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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

Changes in the sensitivity to NASPM after fear conditioning. (A) Diagram showing the positions of the stimulating and recording electrode. BA, basal nucleus of amygdala; CeA, central nucleus of amygdala; LA, lateral nucleus of amygdale; R, recording electrode; S, stimulating electrode. (B–E) NASPM (50 μM) treatment reduced the EPSC amplitude in the presence of D-AP5 (50 μM) in slices prepared 12 h after conditioning but not 48 h after conditioning or from naïve rats. (F) UBP302 treatment displayed no significant effects on the EPSC amplitude in slices prepared 12 h after conditioning. (G) The input-output relationship was not different between the groups of slices prepared 12 and 48 h after conditioning. * p < 0.05. Scale bars: 50 pA and 10 ms.
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Figure 1: Changes in the sensitivity to NASPM after fear conditioning. (A) Diagram showing the positions of the stimulating and recording electrode. BA, basal nucleus of amygdala; CeA, central nucleus of amygdala; LA, lateral nucleus of amygdale; R, recording electrode; S, stimulating electrode. (B–E) NASPM (50 μM) treatment reduced the EPSC amplitude in the presence of D-AP5 (50 μM) in slices prepared 12 h after conditioning but not 48 h after conditioning or from naïve rats. (F) UBP302 treatment displayed no significant effects on the EPSC amplitude in slices prepared 12 h after conditioning. (G) The input-output relationship was not different between the groups of slices prepared 12 and 48 h after conditioning. * p < 0.05. Scale bars: 50 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)

Changes in the sensitivity to NASPM after fear conditioning. (A) Diagram showing the positions of the stimulating and recording electrode. BA, basal nucleus of amygdala; CeA, central nucleus of amygdala; LA, lateral nucleus of amygdale; R, recording electrode; S, stimulating electrode. (B–E) NASPM (50 μM) treatment reduced the EPSC amplitude in the presence of D-AP5 (50 μM) in slices prepared 12 h after conditioning but not 48 h after conditioning or from naïve rats. (F) UBP302 treatment displayed no significant effects on the EPSC amplitude in slices prepared 12 h after conditioning. (G) The input-output relationship was not different between the groups of slices prepared 12 and 48 h after conditioning. * p < 0.05. Scale bars: 50 pA and 10 ms.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: Changes in the sensitivity to NASPM after fear conditioning. (A) Diagram showing the positions of the stimulating and recording electrode. BA, basal nucleus of amygdala; CeA, central nucleus of amygdala; LA, lateral nucleus of amygdale; R, recording electrode; S, stimulating electrode. (B–E) NASPM (50 μM) treatment reduced the EPSC amplitude in the presence of D-AP5 (50 μM) in slices prepared 12 h after conditioning but not 48 h after conditioning or from naïve rats. (F) UBP302 treatment displayed no significant effects on the EPSC amplitude in slices prepared 12 h after conditioning. (G) The input-output relationship was not different between the groups of slices prepared 12 and 48 h after conditioning. * p < 0.05. Scale bars: 50 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