An autoradiographic method for labelling beta(1)- and beta(2)-adrenoceptors using [3H]CGP 12177 as a radioligand is described as well as the procedure for an autoradiographic saturation kinetic study. The method afforded higher quality autoradiographs as well as an improvement in the tissue preservation when assayed in birds and chick embryos. The results confirmed the K(d) values previously reported for membrane homogenate binding. The use of different radioligands to characterise beta-adrenoceptors, the higher B(max) values found with autoradiography than those obtained by the membrane homogenate binding method and the typical errors in quantifying autoradiography are discussed. It is concluded that the method described here considerably improves autoradiographic beta-adrenergic characterisation.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/s1385-299x(00)00005-2 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Characterization of bovine neutrophil beta2-adrenergic receptor function.
J Vet Pharmacol Ther
August 2010
Department of Biomedical Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061-0442, USA.
This study compares bovine leukocyte beta-adrenergic receptor densities to that of the rat, demonstrates for the first time a functional beta(2)-adrenergic receptor signaling pathway in steer neutrophils, and investigates the effect of an inflammatory stimulus on that signaling pathway. The beta(1)-/beta(2)-adrenergic antagonist ([3H])CGP-12177 demonstrated that rat lymphocyte specific binding-site density was highest, followed by steer and dairy cow lymphocytes, and lastly steer and dairy cow neutrophils. The beta(2)-adrenergic agonist terbutaline stimulated steer neutrophil adenosine 3,5-cyclic monophosphate (cAMP) production, an effect increased by inclusion of > or = 1 x 10(-8) M phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C.
View Article and Find Full Text PDFParoxetine pretreatment does not change the effects induced in the rat cortical beta-adrenergic receptor system by repetitive transcranial magnetic stimulation and electroconvulsive shock.
Int J Neuropsychopharmacol
July 2010
Department of Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland.
Repetitive transcranial magnetic stimulation (rTMS) has been proposed as a clinically effective antidepressant treatment, but meta-analysis suggests that its efficacy is marginal. We investigated whether the administration of rTMS together with paroxetine would enhance its effects on the beta-adrenergic system of the rat. We compared our results with the effects of electroconvulsive shock therapy (ECS).
View Article and Find Full Text PDFIdentification of second lipolysis activating protein from scorpion Buthus occitanus tunetanus.
Arch Inst Pasteur Tunis
September 2006
Laboratoire des venins et toxines, Institut Pasteur de Tunis, BP 74-1002 Tunis, Tunisie.
Besides the previously described LVP1, a second protein, LVP2, inducing a lipolytic response in adipose cells, was purified from scorpion Buthus occitanus tunetanus venom. It represented 2% of crude venom proteins, with pHi = 6 and molecular mass of 16889 Da. The reduction and the alkylation of LVP2 revealed an heterodimeric structure.
View Article and Find Full Text PDFExpression of beta-adrenergic receptor up-regulation is mediated by two different processes.
Brain Res
September 2006
Department of Pharmacology, Kawasaki Medical School, Kurashiki 701-0192, Japan.
Mechanisms of up-regulation of beta-adrenergic receptors (beta-ARs) induced by sustained exposure to 10(-8) M nadolol, a non-selective beta-AR antagonist, were examined using mouse cerebrocortical neurons. Nadolol dose- and time-dependently increased [3H]CGP-12177 bindings to the particulate fractions. This increase occurred 6 h and attained its plateau 12 h after the exposure, whereas beta1- and beta2-AR mRNA significantly increased 24 h and attained their plateaus 3 days after the exposure.
View Article and Find Full Text PDFMetabotropic glutamate receptors and neuroadaptation to antidepressants: imipramine-induced down-regulation of beta-adrenergic receptors in mice treated with metabotropic glutamate 2/3 receptor ligands.
J Neurochem
June 2005
Department of Human Physiology and Pharmacology, University of Rome La Sapienza, Rome, Italy.
Antidepressant drugs have a clinical latency that correlates with the development of neuroadaptive changes, including down-regulation of beta-adrenergic receptors in different brain regions. The identification of drugs that shorten this latency will have a great impact on the treatment of major depressive disorders. We report that the time required for the antidepressant imipramine to reduce the expression of beta-adrenergic receptors in the hippocampus is reduced by a co-administration with centrally active ligands of type 2/3 metabotropic glutamate (mGlu2/3) receptors.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!