Quantification and pharmacological characterization of dialysate levels of noradrenaline in the striatum of freely-moving rats: release from adrenergic terminals and modulation by α2-autoreceptors

Gobert, Alain P.; Billiras, Rodolphe; Cistarelli, Laetitia; Millan, Mark J.

doi:10.1016/j.jneumeth.2004.04.040

Cited by 56 publications

(41 citation statements)

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“…DA is an intermediate in the synthesis of NA, and a brief review of the extensive literature and phylogenetic studies emphasizes the intertwined pharmacology between the two transmitters: For example, electrical stimulation of the LC elicits both NA and DA release in the cortex (Devoto et al 2005), and both DA and NA appear to be released by most NA terminals (Devoto et al 2004). The DA transporter is able to reuptake NA (Gobert et al 2004), and both DA and NA appear to be able to bind to each other's specific type of receptors (Cornil and Ball 2008;Millan et al 2000;Uhlen et al 1998). More specifically in our study, while amphetamine-type stimulants release NA more potently than DA (Rothman et al 2001), amphetamine induces both DA and NA synaptic release, and the possible Fig.…”

Section: Discussionmentioning

confidence: 49%

Amphetamine challenge decreases yohimbine binding to α2 adrenoceptors in Landrace pig brain

2012

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Section: Discussionmentioning

confidence: 49%

Amphetamine challenge decreases yohimbine binding to α2 adrenoceptors in Landrace pig brain

2012

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“…Alternatively, in a parkinsonian state, dopamine can be synthesized in nondopaminergic neurons, including serotonergic neurones (Tanaka et al, 1999;Carta et al, 2007). We have demonstrated previously that stimulation of the ␣ 1 -adrenoceptor has an excitatory effect on serotonergic neurons in the striatum and that prazosin can reduce striatal serotonin release (Lejeune et al, 1994;Rouquier et al, 1994;Gobert et al, 2004). Such an effect would probably be reflected in a similar ability of prazosin to reduce the release of dopamine synthesized in serotonergic terminals.…”

Section: Discussionmentioning

confidence: 97%

α₁-Adrenoceptors Mediate Dihydroxyphenylalanine-Induced Activity in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Lesioned Macaques

Visanji¹,

Fox²,

Johnston³

et al. 2008

J Pharmacol Exp Ther

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The mechanisms underlying actions of dihydroxyphenylalanine (L-DOPA) in Parkinson's disease remain to be fully elucidated. Noradrenaline formed from L-DOPA may stimulate ␣ 1 -adrenoceptors. We assessed the involvement of ␣ 1 -adrenoceptors in actions of L-DOPA in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned macaques. In each animal, the minimal dose of L-DOPA required to alleviate parkinsonian symptoms was defined (12.5-25 mg/kg p.o.). The effects of coadministration of the ␣ 1 -adrenoceptor antagonist prazosin ([4-(4-amino-6,7-dimethoxy-quinazolin-2-yl) piperazin-1-yl]-(2-furyl)methanone) on motor activity, parkinsonism, and dyskinesia were assessed. Antiparkinsonian benefit was accompanied by mild dyskinesia. L-DOPA also elicited hyperactivity, i.e., activity greater than that seen in normal animals. Coadministration of prazosin (0.16 -0.63 mg/kg p.o.) with L-DOPA did not significantly affect either its antiparkinsonian actions or dyskinesia. However, prazosin significantly and dose-dependently attenuated L-DOPA-induced activity, reducing it to a level equivalent to that of normal animals. More specifically, during periods of pronounced L-DOPA-induced activity, prazosin attenuated the total and duration of activity by 80 and 76%, respectively. These actions of prazosin were expressed in the absence of sedation. Although activation of ␣ 1 -adrenoceptors plays no major role in the antiparkinsonian and dyskinetic effects of L-DOPA per se, it does contribute to the induction of hyperactivity. ␣ 1 -Adrenoceptors may be involved in pathological responses to L-DOPA treatment, including the dopamine dysregulation syndrome.Since its first use in the early 1960s, dopamine replacement by treatment with the dopamine precursor dihydroxyphenylalanine (L-DOPA) has remained the mainstay of therapy for the motor symptoms of Parkinson's disease (PD) (Lang and Lozano, 1998). Although the antiparkinsonian actions of L-DOPA resulting from dopamine replacement are undisputed, it has long been suggested that L-DOPA therapy may also involve alternate neurotransmitter systems, including noradrenergic pathways (Mercuri and Bernardi, 2005). In this way, L-DOPA may combine both dopaminergic and nondopaminergic mechanisms. Such mechanisms may underlie the superior clinical profile of L-DOPA compared with selective dopamine receptor agonists (Holloway et al., 2004;Oertel et al., 2006). In addition, the nonmotor effects of L-DOPA may reflect involvement of noradrenergic mechanisms. Thus, L-DOPA treatment can result in excessively heightened mood and psychomotor activity, even to the extent of psychosis (Racette et al., 2002;Witjas et al., 2002). In addition, some patients experience hyperactivity with compulsive, repetitive, nongoal-directed motor activity (e.g., "punding," stereotypies, "hobbyism," and "walkabouts") (part of the dopamine dysregulation syndrome), which are related to but probably distinct from impulse control disorders, such as pathological gambling, excessive eating, shopping, and hypersexuality Potenza et...

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“…volume transmission) may play an important role in mediating the neurochemical actions of norepinephrine within both ventral and dorsal striatum. Despite extremely low levels of DBH immunostaining and extracellular norepinephrine in accumbens core and dorsal striatum (Gobert et al 2004), relatively high densities of a-and b-adrenergic receptors have been found in these regions (Rainbow et al 1984;Boyajian et al 1987;Fagerholm et al 2004). Activation of these receptors modulates dopaminergic, cholinergic, glutamatergic and GABAergic activity within striatal slices (Bücheler et al 2002;Dohovics et al 2003;Pisani et al 2003;Zhang and Ordway 2003); it is possible that norepinephrine diffusing from accumbens shell may have similar effects in vivo.…”

Section: Discussionmentioning

confidence: 99%

Catecholamine mapping within nucleus accumbens: differences in basal and amphetamine‐stimulated efflux of norepinephrine and dopamine in shell and core

McKittrick

Abercrombie

2006

Journal of Neurochemistry

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The nucleus accumbens is believed to play a critical role in mediating the behavioral responses to rewarding stimuli. Although most studies of the accumbens focus on dopamine, it receives afferents from many other nuclei, including noradrenergic cell groups in the brainstem. We used in vivo microdialysis to measure extracellular levels of both norepinephrine and dopamine in the accumbens shell and core. Regional analysis of shell and core and border regions demonstrated that norepinephrine was high in shell and decreased from medial shell to lateral core, where baseline levels were low or undetectable. Conversely, extracellular dopamine in core was twice the level seen in shell. Both catecholamines increased following a single injection of amphetamine (2 mg/kg, i.p.). The norepinephrine response was greater and long-lasting in shell compared with core. The maximal dopamine response was higher in core than in shell, but the duration of the effect was comparable in both regions. The distinct neurochemical characteristics of shell and core are likely to contribute to the functional heterogeneity of the two subregions. Furthermore, norepinephrine may be involved in many of the functions generally attributed to the accumbens, either directly or indirectly via modulation of extracellular dopamine.

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Quantification and pharmacological characterization of dialysate levels of noradrenaline in the striatum of freely-moving rats: release from adrenergic terminals and modulation by α2-autoreceptors

Cited by 56 publications

References 64 publications

Amphetamine challenge decreases yohimbine binding to α2 adrenoceptors in Landrace pig brain

Amphetamine challenge decreases yohimbine binding to α2 adrenoceptors in Landrace pig brain

α₁-Adrenoceptors Mediate Dihydroxyphenylalanine-Induced Activity in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Lesioned Macaques

Catecholamine mapping within nucleus accumbens: differences in basal and amphetamine‐stimulated efflux of norepinephrine and dopamine in shell and core

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Quantification and pharmacological characterization of dialysate levels of noradrenaline in the striatum of freely-moving rats: release from adrenergic terminals and modulation by α2-autoreceptors

Cited by 56 publications

References 64 publications

Amphetamine challenge decreases yohimbine binding to α2 adrenoceptors in Landrace pig brain

Amphetamine challenge decreases yohimbine binding to α2 adrenoceptors in Landrace pig brain

α1-Adrenoceptors Mediate Dihydroxyphenylalanine-Induced Activity in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Lesioned Macaques

Catecholamine mapping within nucleus accumbens: differences in basal and amphetamine‐stimulated efflux of norepinephrine and dopamine in shell and core

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α₁-Adrenoceptors Mediate Dihydroxyphenylalanine-Induced Activity in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Lesioned Macaques