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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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The agonist of metabotropic glutamate receptors, 3,5-dihydroxyphenylglycine (3,5-DHPG), improves anxiety-like behavior in DBA mice. An elevated plus-maze was used to evaluate anxiety-like behavior in two groups of DBA/2 mice that were given 3,5-DHPG (0.183 mg/kg) and PBS saline. A) shows the duration of staying in the closed arms vs. total duration for each experiment for DHPG-given mice (gray bar) versus PBS-given mice (white bar; p < 0.05, n = 9). B) shows exploration times toward the open arms in DHPG-given mice (gray bar) vs. PBS-given mice (white bar; p < 0.05, n = 9).
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Figure 7: The agonist of metabotropic glutamate receptors, 3,5-dihydroxyphenylglycine (3,5-DHPG), improves anxiety-like behavior in DBA mice. An elevated plus-maze was used to evaluate anxiety-like behavior in two groups of DBA/2 mice that were given 3,5-DHPG (0.183 mg/kg) and PBS saline. A) shows the duration of staying in the closed arms vs. total duration for each experiment for DHPG-given mice (gray bar) versus PBS-given mice (white bar; p < 0.05, n = 9). B) shows exploration times toward the open arms in DHPG-given mice (gray bar) vs. PBS-given mice (white bar; p < 0.05, n = 9).

Mentions: The effects of mGluR on anxiety and its neural pathophysiology were studied by using mGluR1,5 agonist, 3,5-dihydroxyphenylglycine (3,5-DHPG). DBA/2 mice were randomly divided to two groups that were given the intraperitoneal injections of 3,5-DHPG (0.183 mg/kg, one time per day) and PBS, respectively. Five days after this treatment, their anxiety-like behaviors were evaluated on an elevated plus-maze. The duration of staying in the closed arms is shorter in DHPG-given mice (gray bar) than PBS-given mice (white; p < 0.05, n = 9; Figure 7A). Exploration times toward the open arms are higher in DHPG-given mice (gray bar) vs. PBS-given mice (white; p < 0.05, n = 9; Figure 7B). The activation of mGluR1,5 improves anxiety-like behaviors in DBA/2 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)

The agonist of metabotropic glutamate receptors, 3,5-dihydroxyphenylglycine (3,5-DHPG), improves anxiety-like behavior in DBA mice. An elevated plus-maze was used to evaluate anxiety-like behavior in two groups of DBA/2 mice that were given 3,5-DHPG (0.183 mg/kg) and PBS saline. A) shows the duration of staying in the closed arms vs. total duration for each experiment for DHPG-given mice (gray bar) versus PBS-given mice (white bar; p < 0.05, n = 9). B) shows exploration times toward the open arms in DHPG-given mice (gray bar) vs. PBS-given mice (white bar; p < 0.05, n = 9).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 7: The agonist of metabotropic glutamate receptors, 3,5-dihydroxyphenylglycine (3,5-DHPG), improves anxiety-like behavior in DBA mice. An elevated plus-maze was used to evaluate anxiety-like behavior in two groups of DBA/2 mice that were given 3,5-DHPG (0.183 mg/kg) and PBS saline. A) shows the duration of staying in the closed arms vs. total duration for each experiment for DHPG-given mice (gray bar) versus PBS-given mice (white bar; p < 0.05, n = 9). B) shows exploration times toward the open arms in DHPG-given mice (gray bar) vs. PBS-given mice (white bar; p < 0.05, n = 9).
Mentions: The effects of mGluR on anxiety and its neural pathophysiology were studied by using mGluR1,5 agonist, 3,5-dihydroxyphenylglycine (3,5-DHPG). DBA/2 mice were randomly divided to two groups that were given the intraperitoneal injections of 3,5-DHPG (0.183 mg/kg, one time per day) and PBS, respectively. Five days after this treatment, their anxiety-like behaviors were evaluated on an elevated plus-maze. The duration of staying in the closed arms is shorter in DHPG-given mice (gray bar) than PBS-given mice (white; p < 0.05, n = 9; Figure 7A). Exploration times toward the open arms are higher in DHPG-given mice (gray bar) vs. PBS-given mice (white; p < 0.05, n = 9; Figure 7B). The activation of mGluR1,5 improves anxiety-like behaviors in DBA/2 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