Email updates

Keep up to date with the latest news and content from Molecular Brain and BioMed Central.

Open Access Research

mGluR1,5 activation improves network asynchrony and GABAergic synapse attenuation in the amygdala: implication for anxiety-like behavior in DBA/2 mice

Fengyu Zhang12, Bei Liu12, Zhuofan Lei1 and Jin-Hui Wang12*

Author Affiliations

1 State Key Laboratory, Institute of Biophysics, Chinese Academy of Sciences, 15 Datun Road, Beijing, 100101, China

2 College of Life Science, University of Science and Technology in China, Hefei, Anhui, 230026, China

For all author emails, please log on.

Molecular Brain 2012, 5:20  doi:10.1186/1756-6606-5-20

Published: 9 June 2012

Abstract

Anxiety is a prevalent psychological disorder, in which the atypical expression of certain genes and the abnormality of amygdala are involved. Intermediate processes between genetic defects and anxiety, pathophysiological characteristics of neural network, remain unclear. Using behavioral task, two-photon cellular imaging and electrophysiology, we studied the characteristics of neural networks in basolateral amygdala and the influences of metabotropic glutamate receptor (mGluR) on their dynamics in DBA/2 mice showing anxiety-related genetic defects. Amygdala neurons in DBA/2 high anxiety mice express asynchronous activity and diverse excitability, and their GABAergic synapses demonstrate weak transmission, compared to those in low anxiety FVB/N mice. mGluR1,5 activation improves the anxiety-like behaviors of DBA/2 mice, synchronizes the activity of amygdala neurons and strengthens the transmission of GABAergic synapses. The activity asynchrony of amygdala neurons and the weakness of GABA synaptic transmission are associated with anxiety-like behavior.

Keywords:
Anxiety; Amygdala; GABA; Neuron; Synapse and neural network