			Home About us Contact

Adrenergic System (adrenergic + system)

Distribution by Scientific Domains

Medical Sciences	40%
Life Sciences	40%

Selected Abstracts

An abnormal gene expression of the ,-adrenergic system contributes to the pathogenesis of cardiomyopathy in cirrhotic rats,

HEPATOLOGY, Issue 6 2008
Giulio Ceolotto
Decreased cardiac contractility and ,-adrenergic responsiveness have been observed in cirrhotic cardiomyopathy, but their molecular mechanisms remain unclear. To study ,-adrenergic,stimulated contractility and ,-adrenergic gene expression patterns, 20 Wistar Kyoto rats were treated with carbon tetrachloride to induce cirrhosis and 20 rats were used as controls. Left ventricular contractility was recorded in electrically driven isolated hearts perfused at constant flow with isoproterenol (10,10 to 10,6 M). A cardiac gene expression profile was obtained using a microarray for the myocyte adrenergic pathway. The cardiac contractility maximal response to isoproterenol was significantly reduced in cirrhotic rats in comparison to control rats, whereas the half-maximal effective concentration was not different. In cirrhotic rats, cardiac gene expression analysis showed a significant overexpression of G protein alpha,inhibiting subunit 2 (G,i2), cyclic nucleotide phosphodiesterase (PDE2a), regulator of G-protein signaling 2 (RGS2), and down-expression of adenylate cyclase (Adcy3). These results indicate that overexpression of G,i2, PDE2a, and RGS2 down-regulates the ,-adrenergic signaling pathway, thus contributing to the pathogenesis of cirrhotic cardiomyopathy. (HEPATOLOGY 2008;48:1913-1923.) [source]

Translation of striatal-enriched protein tyrosine phosphatase (STEP) after ,1-adrenergic receptor stimulation

JOURNAL OF NEUROCHEMISTRY, Issue 2 2007
Yaer Hu
Abstract The ,-adrenergic system is implicated in long-term synaptic plasticity in the CNS, a process that requires protein synthesis. To identify proteins that are translated in response to ,-adrenergic receptor stimulation and the pathways that regulate this process, we investigated the effects of isoproterenol on the translation of striatal-enriched protein tyrosine phosphatase (STEP) in both cortico-striatal slices and primary neuronal cultures. Isoproterenol stimulation induced a rapid dose-dependent increase in STEP expression. Anisomycin blocked the increase in STEP expression while actinomycin D had no effect, suggesting a translation-dependent mechanism. Isoproterenol-induced STEP translation required activation of ,1-receptors. Application of the MAPK/ERK kinase (MEK) inhibitor SL327 blocked both isoproterenol-induced activation of pERK and subsequent STEP translation. Inhibitors of PI3K (LY294002) or mTOR (rapamycin) also completely blocked STEP translation. These results suggest that co-activation of both the ERK and PI3K-Akt-mTOR pathways are required for STEP translation. As one of the substrates of STEP includes ERK itself, these results suggest that STEP is translated upon ,-adrenergic activation as part of a negative feedback mechanism. [source]

Morphological Characteristics of C1 and C2 Adrenergic Neurone Groups in Marmoset Monkey Brainstem by using Antibody against Phenylethanolamine-N-methyltransferase

ANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 6 2002
Y.-G. Jeong
Summary This work describes a mapping study of phenylethanolamine-N-methyltransferase (PNMT) immunoreactive neurones and fibres in the medulla oblongata of the marmoset monkey, Callithrix jacchus. Two groups of PNMT-immunoreactive neurones were found in the marmoset monkey medulla oblongata: a ventrolateral (C1 group) and a dorsomedial PNMT-immunoreactive cells group (C2 group). The PNMT-immunoreactive cells in the ventrolateral group C1 were found to be located around the lateral reticular nucleus. The PNMT-immunoreactive somata within the ventrolateral medulla are round to oval, and mostly multipolar with branched processes. In the dorsomedial group C2, PNMT-immunoreactive cell bodies appeared near the obex. The majority of the dorsomedial PNMT-immunoreactive neurones were observed in the nucleus tractus solitarius; although some were present in the dorsal motor nucleus of the vagus. The PNMT-immunoreactive somata in the dorsomedial medulla were small and round or ovoid. These results provide information upon the adrenergic system in the medulla oblongata of a species that presents a useful model of a small primate brain, the marmoset monkey. [source]

Trance and Shamanic Cure on the South American Continent: Psychopharmacological and Neurobiological Interpretations

ANTHROPOLOGY OF CONSCIOUSNESS, Issue 1 2010
FRANCOIS BLANC
ABSTRACT This article examines the neurobiological basis of the healing power attributed to shamanic practices in the Andes and Brazil in light of the pharmacology of neurotransmitters and the new technological explorations of brain functioning. The psychotropic plants used in shamanic psychiatric cures interfere selectively with the intrinsic neuromediators of the brain. Mainly they may alter: (1) the neuroendocrine functioning through the adrenergic system by controlling stressful conditions, (2) the dopaminergic system in incentive learning and emotions incorporation, (3) the serotoninergic system in modulating behaviors, and mood, and (4) basic functions implied in anxiety or depression. PET scans and functional magnetic resonance imaging studies of hypnotic trance and altered states of consciousness may provide a useful model for the neurophysiological phenomena of shamanic drum-and-dance trance. The reorganization of cortical areas and the direct interconnections between the prefrontal cortex and the dopaminergic reward centers in the limbic system are of particular significance for human social judgment and symbolic processing. Those centers,including the hypothalamus and the amygdala (associated with psychosomatic equilibrium, memory, and emotion) are enhanced. This arousal may be amplified in order to induce a cathartic crisis,the shamanic trance. It is suggested that through this holistic approach the shaman empirically interferes in neurobiological dysfunctions. [source]

RESEARCH PAPER: The antihyperalgesic effect of levetiracetam in an inflammatory model of pain in rats: mechanism of action

BRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2010
A Micov
BACKGROUND AND PURPOSE Levetiracetam, a novel antiepileptic drug, has recently been shown to have antinociceptive effects in various animal models of pain. The purpose of this study was to investigate the antihyperalgesic effect of levetiracetam and its mechanism of action, by examining the involvement of GABAergic, opioidergic, 5-hydroxytryptaminergic (5-HTergic) and adrenergic systems in its effect, in a rat model of inflammatory pain. EXPERIMENTAL APPROACH Rats were intraplantarly injected with the pro-inflammatory compound carrageenan. A paw pressure test was used to determine: (i) the effect of levetiracetam on carrageenan-induced hyperalgesia; and (ii) the effects of bicuculline (selective GABAA receptor antagonist), naloxone (non-selective opioid receptor antagonist), methysergide (non-selective 5-HT receptor antagonist) and yohimbine (selective ,2 -adrenoceptor antagonist) on the antihyperalgesic action of levetiracetam. RESULTS Levetiracetam (10,200 mg·kg,1; p.o.) significantly reduced, in a dose-dependent manner, the inflammatory hyperalgesia induced by carrageenan. The antihyperalgesic effect of levetiracetam was significantly decreased after administration of bicuculline (0.5,2 mg·kg,1; i.p.), naloxone (1,3 mg·kg,1; i.p.), methysergide (0.25,1 mg·kg,1; i.p.) and yohimbine (1,3 mg·kg,1; i.p.). CONCLUSIONS AND IMPLICATIONS These results show that levetiracetam produced antihyperalgesia which is at least in part mediated by GABAA, opioid, 5-HT and ,2 -adrenergic receptors, in an inflammatory model of pain. The efficacy of levetiracetam in this animal model of inflammatory pain suggests that it could be a potentially important agent for treating inflammatory pain conditions in humans. [source]