Blood sampling methodology is crucial for precise measurement of plasma catecholamines concentrations in mice

Grouzmann, Eric; Cavadas, Cláudia; Grand, Daniela; Moratel, Martine; Aubert, Jean‐François; Brunner, Hans R.; Mazzolai, Lucia

doi:10.1007/s00424-003-1140-x

Cited by 65 publications

(54 citation statements)

References 20 publications

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“…Supernatants were then filtered through 0.45 m Ultrafree-MC centrifugal filter units (Millipore Corporation, Billerica, MA) and stored at Ϫ70°C. Catecholamine measurements were performed by HPLC with amperometric detection similar to that described previously (Grouzmann et al, 2003). Acidified tissues extracts (1 ml) were spiked with 40,000 ng of DHBA as internal standard to assess recovery.…”

Section: Methodsmentioning

confidence: 99%

Absence and Rescue of Morphine Withdrawal in GIRK/Kir3 Knock-out Mice

Cruz¹,

Berton²,

Sollini³

et al. 2008

J. Neurosci.

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Although morphine induces both analgesia and dependence through -opioid receptors (MORs), the respective contributions of the intracellular effectors engaged by MORs remain unknown. To examine the contribution of G-protein-gated inwardly rectifying K ϩ (GIRK, Kir3) channels to morphine dependence and analgesia, we quantified naloxone-precipitated withdrawal behavior and morphine analgesia using GIRK knock-out ( Ϫ/Ϫ ) mice. The morphine withdrawal syndrome was strongly attenuated, whereas morphine analgesia was mostly preserved in mice lacking both GIRK2 and GIRK3 (GIRK2/3 Ϫ/Ϫ mice). In acute slices containing the locus ceruleus (LC) from GIRK2/3 Ϫ/Ϫ mice, the increase in spontaneous firing typically associated with morphine withdrawal was absent. Moreover, although morphine elicited normal presynaptic inhibition in the LC, postsynaptic GIRK currents were completely abolished in GIRK2/3 Ϫ/Ϫ mice. Altogether, these data suggested that morphine-evoked postsynaptic inhibition of the LC was required for the induction of dependence. Consistent with this hypothesis, morphine withdrawal behavior was rescued in GIRK2/3 Ϫ/Ϫ mice by ablation of adrenergic fibers using the neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine. Our data suggest that inhibition of adrenergic tone is required for the induction of dependence, and that channels containing GIRK2 and GIRK3 serve as an inhibitory gate.

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Section: Methodsmentioning

confidence: 99%

Absence and Rescue of Morphine Withdrawal in GIRK/Kir3 Knock-out Mice

Cruz¹,

Berton²,

Sollini³

et al. 2008

J. Neurosci.

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“…Blood plasma was collected from the retro‐orbital venous plexus under short isoflurane inhalation (2% in O 2 )20 and stored at −80 °C until BNP, catecholamine, and cortisol concentrations were determined. Plasma BNP levels were measured using a commercially available kit from Sigma‐Aldrich (RAB0386, St. Louis, MO).…”

Section: Determination Of Plasma Bnp Epinephrine Norepinephrine Anmentioning

confidence: 99%

Stroke‐induced chronic systolic dysfunction driven by sympathetic overactivity

Bieber

Werner

Tanai

et al. 2017

Annals of Neurology

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ObjectiveCardiac diseases are established risk factors for ischemic stroke incidence and severity. Conversely, there is increasing evidence that brain ischemia can cause cardiac dysfunction. The mechanisms underlying this neurogenic heart disease are incompletely understood. Although it is established that ischemic stroke is associated with cardiac arrhythmias, myocardial damage, elevated cardiac enzymes, and plasma catecholamines in the acute phase, nothing is known about the delayed consequences of ischemic stroke on cardiovascular function.MethodsTo determine the long‐term cardiac consequences of a focal cerebral ischemia, we subjected young and aged mice to a 30‐minute transient middle cerebral artery occlusion and analyzed cardiac function by serial transthoracic echocardiography and hemodynamic measurements up to week 8 after surgery. Finally, animals were treated with metoprolol to evaluate a pharmacologic treatment option to prevent the development of heart failure.ResultsFocal cerebral ischemia induced a long‐term cardiac dysfunction with a reduction in left ventricular ejection fraction and an increase in left ventricular volumes; this development was associated with higher peripheral sympathetic activity. Metoprolol treatment prevented the development of chronic cardiac dysfunction by decelerating extracellular cardiac remodeling and inhibiting sympathetic signaling relevant to chronic autonomic dysfunction.InterpretationFocal cerebral ischemia in mice leads to the development of chronic systolic dysfunction driven by increased sympathetic activity. If these results can be confirmed in a clinical setting, treating physicians should be attentive to clinical signs of heart failure in every patient after ischemic stroke. Therapeutically, the successful β‐blockade with metoprolol in mice could also have future clinical implications. Ann Neurol 2017;82:729–743

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“…Resting epinephrine concentrations in human and mouse plasma are reportedly below 1 nM. In response to acute stress, epinephrine concentrations may increase to 25 nM (27,28). To determine a minimal dose of epinephrine that induces BAD phosphorylation and protects from apoptosis, we tested a range of epinephrine concentrations in LNCaP cells.…”

Section: Antiapoptotic Effect Of Epinephrine Partially Depends On Andmentioning

confidence: 99%

Epinephrine Protects Cancer Cells from Apoptosis via Activation of cAMP-dependent Protein Kinase and BAD Phosphorylation

Sastry

Karpova

Prokopovich

et al. 2007

Journal of Biological Chemistry

174

146

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The stress hormone epinephrine is known to elicit multiple systemic effects that include changes in cardiovascular parameters and immune responses. However, information about its direct action on cancer cells is limited. Here we provide evidence that epinephrine reduces sensitivity of cancer cells to apoptosis through interaction with ␤ 2 -adrenergic receptors. The antiapoptotic mechanism of epinephrine primarily involves phosphorylation and inactivation of the proapoptotic protein BAD by cAMP-dependent protein kinase. Moreover, BAD phosphorylation was observed at epinephrine concentrations found after acute and chronic psychosocial stress. Antiapoptotic signaling by epinephrine could be one of the mechanisms by which stress promotes tumorigenesis and decreases the efficacy of anti-cancer therapies.Epinephrine levels are sharply increased in response to acute stress and can be continuously elevated during persistent stress and depression (1, 2). Sustained increases of epinephrine were implicated in pathogenesis of stress-related immunosuppression proposed as the primary mechanism by which stress and depression may increase tumor incidence and promote metastatic growth (2, 3). However, several reports have questioned whether immunosuppression alone is sufficient to explain stress-induced tumor growth, and some studies have found no correlation between stress and cancer (2, 4). Thus, more information about the mechanisms by which stress hormones affect tumors is necessary to resolve the controversy over the connection between stress and cancer. One potential mechanism may involve direct effects of epinephrine on cancer cells.Cancer cell lines of various origins, including prostate tumors, express ␤ 2 -adrenergic receptors (␤ 2 -ARs) 4 that bind epinephrine and norepinephrine (5-7). ␤ 2 -ARs belong to superfamily A of seven-transmembrane G protein-coupled receptors (GPCRs) (8). Epinephrine binding leads to activation of GTPase and dissociation of ␣ and ␤␥ subunits of heterotrimeric G proteins. Depending on the cell context, this may trigger multiple signaling pathways, including the Ras/extracellular signal-regulated kinase, NFB, and cAMP-dependent protein kinase (PKA) pathways, which regulate diverse cellular responses, such as proliferation, differentiation, secretion, or apoptosis (9).Since resistance to apoptosis has been implicated in cancer pathogenesis (10), we decided to analyze the effects of the ␤ 2 -AR agonist epinephrine on apoptosis in prostate cancer cells. In this paper, we demonstrate that epinephrine reduces sensitivity of prostate cancer cells to apoptosis via ␤ 2 -AR/PKA signaling that triggers BAD phosphorylation at S112. This antiapoptotic mechanism operates in the prostate cancer cell lines LNCaP and C4-2 and in the breast cancer cell line MDA-MB231. Our findings suggest that stress may contribute to cancer etiology and therapeutic resistance by decreasing sensitivity of cancer cells to apoptosis. EXPERIMENTAL PROCEDURESCell Lines and Transfection-LNCaP and C4-2 cells were a gift from Leland C...

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Blood sampling methodology is crucial for precise measurement of plasma catecholamines concentrations in mice

Cited by 65 publications

References 20 publications

Absence and Rescue of Morphine Withdrawal in GIRK/Kir3 Knock-out Mice

Absence and Rescue of Morphine Withdrawal in GIRK/Kir3 Knock-out Mice

Stroke‐induced chronic systolic dysfunction driven by sympathetic overactivity

Epinephrine Protects Cancer Cells from Apoptosis via Activation of cAMP-dependent Protein Kinase and BAD Phosphorylation

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