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Group I mGluR-dependent depotentiation in the lateral amygdala does not require the removal of calcium-permeable AMPA receptors.

Park K, Song S, Hong I, Song B, Kim J, Park S, Lee J, Song S, An B, Kim J, Lee CJ, Shin KS, Choi S, Lee S - Front Behav Neurosci (2014)

Bottom Line: Here, we examined whether CP-AMPARs are removed by mGluR1-mediated depotentiation of fear conditioning-induced synaptic potentiation.The synaptic expression of CP-AMPARs was negligible before, increased significantly 12 h after, and returned to baseline 48 h after fear conditioning, as evidenced by the changes in the sensitivity of lateral amygdala synaptic responses to NASPM.Our findings, together with previous results, suggest that the removal of CP-AMPARs is not required for the depotentiation of fear conditioning-induced synaptic potentiation at lateral amygdala synapses.

View Article: PubMed Central - PubMed

Affiliation: School of Biological Sciences, College of Natural Sciences, Seoul National University Seoul, Korea (ROK).

ABSTRACT
There is conflicting evidence regarding whether calcium-permeable receptors are removed during group I mGluR-mediated synaptic depression. In support of this hypothesis, AMPAR rectification, a correlative index of the synaptic expression of GluA2-lacking calcium-permeable AMPARs (CP-AMPARs), is known to decrease after the induction of several types of group I mGluR-mediated long-term depression (LTD), suggesting that a significant proportion of synaptic CP-AMPARs is removed during synaptic depression. We have previously demonstrated that fear conditioning-induced synaptic potentiation in the lateral amygdala is reversed by group 1 mGluR-mediated depotentiation. Here, we examined whether CP-AMPARs are removed by mGluR1-mediated depotentiation of fear conditioning-induced synaptic potentiation. The synaptic expression of CP-AMPARs was negligible before, increased significantly 12 h after, and returned to baseline 48 h after fear conditioning, as evidenced by the changes in the sensitivity of lateral amygdala synaptic responses to NASPM. Importantly, the sensitivity to NASPM was not altered after induction of depotentiation. Our findings, together with previous results, suggest that the removal of CP-AMPARs is not required for the depotentiation of fear conditioning-induced synaptic potentiation at lateral amygdala synapses.

No MeSH data available.


Related in: MedlinePlus

Sensitivity to NASPM is maintained after DHPG-induced depotentiation. (A) DHPG-induced depression was not significantly altered after vehicle treatment. The slices were prepared 12 h after conditioning. (B) NASPM treatment induced further depression after the onset of DHPG-induced depression. The slices were prepared 12 h after conditioning. (C) NASPM did not induce further changes in EPSCs after the onset of DHPG-induced depression. The slices were prepared 48 h after conditioning. All the experiments shown in this figure were performed in the presence of D-AP5 (50 μM). (D) A summary of the results shown in (A–C) (percent inhibition due to NASPM treatment for the three experiments). *** p < 0.001. Scale bars: 100 pA and 10 ms.
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Figure 2: Sensitivity to NASPM is maintained after DHPG-induced depotentiation. (A) DHPG-induced depression was not significantly altered after vehicle treatment. The slices were prepared 12 h after conditioning. (B) NASPM treatment induced further depression after the onset of DHPG-induced depression. The slices were prepared 12 h after conditioning. (C) NASPM did not induce further changes in EPSCs after the onset of DHPG-induced depression. The slices were prepared 48 h after conditioning. All the experiments shown in this figure were performed in the presence of D-AP5 (50 μM). (D) A summary of the results shown in (A–C) (percent inhibition due to NASPM treatment for the three experiments). *** p < 0.001. Scale bars: 100 pA and 10 ms.

Mentions: Between-group comparisons of the data were performed using either an unpaired t-test or one-way ANOVA with subsequent Newman-Keuls post-hoc comparison. A paired t-test was used to determine whether the post-treatment responses differed significantly from the baseline responses (Figures 1E, 3D). A p-value < 0.05 was considered to be statistically significant. The data from each neuron/slice were treated as independent samples. In all experiments using behaviorally trained rats, the data included samples from three or more animals.


Group I mGluR-dependent depotentiation in the lateral amygdala does not require the removal of calcium-permeable AMPA receptors.

Park K, Song S, Hong I, Song B, Kim J, Park S, Lee J, Song S, An B, Kim J, Lee CJ, Shin KS, Choi S, Lee S - Front Behav Neurosci (2014)

Sensitivity to NASPM is maintained after DHPG-induced depotentiation. (A) DHPG-induced depression was not significantly altered after vehicle treatment. The slices were prepared 12 h after conditioning. (B) NASPM treatment induced further depression after the onset of DHPG-induced depression. The slices were prepared 12 h after conditioning. (C) NASPM did not induce further changes in EPSCs after the onset of DHPG-induced depression. The slices were prepared 48 h after conditioning. All the experiments shown in this figure were performed in the presence of D-AP5 (50 μM). (D) A summary of the results shown in (A–C) (percent inhibition due to NASPM treatment for the three experiments). *** p < 0.001. Scale bars: 100 pA and 10 ms.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4126548&req=5

Figure 2: Sensitivity to NASPM is maintained after DHPG-induced depotentiation. (A) DHPG-induced depression was not significantly altered after vehicle treatment. The slices were prepared 12 h after conditioning. (B) NASPM treatment induced further depression after the onset of DHPG-induced depression. The slices were prepared 12 h after conditioning. (C) NASPM did not induce further changes in EPSCs after the onset of DHPG-induced depression. The slices were prepared 48 h after conditioning. All the experiments shown in this figure were performed in the presence of D-AP5 (50 μM). (D) A summary of the results shown in (A–C) (percent inhibition due to NASPM treatment for the three experiments). *** p < 0.001. Scale bars: 100 pA and 10 ms.
Mentions: Between-group comparisons of the data were performed using either an unpaired t-test or one-way ANOVA with subsequent Newman-Keuls post-hoc comparison. A paired t-test was used to determine whether the post-treatment responses differed significantly from the baseline responses (Figures 1E, 3D). A p-value < 0.05 was considered to be statistically significant. The data from each neuron/slice were treated as independent samples. In all experiments using behaviorally trained rats, the data included samples from three or more animals.

Bottom Line: Here, we examined whether CP-AMPARs are removed by mGluR1-mediated depotentiation of fear conditioning-induced synaptic potentiation.The synaptic expression of CP-AMPARs was negligible before, increased significantly 12 h after, and returned to baseline 48 h after fear conditioning, as evidenced by the changes in the sensitivity of lateral amygdala synaptic responses to NASPM.Our findings, together with previous results, suggest that the removal of CP-AMPARs is not required for the depotentiation of fear conditioning-induced synaptic potentiation at lateral amygdala synapses.

View Article: PubMed Central - PubMed

Affiliation: School of Biological Sciences, College of Natural Sciences, Seoul National University Seoul, Korea (ROK).

ABSTRACT
There is conflicting evidence regarding whether calcium-permeable receptors are removed during group I mGluR-mediated synaptic depression. In support of this hypothesis, AMPAR rectification, a correlative index of the synaptic expression of GluA2-lacking calcium-permeable AMPARs (CP-AMPARs), is known to decrease after the induction of several types of group I mGluR-mediated long-term depression (LTD), suggesting that a significant proportion of synaptic CP-AMPARs is removed during synaptic depression. We have previously demonstrated that fear conditioning-induced synaptic potentiation in the lateral amygdala is reversed by group 1 mGluR-mediated depotentiation. Here, we examined whether CP-AMPARs are removed by mGluR1-mediated depotentiation of fear conditioning-induced synaptic potentiation. The synaptic expression of CP-AMPARs was negligible before, increased significantly 12 h after, and returned to baseline 48 h after fear conditioning, as evidenced by the changes in the sensitivity of lateral amygdala synaptic responses to NASPM. Importantly, the sensitivity to NASPM was not altered after induction of depotentiation. Our findings, together with previous results, suggest that the removal of CP-AMPARs is not required for the depotentiation of fear conditioning-induced synaptic potentiation at lateral amygdala synapses.

No MeSH data available.


Related in: MedlinePlus