期刊
CELL CALCIUM
卷 45, 期 3, 页码 310-317出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.ceca.2008.11.003
关键词
Potassium channels; Pharmacology; IP3 receptor; Internal calcium release
类别
资金
- Kavli Foundation
- Dart Foundation
- NIMH [R01-MH067830, P50-MH068789]
- NIAAA [1RL1AA017536-01]
- NIH
- NSF
Calcium ions (Ca2+) released from inositol trisphosphate (IP3)-sensitive intracellular stores may participate in both the transient and extended regulation of neuronal excitability in neocortical and hippocampal pyramidal neurons. IP3 receptor (IP3R) antagonists represent an important tool for dissociating these consequences of IP3 generation and IP3R-dependent internal Ca2+ release from the effects of other, concurrently stimulated second messenger signaling cascades and Ca2+ sources. In this study, we have described the actions of the IP3R and store-operated Ca2+ channel antagonist, 2-aminoethoxydiphenyl-borate (2-APB), on internal Ca2+ releaseand plasma membrane excitability in neocortical and hippocampal pyramidal neurons. Specifically, we found that a dose of 2-APB (100 mu M) sufficient for attenuating or blocking IP3-mediated internal Ca2+ release also raised pyramidal neuron excitability. The 2-APB-dependent increase in excitability reversed upon washout and was characterized by an increase in input resistance, a decrease in the delay to action potential onset, an increase in the width of action potentials, a decrease in the magnitude of afterhyperpolarizations (AHPs), and an increase in the magnitude of post-spike afterdepolarizations (ADPs). From these observations, we conclude that 2-APB potently and reversibly increases neuronal excitability, likely via the inhibition of voltage- and Ca2+-dependent potassium (K+) conductances. (c) 2008 Elsevier Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据