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

Landau, Anne M.; Doudet, Doris J.; Jakobsen, Steen

doi:10.1007/s00213-011-2632-6

Cited by 23 publications

(18 citation statements)

References 56 publications

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“…When the BP ND declined significantly in response to the amphetamine challenge, the Inhibition plot yielded the V ND value that must be known to calculate the BP ND of radiotracers with displaceable accumulation in all parts of the brain. Similar findings were reported in recent PET studies in pigs, where [ 11 C]-yohimbine binding was significantly displaced by competition with endogenous transmitters, as shown by a decline of the V T in response to acute amphetamine treatment, 6 although the binding potential was not calculated because the magnitude of V ND varied among the few subjects studied.…”

Section: Discussionsupporting

confidence: 88%

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Quantification of [¹¹C]yohimbine Binding to α₂ Adrenoceptors in Rat Brain in vivo

Phan

Landau

Wong

et al. 2015

J Cereb Blood Flow Metab

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We quantified the binding potentials (BPND) of [11C]yohimbine binding in rat brain to alpha-2 adrenoceptors to evaluate [11C]yohimbine as an in vivo marker of noradrenergic neurotransmission and to examine its sensitivity to the level of noradrenaline. Dual [11C]yohimbine dynamic positron emission tomography (PET) recordings were applied to five Sprague Dawley rats at baseline, followed by acute amphetamine administration (2 mg/kg) to induce elevation of the endogenous level of noradrenaline. The volume of distribution (VT) of [11C]yohimbine was obtained using Logan plot with arterial plasma input. Because alpha-2 adrenoceptors are distributed throughout the brain, the estimation of the BPND is complicated by the absence of an anatomic region of no displaceable binding. We used the Inhibition plot to acquire the reference volume, VND, from which we calculated the BPND. Acute pharmacological challenge with amphetamine induced a significant decline of [11C]yohimbine BPND of ~38% in all volumes of interest. The BPND was greatest in the thalamus and striatum, followed in descending order by, frontal cortex, pons, and cerebellum. The experimental data demonstrate that [11C]yohimbine binding is sensitive to a challenge known to increase the extracellular level of noradrenaline, which can benefit future PET investigations of pathologic conditions related to disrupted noradrenergic neurotransmission.

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Section: Discussionsupporting

confidence: 88%

“…However, partial volume effects cannot fully explain the [ 11 C]yohimbine binding in striatum, because recent in vivo studies in pigs with much larger brains show [ 11 C]-yohimbine binding in caudate nucleus and putamen that is similar to the binding in cortical regions. 5, 6 …”

Section: Discussionmentioning

confidence: 99%

Quantification of [¹¹C]yohimbine Binding to α₂ Adrenoceptors in Rat Brain in vivo

Phan

Landau

Wong

et al. 2015

J Cereb Blood Flow Metab

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“…For verifying if the metabolic and hemodynamic effects of octopamine in the liver are mediated by adrenergic receptors, we performed experiments using several antagonists: (a) yohimbine (α 1 and α 2 -antagonist), (b) prazosin (mainly α 1 -antagonist) [28–30] and (c) propranolol (non-specific β-antagonist) [31,32]. Livers from fed rats were used in all experiments.…”

Section: Resultsmentioning

confidence: 99%

Adrenergic Metabolic and Hemodynamic Effects of Octopamine in the Liver

Oliveira

Paula

Comar

et al. 2013

IJMS

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The fruit extracts of Citrus aurantium (bitter orange) are traditionally used as weight-loss products and as appetite suppressants. A component of these extracts is octopamine, which is an adrenergic agent. Weight-loss and adrenergic actions are always related to metabolic changes and this work was designed to investigate a possible action of octopamine on liver metabolism. The isolated perfused rat liver was used to measure catabolic and anabolic pathways and hemodynamics. Octopamine increased glycogenolysis, glycolysis, oxygen uptake, gluconeogenesis and the portal perfusion pressure. Octopamine also accelerated the oxidation of exogenous fatty acids (octanoate and oleate), as revealed by the increase in 14CO2 production derived from 14C labeled precursors. The changes in glycogenolysis, oxygen uptake and perfusion pressure were almost completely abolished by α1-adrenergic antagonists. The same changes were partly sensitive to the β-adrenergic antagonist propranolol. It can be concluded that octopamine accelerates both catabolic and anabolic processes in the liver via adrenergic stimulation. Acceleration of oxygen uptake under substrate-free perfusion conditions also means acceleration of the oxidation of endogenous fatty acids, which are derived from lipolysis. All these effects are compatible with an overall stimulating effect of octopamine on metabolism, which is compatible with its reported weight-loss effects in experimental animals.

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“…Despite some antihypertensive properties, it generally increases blood pressure at rest, which is thought to be mediated via central antagonism of a2 adrenergic receptors (Biaggioni et al, 1994). Our earlier studies have found that in tracer concentrations, yohimbine exhibits high selectivity for a2 sites in vivo in pigs (Jakobsen et al, 2006) which is displaceable by amphetamine challenge (Landau et al, 2012a). Central a2 NA receptors are widely expressed pre-synaptically primarily on NA cell bodies and dendrites in the locus coeruleus (LC).…”

Section: Introductionmentioning

confidence: 99%

Decreased in vivo α2 adrenoceptor binding in the Flinders Sensitive Line rat model of depression

et al. 2015

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Depression is a debilitating heterogeneous disorder and the underlying mechanisms remain elusive. Alterations in monoaminergic neurotransmission, including noradrenergic, have been implicated in the etiology of depression. Although depression is difficult to model in animals, the availability of animal models with face, predictive and construct validity permits more in-depth investigations resulting in a greater understanding of the disease. We investigated the role of noradrenaline (NA) and α2 adrenoceptors in vivo in a genetic model of depression, the Flinders Sensitive Line (FSL) rat. We determined baseline differences in NA receptor volume of distribution to α2 adrenoceptors in FSL, in comparison with two routinely used controls, Flinders Resistant Line (FRL) and Sprague-Dawley (SD) rats using positron emission tomography (PET) imaging and the carbon-11 labeled radioligand yohimbine. We demonstrate a 42-47% reduction in the binding of the tracer in the cortex, striatum, cerebellum, thalamus and pons of FSL rats compared to the two control groups. Our results suggest that the behavioral deficits expressed in the FSL depression model are associated with functional over-activity of the NA system.

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

Cited by 23 publications

References 56 publications

Quantification of [¹¹C]yohimbine Binding to α₂ Adrenoceptors in Rat Brain in vivo

Quantification of [¹¹C]yohimbine Binding to α₂ Adrenoceptors in Rat Brain in vivo

Adrenergic Metabolic and Hemodynamic Effects of Octopamine in the Liver

Decreased in vivo α2 adrenoceptor binding in the Flinders Sensitive Line rat model of depression

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

Cited by 23 publications

References 56 publications

Quantification of [11C]yohimbine Binding to α2 Adrenoceptors in Rat Brain in vivo

Quantification of [11C]yohimbine Binding to α2 Adrenoceptors in Rat Brain in vivo

Adrenergic Metabolic and Hemodynamic Effects of Octopamine in the Liver

Decreased in vivo α2 adrenoceptor binding in the Flinders Sensitive Line rat model of depression

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Quantification of [¹¹C]yohimbine Binding to α₂ Adrenoceptors in Rat Brain in vivo

Quantification of [¹¹C]yohimbine Binding to α₂ Adrenoceptors in Rat Brain in vivo