Nelles, Eric and Bützler, Christoph and Jung, Dirk and Temme, Achim and Gabriel, Heinz-Dieter and Dahl, Ursula and Traub, Otto and Stümpel, Frank and Jungermann, Kurt and Zielasek, Jürgen and Toyka, Klaus V. and Dermietzel, Rolf and Willecke, Klaus (1996) Defective propagation of signals generated by sympathetic nerve stimulation in the liver of connexin32-deficient mice. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 93 (18). pp. 9565-9570. ISSN 0027-8424, 1091-6490
Full text not available from this repository.Abstract
The gap junctional protein connexin32 is expressed in hepatocytes, exocrine pancreatic cells, Schwann cells, and other cell types. We have inactivated the connexin32 gene by homologous recombination in the mouse genome and have generated homozygous connexin32-deficient mice that were viable and fertile but weighed on the average approximate to 17% less than wild-type controls, Electrical stimulation of sympathetic nerves in connexin32-deficient liver triggered a 78% lower amount of glucose mobilization from glycogen stores, when compared with wild-type liver. Thus, connexin32-containing gap junctions are essential in mouse liver for maximal intercellular propagation of the noradrenaline signal from the periportal (upstream) area, where it is received from sympathetic nerve endings, to perivenous (downstream) hepatocytes, In connexin32-defective liver, the amount of connexin26 protein expressed was found to be lower than in wild-type liver, and the total area of gap junction plaques was approximate to 1000-fold smaller than in wild-type liver, In contrast to patients with connexin32 defects suffering from X chromosome-linked Charcot-Marie-Tooth disease (CMTX) due to demyelination in Schwann cells of peripheral nerves, connexin32-deficient mice did not show neurological abnormalities when analyzed at 3 months of age. It is possible, however, that they may develop neurodegenerative symptoms at older age.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | MARIE-TOOTH DISEASE; GAP JUNCTION PROTEINS; RAT-LIVER; MUTATIONS; CELLS; GENE; CONNEXIN-32; HEPATOCYTES; METABOLISM; MYELIN; gap junction; glucose release; metabolic cooperation; Charcot-Marie-Tooth disease (CMTX) |
| Subjects: | 500 Science > 570 Life sciences |
| Divisions: | Biology, Preclinical Medicine > Institut für Anatomie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 22 Jun 2023 10:52 |
| Last Modified: | 22 Jun 2023 10:52 |
| URI: | https://pred.uni-regensburg.de/id/eprint/51481 |
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