Chemical and electrical stimulation of the caudate nucleus in freely moving cats: The role of dopamine

1973 ◽  
Vol 58 (2) ◽  
pp. 437-451 ◽  
Author(s):  
A.R. Cools
2017 ◽  
Vol 10 (1) ◽  
pp. 116-125 ◽  
Author(s):  
D. Martínez-Vargas ◽  
A. Valdés-Cruz ◽  
V.M. Magdaleno-Madrigal ◽  
R. Fernández-Mas ◽  
S. Almazán-Alvarado

1971 ◽  
Vol 28 (3) ◽  
pp. 567-572 ◽  
Author(s):  
Josef Syka ◽  
Toma´sˇ Radil-Weiss

2004 ◽  
Vol 287 (4) ◽  
pp. H1721-H1729 ◽  
Author(s):  
Koji Miyazaki ◽  
Satoshi Komatsu ◽  
Mitsuo Ikebe ◽  
Richard A. Fenton ◽  
James G. Dobson

Adenosine-induced antiadrenergic effects in the heart are mediated by adenosine A1 receptors (A1R). The role of PKCε in the antiadrenergic action of adenosine was explored with adult rat ventricular myocytes in which PKCε was overexpressed. Myocytes were transfected with a pEGFP-N1 vector in the presence or absence of a PKCε construct and compared with normal myocytes. The extent of myocyte shortening elicited by electrical stimulation of quiescent normal and transfected myocytes was recorded with video imaging. PKCε was found localized primarily in transverse tubules. The A1R agonist chlorocyclopentyladenosine (CCPA) at 1 μM rendered an enhanced localization of PKCε in the t-tubular system. The β-adrenergic agonist isoproterenol (Iso; 0.4 μM) elicited a 29–36% increase in myocyte shortening in all three groups. Although CCPA significantly reduced the Iso-produced increase in shortening in all three groups, the reduction caused by CCPA was greatest with PKCε overexpression. The CCPA reduction of the Iso-elicited shortening was eliminated in the presence of a PKCε inhibitory peptide. These results suggest that the translocation of PKCε to the t-tubular system plays an important role in A1R-mediated antiadrenergic actions in the heart.


1996 ◽  
Vol 739 (1-2) ◽  
pp. 192-200 ◽  
Author(s):  
Franco Marrosu ◽  
Casimir A. Fornal ◽  
Christine W. Metzler ◽  
Barry L. Jacobs

Sign in / Sign up

Export Citation Format

Share Document