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.
Highlights
Anxiety, characterized as unstable mood, elevated attention, negative interpretation and social phobia under the conditions of potential threatening signs, is one of prevalent psychological disorders [1,2,3]
In order to study how genetic deficits impair neuronal networks in amygdala and lead to anxiety disorder, we have to select an appropriate model of animals that show anxiety-related phenotype and genotype
These two strains of mice were used to study the correlation among anxiety, genes and amygdala neuron networks
Summary
Anxiety, characterized as unstable mood, elevated attention, negative interpretation and social phobia under the conditions of potential threatening signs, is one of prevalent psychological disorders [1,2,3]. The studies by neural imaging indicate the hyperactivity of amygdala in anxiety disorder [4,5]. The grafts of GABAergic-rich neural tissue into amygdala improve anxiety-like signs [7]. The abnormality of amygdala is presumably a major origin of anxiety pathogenesis [1,4,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24]. Anxiety-related pathological characteristics and mechanisms in amygdala remain to be elusive
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