Science and Technology Production

A quantitative immunocytochemical study of a G-protein-gated inward rectifier potassium channel (GIRK2) in the weaver mice mesencephalon.

Article

Authorship:

Adelbrecht C ; MURER, MARIO GUSTAVO ; Lauritzen I ; Lesage F ; Lazdunski M ; Agid Y ; Raisman-Vozari R

Date:

1997

Publishing House and Editing Place:

LIPPINCOTT WILLIAMS & WILKINS

Magazine:

NEUROREPORT, vol. 8 (pp. 979-984) LIPPINCOTT WILLIAMS & WILKINS

Summary *

It has been suggested that a mutation in a G-protein-gated inward rectifier K+ channel (GIRK2) is responsible for inducing cell death in the cerebellum of homozygous weaver (wv/wv) mutant mice. These mice also display a progressive, massive loss of mesencephalic dopaminergic neurones. Using an immunocytochemical method, we detected GIRK2-positive cell bodies and fibres in the substantia nigra pars compacta (SNC) and the ventral tegmental area (VTA) of control (+/+) mice. Cell counts of both GIRK2- and tyrosine hydroxylase (TH)-positive neurones demonstrated a marked loss of SNC cell bodies, especially in 12-month-old (12M) wv/wv mice. A considerable proportion of GIRK2-positive cell bodies were preserved, however. In addition, no loss of GIRK2-positive neurones was observed in the VTA of 12M wv/wv mice, despite of a significant reduction in TH-positive cell bodies. These results suggest that expression of the mutated channel is not a sufficient condition to induce cell death in the ventral mesencephalon of the wv/wv mice. Information provided by the agent in SIGEVA

Key Words

WEAVERPARKINSONGIRK2DOPAMINA