Opposite effects of midazolam and β-carboline-3-carboxylate ethyl ester on the release of dopamine from rat nucleus accumbens measured by in vivo mudialysis
References (43)
- et al.
mudialysis - theory and application
Prog. Neurobiol.
(1990) - et al.
Dopamine in the basal ganglia and benzodiazepine-induced sedation
Neuropharmacology
(1988) - et al.
Tail-pinch stress increases extracellular DOPAC levels (as measured by in vivo voltammetry) in rat nucleus accumbens but not frontal cortex: antagonism by diazepam and zolpidem
Brain Res.
(1987) - et al.
Stress-induced increase in 3,4-dihydroxyphenyl-acetic acid (DOPAC) levels in the cerebral cortex and in nucleus accumbens: reversal by diazepam
Life Sci.
(1978) - et al.
The anxiogenic action of benzodiazepine antagonists
Neuropharmacology
(1982) - et al.
Tonic inhibition of striatal dopamine transmission: effects of benzodiazepine and GABAA receptor antagonists on extracellular dopamine levels
Brain Res.
(1992) - et al.
Chronic administration of diazepam downregulates adenosine receptors in the rat brain
Pharmacol. Biochem. Behav.
(1988) - et al.
Release of dopamine is reduced by diazepam more in the nucleus accumbens that in the caudate nucleus of conscious rats
Neuropharmacology
(1991) - et al.
The anxiogenic β-carboline FG-7142 increases in vivo and in vivo tyrosine hydroxylation in the prefrontal cortex
Brain Res.
(1989) - et al.
Intracerebral mudialysis. I. Experimental studies of diffusion kinetics
J. Pharmacol. Meth.
(1989)
Benzodiazepine inhibition of adenosine uptake is not prevented by benzodiazepine antagonists
Eur. J. Pharmacol.
Inhibition of adenosine accumulation by a CNS benzodiazepine antagonist (Ro 15-1788) and a peripheral benzodiazepine receptor ligandd (Ro 05-4864)
Neurosci. Lett.
Intrinsic and antagonistic effects of beta-carboline FG-7142 on behavioral and EEG actions of benzodiazepines and pentobarbital in cats
Eur. J. Pharmacol.
Proconflict effect of benzodiazepine inverse agonists and other inhibitors of GABA function
Eur. J. Pharmacol.
Benzodiazepine interaction with adenosine systems explains some anomalies in GABA hypothesis
Trends Pharmacol. Sci.
Inhibition of adenosine uptake into rat brain synaptosomes by prostaglandins, benzodiazepines and other centrally active compounds
Gen. Pharmacol.
Differential modulation of striatal dopamine release by intranigral injection of gamma-aminobutyric acid (GABA), dynorphin A and substance P
Eur. J. Pharmacol.
The role of GABA receptors in the control of nigrostriatal dopaminergic neurons: dual probe mudialysis study in awake rats
Eur. J. Pharmacol.
3.7-Dimethyl-1-propargylxanthine: a potent and selective in vivo antagonist of adenosine analogues
Life Sci.
Intranigral GABAergic drugs effects on striatal dopamine activity
Pharmacol. Biochem. Behav.
Discriminative and aversive properties of beta-carboline-3-carboxylic acid ethyl ester, a benzodiazepine receptor inverse agonist, in rhesus monkeys
Life Sci.
Cited by (54)
Hooked on benzodiazepines: GABA<inf>A</inf> receptor subtypes and addiction
2011, Trends in NeurosciencesCitation Excerpt :Indeed, subcutaneous acute or chronic (twice a day for 14 days) injections of midazolam decreased extracellular DA concentrations in the nucleus accumbens (NAc) (as measured 40 min after the injection). Similar results were obtained in rats when midazolam [52] or flurazepam [53] was locally injected into the NAc. However, in this latter case, because the drug is restricted to the NAc, GABAARs of VTA cells are not potentiated, which could explain this result.
Intra-VTA adenosine A<inf>1</inf> receptor activation blocks morphine stimulation of motor behavior and cortical and limbic Fos immunoreactivity
2009, European Journal of PharmacologyBiological substrates of reward and aversion: A nucleus accumbens activity hypothesis
2009, NeuropharmacologyCitation Excerpt :While on the surface this finding might appear to invalidate our working hypothesis, electrophysiological evidence suggests that co-activation of D1 and D2 receptors on NAc neurons can, under some conditions, cause a reduction in their membrane excitability that is not seen in response to either agonist alone (O'Donnell and Grace, 1996). In addition, more work is needed to study the behavioral effects of intra-NAc microinfusions of GABA agonists; historically, this work has been hindered by poor solubility of benzodiazepines – which are known to be addictive (Griffiths and Ator, 1980) despite their tendency to decrease dopamine function in the NAc (Wood, 1982; Finlay et al., 1992: Murai et al., 1994) – and the relatively small number of researchers who use brain microinjection procedures together with models of reward. Still other ways of testing our hypothesis would be to study the effects of manipulations in brain areas downstream of D2 receptor-containing MSNs.
Abuse and dependence liability of benzodiazepine-type drugs: GABA<inf>A</inf> receptor modulation and beyond
2008, Pharmacology Biochemistry and BehaviorPentobarbital inhibits l-DOPA-induced dopamine increases in the rat striatum: An in vivo microdialysis study
2006, Brain Research Bulletin