In vivo pharmacological profile of S 38093, a novel histamine H3 receptor inverse agonist.

S 38093, a novel histamine H3 receptor inverse agonist, was tested in a series of neurochemical and behavioral paradigms designed to evaluate its procognitive and arousal properties. In intracerebral microdialysis studies performed in rats, S 38093 dose-dependently increased histamine extracellular levels in the prefrontal cortex and facilitated cholinergic transmission in the prefrontal cortex and hippocampus of rats after acute and chronic administration (10mg/kg i.p.

Quetiapine anxiolytic-like effect in the Vogel conflict test is serotonin dependent.

There is growing evidence to show that atypical antipsychotic quetiapine might exert an anxiolytic effect in patients. Nevertheless, the mechanism underlying this effect has not yet been fully explored. Like other anxiolytic drugs, quetiapine exhibits partial agonistic activity toward serotonergic 1A (5HT1A) receptors.

Antipsychotic efficacy: relationship to optimal D2-receptor occupancy.

Clinically important differences exist between antipsychotic agents and formulations in terms of safety and tolerability. Features of the biochemical interaction between the antipsychotic and the D2-receptor may underlie these differences. This article reviews current information on the relationship between antipsychotic receptor occupancy and clinical response.

The atypical antipsychotic quetiapine increases both noradrenaline and dopamine release in the rat prefrontal cortex.

Quetiapine is a novel atypical antipsychotic drug with multi-receptorial affinity. Using in vivo microdialysis, we investigated if quetiapine modulates extracellular noradrenaline and dopamine in brain areas generally believed to be involved in the pathophysiology of schizophrenia and in the action of antipsychotic drugs. Quetiapine (5, 10 and 20 mg/kg, i.

Mirtazapine-induced corelease of dopamine and noradrenaline from noradrenergic neurons in the medial prefrontal and occipital cortex.

The 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 alpha(2)-adrenoceptors. Because mirtazapine inhibits alpha(2)-adrenoceptors, the possibility that it might corelease dopamine and noradrenaline was investigated.

Alpha2-adrenoceptor mediated co-release of dopamine and noradrenaline from noradrenergic neurons in the cerebral cortex.

Previous 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 alpha2-adrenoceptor antagonist RS 79948 and the D2-receptor antagonist haloperidol on extracellular DA, DOPAC and NA was investigated.

Origin of extracellular dopamine from dopamine and noradrenaline neurons in the medial prefrontal and occipital cortex.

Our recent studies suggest that extracellular dopamine (DA) in the cerebral cortex not only originates from dopaminergic terminals but is also coreleased with noradrenaline (NA) from noradrenergic terminals [Devoto et al. (2001) Mol Psychiatry 6:657-664]. To further clarify this issue, the concentrations of extracellular DA, its deaminated metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), and NA were compared by microdialysis in the medial prefrontal cortex (mPFC), an area densely innervated by NA and DA neurons, and in the occipital cortex (OCC), equally innervated by NA but receiving scarce DA projections.

Co-release of noradrenaline and dopamine from noradrenergic neurons in the cerebral cortex induced by clozapine, the prototype atypical antipsychotic.

Rationale: Clozapine has been shown to increase extracellular dopamine (DA) and noradrenaline (NA) in the medial prefrontal cortex (mPFC). A recent study of ours suggested that extracellular DA in the PFC originates not only from dopaminergic but also from noradrenergic terminals, its release being controlled by alpha(2)-adrenoceptors.

Objectives: Since clozapine binds to alpha(2)-adrenoceptors, the possibility that it might co-release DA and NA was studied.

Delta(9)-tetrahydrocannabinol decreases extracellular GABA and increases extracellular glutamate and dopamine levels in the rat prefrontal cortex: an in vivo microdialysis study.

Cannabinoid modulation of prefrontal cortex and hippocampus neuronal functioning has been correlated to the disruptive action of marijuana on memory tasks. This study investigates the effects of delta(9)-tetrahydrocannabinol (delta(9)-THC) on dopamine, glutamate and GABA levels in vivo by brain microdialysis in the prefrontal cortex. Delta(9)-THC (1 mg/kg, i.

Co-release of noradrenaline and dopamine in the prefrontal cortex after acute morphine and during morphine withdrawal.

Rationale: Acute morphine and abstinence from chronic morphine have been shown to increase and to decrease extracellular dopamine (DA) in the nucleus accumbens, respectively. In contrast, extracellular DA in the prefrontal cortex (PFC) is not modified by acute morphine and is markedly increased during abstinence syndrome.

Objectives: We investigated whether the peculiar behaviour of PFC DA might depend on the fact that extracellular DA originates not only from DA but, mainly, noradrenaline (NA) terminals.

Chronic treatment with imipramine or mirtazapine antagonizes stress- and FG7142-induced increase in cortical norepinephrine output in freely moving rats.

The effect of repeated administration of imipramine or mirtazapine, two antidepressant drugs with different mechanisms of action, was studied on the stress-induced increase in the extracellular concentration of norepinephrine in the prefrontal cortex of freely moving rats. Exposure to footshock in control rats induced a marked increase in extracellular norepinephrine concentrations in the prefrontal cortex (+120%). Long-term administration with imipramine or mirtazapine (10 mg/kg, i.