Alpha2-adrenoceptor mediated co-release of @entity935 and XXXX from noradrenergic neurons in the cerebral cortex.

@entity4925 @entity5829 @entity935 @entity49739 @entity11719 @entity9956 @entity1767 @entity35 @entity1063 @entity16750
Previous results suggest that extracellular @entity935 (DA) in the @entity35 cerebral cortex originates from dopaminergic and noradrenergic terminals. To further clarify this issue, dialysate DA, @entity16750 ( @entity4925 ) and @entity1063 (NA) were measured both in the medial prefrontal cortex (mPFC) and in the occipital cortex (OCC), with dense and scarce dopaminergic projections, respectively. Moreover, the effect of the alpha2-adrenoceptor antagonist @entity49739 and the D2-receptor antagonist @entity1767 on extracellular DA, @entity4925 and NA was investigated. Extracellular DA and @entity4925 concentrations in the OCC were 43% and 9%, respectively, those in the mPFC. @entity1767 (0.1 mg/kg i.p.) increased DA and @entity4925 (by 35% and 150%, respectively) in the mPFC, but was ineffective in the OCC. In contrast, @entity49739 (1.5 mg/kg i.p.) increased NA, DA and @entity4925 , both in the mPFC (by approximately 50%, 60% and 130%, respectively) and the OCC (by approximately 50%, 80% and 200%, respectively). Locally perfused, the DA transporter blocker @entity11719 (10 micro m) was ineffective in either cortex, whereas @entity5829 ( @entity9956 , 100 micro m) markedly increased extracellular NA and DA in both cortices. The weak @entity1767 effect on DA efflux was not enhanced after DA- and NA-transporter blockade, whereas after @entity9956 , @entity49739 markedly increased extracellular NA, and especially DA and @entity4925 in both cortices. The results support the hypothesis that most extracellular DA in the cortex is co-released with NA from noradrenergic terminals, such co-release being primarily controlled by alpha2-adrenoceptors.
