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Alpha2-adrenoceptor mediated co-release of dopamine and noradrenaline from noradrenergic neurons in the cerebral cortex
No full textPrevious results suggest that extracellular dopamine (DA) in
the rat cerebral cortex originates from dopaminergic and
noradrenergic terminals. To further clarify this issue, dialysate
DA, dihydroxyphenylacetic acid (DOPAC) and noradrenaline
(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 a2-adrenoceptor antagonist RS 79948 and the
D2-receptor antagonist haloperidol on extracellular DA, DOPAC
and NA was investigated. Extracellular DA and DOPAC
concentrations in the OCC were 43% and 9%, respectively,
those in the mPFC. Haloperidol (0.1 mg/kg i.p.) increased DA
and DOPAC (by 35% and 150%, respectively) in the mPFC,
but was ineffective in the OCC. In contrast, RS 79948
(1.5 mg/kg i.p.) increased NA, DA and DOPAC, 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
GBR 12909 (10 lM) was ineffective in either cortex, whereas
desipramine (DMI, 100 lM) markedly increased extracellular
NA and DA in both cortices. The weak haloperidol effect on
DA efflux was not enhanced after DA- and NA-transporter
blockade, whereas after DMI, RS 79948 markedly increased
extracellular NA, and especially DA and DOPAC 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 a2-adrenoceptors
Recettori della dopamina del tipo DA2 : implicazioni fisiologiche e cliniche in cardiologia
No full textExtraneuronal noradrenaline in the prefrontal cortex of morphine-dependent rats : tolerance and withdrawl mechanism
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No full textMirtazapine-induced corelease of dopamine and noradrenaline from noradrenergic neurons in the medial prefrontal and occipital cortex
No full textThe novel antidepressant mirtazapine has been shown to increase extracellular noradrenaline and dopamine in the medial prefrontal
cortex. Our previous studies indicate that extracellular dopamine in the cerebral cortex originates largely from noradrenergic terminals, such
release being controlled by a2-adrenoceptors. Because mirtazapine inhibits a2-adrenoceptors, the possibility that it might corelease dopamine
and noradrenaline was investigated. By means of microdialysis, the effect of mirtazapine on extracellular dopamine, 3,4-dihydroxyphenylacetic
acid (DOPAC) and noradrenaline in the medial prefrontal cortex, densely innervated by dopaminergic and noradrenergic neurons, and
in the occipital cortex, receiving equal noradrenergic but scarce dopaminergic projections, was compared. Basal extracellular concentration of
noradrenaline was similar in both cortices, while dopamine in the occipital cortex was only about 50% lower than in the medial prefrontal
cortex, reflecting noradrenergic rather than dopaminergic projections. The intraperitoneal (i.p.) administration of mirtazapine (5 and 10 mg/
kg) increased extracellular dopamine, DOPAC and noradrenaline to approximately the same extent in both cortices, an effect totally
suppressed by the a2-adrenoceptors agonist clonidine (0.15 mg/kg, i.p.). To exclude the possibility that mirtazapine-induced increase in
dopamine might result from reduced dopamine removal from extracellular space, noradrenaline and dopamine uptake mechanisms were
blocked by perfusing 100 AM desipramine into either cortex. The combined i.p. administration of mirtazapine (5 mg/kg) and the local
perfusion of desipramine produced an additional increase in extracellular dopamine, DOPAC and noradrenaline in the medial prefrontal
cortex and occipital cortex compared with the increase produced by either drug given alone. The results suggest that mirtazapine by inhibiting
a2-adrenoceptors produces a corelease of noradrenaline and dopamine from noradrenergic terminals in the cerebral cortex.
D 2004 Elsevier B.V. All rights reserved
Alterazioni del flusso ematico e riduzione della riserva di vasodilatazione in donne sane in postmenopausa
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