electrochemical signal, suggesting an increase in somatodendritic DA release. Mean peak signal increases (calibrated in nM DA concentration) were 104, 135 and 161 nM after FD, SI and TP stimulus, respectively. After daily presentation of all four stimuli, one of four DA active drugs was given s.c. When compared with preinjection baseline, apomorphine (APO) caused a decrease while nomifensine (NOMI), cocaine (COC) and haloperidol (HALO) caused an increase in electrochemical signal. When TP was given 30 min after drug injection, APO, NOMI and COC suppressed the TP-induced signal increase compared with the predrug response. HALO, on the other hand, did not alter TP-induced DA release. These data support the hypothesis that the cells of origin of the mesocorticolimbic system release dendritic DA after physiologically relevant stimuli.