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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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3,5-DHPG enhances GABAergic synaptic transmission in the amygdala neurons of DBA mice. Spontaneous GABAergic inhibitory postsynaptic currents (IPSC) were recorded by whole-cell clamp at amygdala neurons in brain slices before and after DHPG (10 μM) was washed onto the slices. A) shows GABAergic sIPSCs under the conditions of control (left panels) and DHPG application (right panels). Bottom panels show sIPSCs in the extended time scales. B) shows cumulative probability vs. sIPSCs amplitudes before (opened symbols) and after using DHPG (filled ones) from an experiment in panel A. C) shows the cumulative probability vs. inter-event intervals for sIPSCs before (opened symbols) and after applying DHPG (filled ones) from an experiment in panel A. D) shows the cumulative probability vs. sIPSCs amplitudes before (opened symbols) and after applying DHPG (filled ones) averaged from all of the experiments (n = 8). E) shows the cumulative probability vs. inter-event intervals for sIPSCs before (opened symbols) and after using DHPG (filled ones) from all of the experiments (n = 8, p < 0.01).
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Figure 9: 3,5-DHPG enhances GABAergic synaptic transmission in the amygdala neurons of DBA mice. Spontaneous GABAergic inhibitory postsynaptic currents (IPSC) were recorded by whole-cell clamp at amygdala neurons in brain slices before and after DHPG (10 μM) was washed onto the slices. A) shows GABAergic sIPSCs under the conditions of control (left panels) and DHPG application (right panels). Bottom panels show sIPSCs in the extended time scales. B) shows cumulative probability vs. sIPSCs amplitudes before (opened symbols) and after using DHPG (filled ones) from an experiment in panel A. C) shows the cumulative probability vs. inter-event intervals for sIPSCs before (opened symbols) and after applying DHPG (filled ones) from an experiment in panel A. D) shows the cumulative probability vs. sIPSCs amplitudes before (opened symbols) and after applying DHPG (filled ones) averaged from all of the experiments (n = 8). E) shows the cumulative probability vs. inter-event intervals for sIPSCs before (opened symbols) and after using DHPG (filled ones) from all of the experiments (n = 8, p < 0.01).

Mentions: If the synchronous activity of network neurons is coordinated by GABAergic neurons, we should see that mGluR activation strengthens GABA synaptic transmission in amygdala neurons of DBA/2 anxiety-like mice. Spontaneous inhibitory postsynaptic currents (sIPSC) were recorded by whole-cell voltage-clamp at amygdala neurons in brain slices before and after 3,5-DHPG (10 μM) was washed on. Figure 9A illustrates sIPSCs recorded before (left panels) and after applying 3,5-DHPG (rights). Cumulative probability versus sIPSC amplitudes and inter-event intervals from 9A experiment before (open symbols) and after using 3,5-DHPG (filled) are showed in Figure 9B-C. Figure 9D shows cumulative probability vs. sIPSC amplitudes averaged from all of the experiments (n = 7) before (open symbols) and after 3,5-DHPG (filled ones). Figure 9E illustrates cumulative probability vs. inter-event intervals before (open symbols) and after 3,5-DHPG (filled, n = 7, p < 0.01). Thus, mGluR1,5 activation enhances GABAergic synaptic transmission in the amygdala neurons of DBA/2 anxiety-like mice.


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)

3,5-DHPG enhances GABAergic synaptic transmission in the amygdala neurons of DBA mice. Spontaneous GABAergic inhibitory postsynaptic currents (IPSC) were recorded by whole-cell clamp at amygdala neurons in brain slices before and after DHPG (10 μM) was washed onto the slices. A) shows GABAergic sIPSCs under the conditions of control (left panels) and DHPG application (right panels). Bottom panels show sIPSCs in the extended time scales. B) shows cumulative probability vs. sIPSCs amplitudes before (opened symbols) and after using DHPG (filled ones) from an experiment in panel A. C) shows the cumulative probability vs. inter-event intervals for sIPSCs before (opened symbols) and after applying DHPG (filled ones) from an experiment in panel A. D) shows the cumulative probability vs. sIPSCs amplitudes before (opened symbols) and after applying DHPG (filled ones) averaged from all of the experiments (n = 8). E) shows the cumulative probability vs. inter-event intervals for sIPSCs before (opened symbols) and after using DHPG (filled ones) from all of the experiments (n = 8, p < 0.01).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3475049&req=5

Figure 9: 3,5-DHPG enhances GABAergic synaptic transmission in the amygdala neurons of DBA mice. Spontaneous GABAergic inhibitory postsynaptic currents (IPSC) were recorded by whole-cell clamp at amygdala neurons in brain slices before and after DHPG (10 μM) was washed onto the slices. A) shows GABAergic sIPSCs under the conditions of control (left panels) and DHPG application (right panels). Bottom panels show sIPSCs in the extended time scales. B) shows cumulative probability vs. sIPSCs amplitudes before (opened symbols) and after using DHPG (filled ones) from an experiment in panel A. C) shows the cumulative probability vs. inter-event intervals for sIPSCs before (opened symbols) and after applying DHPG (filled ones) from an experiment in panel A. D) shows the cumulative probability vs. sIPSCs amplitudes before (opened symbols) and after applying DHPG (filled ones) averaged from all of the experiments (n = 8). E) shows the cumulative probability vs. inter-event intervals for sIPSCs before (opened symbols) and after using DHPG (filled ones) from all of the experiments (n = 8, p < 0.01).
Mentions: If the synchronous activity of network neurons is coordinated by GABAergic neurons, we should see that mGluR activation strengthens GABA synaptic transmission in amygdala neurons of DBA/2 anxiety-like mice. Spontaneous inhibitory postsynaptic currents (sIPSC) were recorded by whole-cell voltage-clamp at amygdala neurons in brain slices before and after 3,5-DHPG (10 μM) was washed on. Figure 9A illustrates sIPSCs recorded before (left panels) and after applying 3,5-DHPG (rights). Cumulative probability versus sIPSC amplitudes and inter-event intervals from 9A experiment before (open symbols) and after using 3,5-DHPG (filled) are showed in Figure 9B-C. Figure 9D shows cumulative probability vs. sIPSC amplitudes averaged from all of the experiments (n = 7) before (open symbols) and after 3,5-DHPG (filled ones). Figure 9E illustrates cumulative probability vs. inter-event intervals before (open symbols) and after 3,5-DHPG (filled, n = 7, p < 0.01). Thus, mGluR1,5 activation enhances GABAergic synaptic transmission in the amygdala neurons of DBA/2 anxiety-like mice.

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