PubMed 18524485
Referenced in: none
Automatically associated channels: Kir6.2
Title: Kir6.2 knockout alters neurotransmitter release in mouse striatum: an in vivo microdialysis study.
Authors: Xue-Ru Shi, Jing Chang, Jian-Hua Ding, Yi Fan, Xiu-Lan Sun, Gang Hu
Journal, date & volume: Neurosci. Lett., 2008 Jul 18 , 439, 230-4
PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/18524485
Abstract
ATP-sensitive potassium (K-ATP) channels have been demonstrated to play important roles in the brain. In the present study, Kir6.2 knockout (Kir6.2-/-) mice were used to examine the contribution of Kir6.2-containing K-ATP channels to the regulation of neurotransmitter release via in vivo microdialysis studies. The results showed that the extracellular levels of monoamine and amino acid neurotransmitters in Kir6.2-/- mouse striatum were similar to those in Kir6.2+/+ mice under basal conditions. After high K+ (100mM) perfusion, the extracellular levels of DA and amino acids were increased in both genotypes. These increases, however, were significantly lower in Kir6.2-/- mice than those in Kir6.2+/+ mice. Extracellular levels of 3,4-dihydroxyphenylacetic acid (DOPAC), a major metabolite of DA, were increased in Kir6.2-/- mice but decreased in Kir6.2+/+ mice in response to high K+ stimulus. The releases of 4-hydroxy-3-methoxy-phenylacetic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) were attenuated to a similar extent in both mouse genotypes. Taken together, this study provides direct in vivo evidence that Kir6.2-containing K-ATP channels play regulatory roles in neurotransmitter release in the striatum.