Distinct molecular components for thalamic- and cortical-dependent plasticity in the lateral amygdala
N-methyl-D-aspartate receptor (NMDAR)-dependent long-term depression (LTD) in the lateral nucleus of the amygdala (LA) is a form of synaptic plasticity thought to be a cellular substrate for the extinction of fear memory. The LA receives converging inputs from the sensory thalamus and neocortex that...
| Main Authors: | , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2014-07-01
|
| Series: | Frontiers in Molecular Neuroscience |
| Subjects: | |
| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fnmol.2014.00062/full |
| _version_ | 1819051577729613824 |
|---|---|
| author | Osvaldo eMirante Osvaldo eMirante Federico eBrandalise Johannes eBohacek Johannes eBohacek Isabelle M Mansuy Isabelle M Mansuy |
| author_facet | Osvaldo eMirante Osvaldo eMirante Federico eBrandalise Johannes eBohacek Johannes eBohacek Isabelle M Mansuy Isabelle M Mansuy |
| author_sort | Osvaldo eMirante |
| collection | DOAJ |
| description | N-methyl-D-aspartate receptor (NMDAR)-dependent long-term depression (LTD) in the lateral nucleus of the amygdala (LA) is a form of synaptic plasticity thought to be a cellular substrate for the extinction of fear memory. The LA receives converging inputs from the sensory thalamus and neocortex that are weakened following fear extinction. Combining field and patch-clamp electrophysiological recordings in mice, we show that a paired-pulse low-frequency stimulation can induce a robust LTD at thalamic and cortical inputs to LA, and we identify different underlying molecular components at these pathways. We show that while LTD depends on NMDARs and activation of the protein phosphatases PP2B and PP1 at both pathways, it requires NR2B-containing NMDARs at the thalamic pathway, but NR2C/D-containing NMDARs at the cortical pathway. LTD appears to be induced postsynaptically at the thalamic input but presynaptically at the cortical input, since postsynaptic calcium chelation and NMDAR blockade prevent thalamic but not cortical LTD. These results highlight distinct molecular features of LTD in LA that may be relevant for traumatic memory and its erasure, and for pathologies such as post-traumatic stress disorder (PTSD). |
| first_indexed | 2024-12-21T12:06:09Z |
| format | Article |
| id | doaj.art-c3faf862b2e64e23816633c2250a1f9a |
| institution | Directory Open Access Journal |
| issn | 1662-5099 |
| language | English |
| last_indexed | 2024-12-21T12:06:09Z |
| publishDate | 2014-07-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Molecular Neuroscience |
| spelling | doaj.art-c3faf862b2e64e23816633c2250a1f9a2022-12-21T19:04:41ZengFrontiers Media S.A.Frontiers in Molecular Neuroscience1662-50992014-07-01710.3389/fnmol.2014.0006298768Distinct molecular components for thalamic- and cortical-dependent plasticity in the lateral amygdalaOsvaldo eMirante0Osvaldo eMirante1Federico eBrandalise2Johannes eBohacek3Johannes eBohacek4Isabelle M Mansuy5Isabelle M Mansuy6University ZurichSwiss Federal Institute of TechnologyUniversity ZurichUniversity ZurichSwiss Federal Institute of TechnologyUniversity ZurichSwiss Federal Institute of TechnologyN-methyl-D-aspartate receptor (NMDAR)-dependent long-term depression (LTD) in the lateral nucleus of the amygdala (LA) is a form of synaptic plasticity thought to be a cellular substrate for the extinction of fear memory. The LA receives converging inputs from the sensory thalamus and neocortex that are weakened following fear extinction. Combining field and patch-clamp electrophysiological recordings in mice, we show that a paired-pulse low-frequency stimulation can induce a robust LTD at thalamic and cortical inputs to LA, and we identify different underlying molecular components at these pathways. We show that while LTD depends on NMDARs and activation of the protein phosphatases PP2B and PP1 at both pathways, it requires NR2B-containing NMDARs at the thalamic pathway, but NR2C/D-containing NMDARs at the cortical pathway. LTD appears to be induced postsynaptically at the thalamic input but presynaptically at the cortical input, since postsynaptic calcium chelation and NMDAR blockade prevent thalamic but not cortical LTD. These results highlight distinct molecular features of LTD in LA that may be relevant for traumatic memory and its erasure, and for pathologies such as post-traumatic stress disorder (PTSD).http://journal.frontiersin.org/Journal/10.3389/fnmol.2014.00062/fullAmygdalaMiceLTDphosphataseNR2BPP1 |
| spellingShingle | Osvaldo eMirante Osvaldo eMirante Federico eBrandalise Johannes eBohacek Johannes eBohacek Isabelle M Mansuy Isabelle M Mansuy Distinct molecular components for thalamic- and cortical-dependent plasticity in the lateral amygdala Frontiers in Molecular Neuroscience Amygdala Mice LTD phosphatase NR2B PP1 |
| title | Distinct molecular components for thalamic- and cortical-dependent plasticity in the lateral amygdala |
| title_full | Distinct molecular components for thalamic- and cortical-dependent plasticity in the lateral amygdala |
| title_fullStr | Distinct molecular components for thalamic- and cortical-dependent plasticity in the lateral amygdala |
| title_full_unstemmed | Distinct molecular components for thalamic- and cortical-dependent plasticity in the lateral amygdala |
| title_short | Distinct molecular components for thalamic- and cortical-dependent plasticity in the lateral amygdala |
| title_sort | distinct molecular components for thalamic and cortical dependent plasticity in the lateral amygdala |
| topic | Amygdala Mice LTD phosphatase NR2B PP1 |
| url | http://journal.frontiersin.org/Journal/10.3389/fnmol.2014.00062/full |
| work_keys_str_mv | AT osvaldoemirante distinctmolecularcomponentsforthalamicandcorticaldependentplasticityinthelateralamygdala AT osvaldoemirante distinctmolecularcomponentsforthalamicandcorticaldependentplasticityinthelateralamygdala AT federicoebrandalise distinctmolecularcomponentsforthalamicandcorticaldependentplasticityinthelateralamygdala AT johannesebohacek distinctmolecularcomponentsforthalamicandcorticaldependentplasticityinthelateralamygdala AT johannesebohacek distinctmolecularcomponentsforthalamicandcorticaldependentplasticityinthelateralamygdala AT isabellemmansuy distinctmolecularcomponentsforthalamicandcorticaldependentplasticityinthelateralamygdala AT isabellemmansuy distinctmolecularcomponentsforthalamicandcorticaldependentplasticityinthelateralamygdala |