The NO-cGMP-PKG Signaling Pathway Coordinately Regulates ERK and ERK-Driven Gene Expression at Pre- and Postsynaptic Sites Following LTP-Inducing Stimulation of Thalamo-Amygdala Synapses
Long-term potentiation (LTP) at thalamic input synapses to the lateral nucleus of the amygdala (LA) has been proposed as a cellular mechanism of the formation of auditory fear memories. We have previously shown that signaling via ERK/MAPK in both the LA and the medial division of the medial genicula...
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| Format: | Article |
| Language: | English |
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Wiley
2010-01-01
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| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/2010/540940 |
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| author | Junli Ping Glenn E. Schafe |
| author_facet | Junli Ping Glenn E. Schafe |
| author_sort | Junli Ping |
| collection | DOAJ |
| description | Long-term potentiation (LTP) at thalamic input synapses to the lateral nucleus of the amygdala (LA) has been proposed as a cellular mechanism of the formation of auditory fear memories. We have previously shown that signaling via ERK/MAPK in both the LA and the medial division of the medial geniculate nucleus/posterior intralaminar nucleus (MGm/PIN) is critical for LTP at thalamo-LA synapses. Here, we show that LTP-inducing stimulation of thalamo-LA inputs regulates the activation of ERK and the expression of ERK-driven immediate early genes (IEGs) in both the LA and MGm/PIN. Further, we show that pharmacological blockade of NMDAR-driven synaptic plasticity, NOS activation, or PKG signaling in the LA significantly impairs high-frequency stimulation-(HFS-) induced ERK activation and IEG expression in both regions, while blockade of extracellular NO signaling in the LA impairs HFS-induced ERK activation and IEG expression exclusively in the MGm/PIN. These findings suggest that NMDAR-driven synaptic plasticity and NO-cGMP-PKG signaling within the LA coordinately regulate ERK-driven gene expression in both the LA and the MGm/PIN following LTP induction at thalamo-LA synapses, and that synaptic plasticity in the LA promotes ERK-driven transcription in MGm/PIN neurons via NO-driven “retrograde signaling”. |
| format | Article |
| id | doaj-art-6a53996af48e4089ac0c44cbc019139f |
| institution | Kabale University |
| issn | 2090-5904 1687-5443 |
| language | English |
| publishDate | 2010-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Neural Plasticity |
| spelling | doaj-art-6a53996af48e4089ac0c44cbc019139f2025-08-20T03:33:39ZengWileyNeural Plasticity2090-59041687-54432010-01-01201010.1155/2010/540940540940The NO-cGMP-PKG Signaling Pathway Coordinately Regulates ERK and ERK-Driven Gene Expression at Pre- and Postsynaptic Sites Following LTP-Inducing Stimulation of Thalamo-Amygdala SynapsesJunli Ping0Glenn E. Schafe1Department of Psychology, Yale University, 2 Hillhouse Avenue, Box 208205, New Haven, CT 06520, USADepartment of Psychology, Yale University, 2 Hillhouse Avenue, Box 208205, New Haven, CT 06520, USALong-term potentiation (LTP) at thalamic input synapses to the lateral nucleus of the amygdala (LA) has been proposed as a cellular mechanism of the formation of auditory fear memories. We have previously shown that signaling via ERK/MAPK in both the LA and the medial division of the medial geniculate nucleus/posterior intralaminar nucleus (MGm/PIN) is critical for LTP at thalamo-LA synapses. Here, we show that LTP-inducing stimulation of thalamo-LA inputs regulates the activation of ERK and the expression of ERK-driven immediate early genes (IEGs) in both the LA and MGm/PIN. Further, we show that pharmacological blockade of NMDAR-driven synaptic plasticity, NOS activation, or PKG signaling in the LA significantly impairs high-frequency stimulation-(HFS-) induced ERK activation and IEG expression in both regions, while blockade of extracellular NO signaling in the LA impairs HFS-induced ERK activation and IEG expression exclusively in the MGm/PIN. These findings suggest that NMDAR-driven synaptic plasticity and NO-cGMP-PKG signaling within the LA coordinately regulate ERK-driven gene expression in both the LA and the MGm/PIN following LTP induction at thalamo-LA synapses, and that synaptic plasticity in the LA promotes ERK-driven transcription in MGm/PIN neurons via NO-driven “retrograde signaling”.http://dx.doi.org/10.1155/2010/540940 |
| spellingShingle | Junli Ping Glenn E. Schafe The NO-cGMP-PKG Signaling Pathway Coordinately Regulates ERK and ERK-Driven Gene Expression at Pre- and Postsynaptic Sites Following LTP-Inducing Stimulation of Thalamo-Amygdala Synapses Neural Plasticity |
| title | The NO-cGMP-PKG Signaling Pathway Coordinately Regulates ERK and ERK-Driven Gene Expression at Pre- and Postsynaptic Sites Following LTP-Inducing Stimulation of Thalamo-Amygdala Synapses |
| title_full | The NO-cGMP-PKG Signaling Pathway Coordinately Regulates ERK and ERK-Driven Gene Expression at Pre- and Postsynaptic Sites Following LTP-Inducing Stimulation of Thalamo-Amygdala Synapses |
| title_fullStr | The NO-cGMP-PKG Signaling Pathway Coordinately Regulates ERK and ERK-Driven Gene Expression at Pre- and Postsynaptic Sites Following LTP-Inducing Stimulation of Thalamo-Amygdala Synapses |
| title_full_unstemmed | The NO-cGMP-PKG Signaling Pathway Coordinately Regulates ERK and ERK-Driven Gene Expression at Pre- and Postsynaptic Sites Following LTP-Inducing Stimulation of Thalamo-Amygdala Synapses |
| title_short | The NO-cGMP-PKG Signaling Pathway Coordinately Regulates ERK and ERK-Driven Gene Expression at Pre- and Postsynaptic Sites Following LTP-Inducing Stimulation of Thalamo-Amygdala Synapses |
| title_sort | no cgmp pkg signaling pathway coordinately regulates erk and erk driven gene expression at pre and postsynaptic sites following ltp inducing stimulation of thalamo amygdala synapses |
| url | http://dx.doi.org/10.1155/2010/540940 |
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