Calcium transient of CA1 pyramidal neurons induced by potassium blocker 4-aminopyridine in acute hippocampal slices

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Author:
SU Tao(Institute of Neuroscience,Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510260, China)
CONG Wen-dong(Institute of Neuroscience,Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510260, China)
LIAO Wei-ping(Institute of Neuroscience,Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510260, China)
Journal Title:
CHINESE JOURNAL OF NEUROMEDICINE
Issue:
Volume 10, Issue 05, 2011
DOI:
10.3760/cma.j.issn.1671-8925.2011.05.010
Key Word:
Potassium channel;Calcium transient;4-aminopyridine;Pyramidal neuron

Abstract: Objective To investigate the calcium transient of CA1 pyramidal neurons induced by potassium blocker 4-aminopyridine (4-AP) in acute hippocampal slices to explore the relation between potassium channel function and calcium transient, and their mechanism. Methods Fluorescent probe was employed to mark the hippocampai neurons in acute brain slices of rats; confocal microscopy was used to perform calcium imaging to observe the influences of different concentrations of 4-AP and perfusate with/without calcium on calcium transient of CA1 pyramidal neurons. Results The response of [Ca2+]I to lower concentration of 4-AP (<15 mmol/L) was in a dose-dependent manner (r2=0.910, P=0.000); the higher the concentration of 4-AP (20-80 mmol/L), the lower the peak level of calcium transient. The latency and amplitude of calcium transient induced by 4-AP were obviously reduced when the extracellular condition was switched to an absence of calcium, which was significantly different as compared with that with calcium (P<0.05). Conclusion Blockade of potassium channels with 4-AP can increase [Ca2+]I in the hippocampal pyramidal neurons of acute slices. The increase of [Ca2+]1 to 4-AP could be ascribe to calcium release from intracellular stores and calcium influx from extracellular matrix.

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