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

Zhang F, Liu B, Lei Z, Wang JH - Mol Brain (2012)

Bottom Line: Anxiety is a prevalent psychological disorder, in which the atypical expression of certain genes and the abnormality of amygdala are involved.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.The activity asynchrony of amygdala neurons and the weakness of GABA synaptic transmission are associated with anxiety-like behavior.

View Article: PubMed Central - HTML - PubMed

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

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.

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Amygdala neurons in DBA/2 mice show more diversified excitability. Neuronal excitability was assessed by a gap (ΔV) between threshold potential (Vts) and resting membrane potential (Vr), in which the membrane potentials were measured by whole-cell current-clamp recording in brain slices. A) shows the measurement and assessment of neuronal excitability from the recorded sequential spikes in an amygdala neuron. B) The histogram shows the number of neurons versus ΔV, i.e., the distributions of amygdala neuron excitability, from FVB/N mice (white bars) and DBA/2 mice (gray bars). The fitting curves in bell-shape are from FVB/N mice (black line) and DBA/2 mice (gray line). The wide curve in DBA/2 mice shows a diversified excitability. C) shows the coefficients of variance (standard deviation over mean) for ΔV of all amygdala neurons in FVB/N (white bar) and DBA/2 (gray bar). D) shows the coefficients of variance for ΔV of all amygdala non-fast spiking neurons in FVB/N (white bar) and DBA/2 (gray bar). E) shows the coefficients of variance for ΔV of amygdala fast spiking neurons in FVB/N (white bar) and DBA/2 (gray bar).
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Figure 5: Amygdala neurons in DBA/2 mice show more diversified excitability. Neuronal excitability was assessed by a gap (ΔV) between threshold potential (Vts) and resting membrane potential (Vr), in which the membrane potentials were measured by whole-cell current-clamp recording in brain slices. A) shows the measurement and assessment of neuronal excitability from the recorded sequential spikes in an amygdala neuron. B) The histogram shows the number of neurons versus ΔV, i.e., the distributions of amygdala neuron excitability, from FVB/N mice (white bars) and DBA/2 mice (gray bars). The fitting curves in bell-shape are from FVB/N mice (black line) and DBA/2 mice (gray line). The wide curve in DBA/2 mice shows a diversified excitability. C) shows the coefficients of variance (standard deviation over mean) for ΔV of all amygdala neurons in FVB/N (white bar) and DBA/2 (gray bar). D) shows the coefficients of variance for ΔV of all amygdala non-fast spiking neurons in FVB/N (white bar) and DBA/2 (gray bar). E) shows the coefficients of variance for ΔV of amygdala fast spiking neurons in FVB/N (white bar) and DBA/2 (gray bar).

Mentions: The sensitivity of amygdala neurons to inputs (i.e., threshold potentials) was used to merit their functional diversity [56,57]. The histogram in Figure 5B shows the number of neurons vs. threshold potential (ΔV), i.e., the distributions of amygdala neuron excitability, from FVB/N mice (white bars/black line for fitting curve, n = 153) and DBA/2 mice (grays, n = 153). A wide fitting-curve in DBA/2 mice indicates the diversity of neuronal excitability. Figure 5C presents the coefficient of variance (CV, standard deviation/mean) for ΔV from all amygdala neurons in FVB/N (white bar) and DBA/2 (gray) mice. Figure 5D illustrates CV for ΔV from amygdala non-fast spiking neurons in FVB/N (white bar, n = 80) and DBA/2 mice (gray, n = 80). Figure 5F illustrates CV for ΔV from amygdala fast-spiking neurons in FVB/N (white bar, n = 73) and DBA/2 mice (gray, n = 73). The excitability of amygdala neurons is diversified in DBA/2 high anxiety mice, leading to their asynchronous activities, especially for non-fast spiking neurons.


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

Zhang F, Liu B, Lei Z, Wang JH - Mol Brain (2012)

Amygdala neurons in DBA/2 mice show more diversified excitability. Neuronal excitability was assessed by a gap (ΔV) between threshold potential (Vts) and resting membrane potential (Vr), in which the membrane potentials were measured by whole-cell current-clamp recording in brain slices. A) shows the measurement and assessment of neuronal excitability from the recorded sequential spikes in an amygdala neuron. B) The histogram shows the number of neurons versus ΔV, i.e., the distributions of amygdala neuron excitability, from FVB/N mice (white bars) and DBA/2 mice (gray bars). The fitting curves in bell-shape are from FVB/N mice (black line) and DBA/2 mice (gray line). The wide curve in DBA/2 mice shows a diversified excitability. C) shows the coefficients of variance (standard deviation over mean) for ΔV of all amygdala neurons in FVB/N (white bar) and DBA/2 (gray bar). D) shows the coefficients of variance for ΔV of all amygdala non-fast spiking neurons in FVB/N (white bar) and DBA/2 (gray bar). E) shows the coefficients of variance for ΔV of amygdala fast spiking neurons in FVB/N (white bar) and DBA/2 (gray bar).
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Figure 5: Amygdala neurons in DBA/2 mice show more diversified excitability. Neuronal excitability was assessed by a gap (ΔV) between threshold potential (Vts) and resting membrane potential (Vr), in which the membrane potentials were measured by whole-cell current-clamp recording in brain slices. A) shows the measurement and assessment of neuronal excitability from the recorded sequential spikes in an amygdala neuron. B) The histogram shows the number of neurons versus ΔV, i.e., the distributions of amygdala neuron excitability, from FVB/N mice (white bars) and DBA/2 mice (gray bars). The fitting curves in bell-shape are from FVB/N mice (black line) and DBA/2 mice (gray line). The wide curve in DBA/2 mice shows a diversified excitability. C) shows the coefficients of variance (standard deviation over mean) for ΔV of all amygdala neurons in FVB/N (white bar) and DBA/2 (gray bar). D) shows the coefficients of variance for ΔV of all amygdala non-fast spiking neurons in FVB/N (white bar) and DBA/2 (gray bar). E) shows the coefficients of variance for ΔV of amygdala fast spiking neurons in FVB/N (white bar) and DBA/2 (gray bar).
Mentions: The sensitivity of amygdala neurons to inputs (i.e., threshold potentials) was used to merit their functional diversity [56,57]. The histogram in Figure 5B shows the number of neurons vs. threshold potential (ΔV), i.e., the distributions of amygdala neuron excitability, from FVB/N mice (white bars/black line for fitting curve, n = 153) and DBA/2 mice (grays, n = 153). A wide fitting-curve in DBA/2 mice indicates the diversity of neuronal excitability. Figure 5C presents the coefficient of variance (CV, standard deviation/mean) for ΔV from all amygdala neurons in FVB/N (white bar) and DBA/2 (gray) mice. Figure 5D illustrates CV for ΔV from amygdala non-fast spiking neurons in FVB/N (white bar, n = 80) and DBA/2 mice (gray, n = 80). Figure 5F illustrates CV for ΔV from amygdala fast-spiking neurons in FVB/N (white bar, n = 73) and DBA/2 mice (gray, n = 73). The excitability of amygdala neurons is diversified in DBA/2 high anxiety mice, leading to their asynchronous activities, especially for non-fast spiking neurons.

Bottom Line: Anxiety is a prevalent psychological disorder, in which the atypical expression of certain genes and the abnormality of amygdala are involved.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.The activity asynchrony of amygdala neurons and the weakness of GABA synaptic transmission are associated with anxiety-like behavior.

View Article: PubMed Central - HTML - PubMed

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

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.

Show MeSH
Related in: MedlinePlus