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Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum
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| Zeitschriftentitel: | The Journal of Neuroscience |
|---|---|
| Personen und Körperschaften: | , , , , , , , |
| In: | The Journal of Neuroscience, 25, 2005, 3, S. 577-583 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Society for Neuroscience
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| Schlagwörter: |
| author_facet |
Liu, Jie Yu, Baojian Orozco-Cabal, Luis Grigoriadis, Dimitri E. Rivier, Jean Vale, Wylie W. Shinnick-Gallagher, Patricia Gallagher, Joel P. Liu, Jie Yu, Baojian Orozco-Cabal, Luis Grigoriadis, Dimitri E. Rivier, Jean Vale, Wylie W. Shinnick-Gallagher, Patricia Gallagher, Joel P. |
|---|---|
| author |
Liu, Jie Yu, Baojian Orozco-Cabal, Luis Grigoriadis, Dimitri E. Rivier, Jean Vale, Wylie W. Shinnick-Gallagher, Patricia Gallagher, Joel P. |
| spellingShingle |
Liu, Jie Yu, Baojian Orozco-Cabal, Luis Grigoriadis, Dimitri E. Rivier, Jean Vale, Wylie W. Shinnick-Gallagher, Patricia Gallagher, Joel P. The Journal of Neuroscience Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum General Neuroscience |
| author_sort |
liu, jie |
| spelling |
Liu, Jie Yu, Baojian Orozco-Cabal, Luis Grigoriadis, Dimitri E. Rivier, Jean Vale, Wylie W. Shinnick-Gallagher, Patricia Gallagher, Joel P. 0270-6474 1529-2401 Society for Neuroscience General Neuroscience http://dx.doi.org/10.1523/jneurosci.4196-04.2005 <jats:p>Corticotropin-releasing factor (CRF) and urocortin (Ucn I) are endogenous members among a family of CRF-related peptides that activate two different and synaptically localized G-protein-coupled receptors, CRF<jats:sub>1</jats:sub>and CRF<jats:sub>2</jats:sub>. These peptides and their receptors have been implicated in stress responses and stress with cocaine abuse.</jats:p><jats:p>In this study, we observed significant alterations in excitatory transmission and CRF-related peptide regulation of excitatory transmission in the lateral septum mediolateral nucleus (LSMLN) after chronic cocaine administration. In brain slice recordings from the LSMLN of control (saline-treated) rats, glutamatergic synaptic transmission was facilitated by activation of CRF<jats:sub>1</jats:sub>receptors with CRF but was depressed after activation of CRF<jats:sub>2</jats:sub>receptors with Ucn I. After acute withdrawal from a chronic cocaine administration regimen, CRF<jats:sub>1</jats:sub>activation remained facilitatory, but CRF<jats:sub>2</jats:sub>activation facilitated rather than depressed LSMLN EPSCs. These alterations in CRF<jats:sub>2</jats:sub>effects occurred through both presynaptic and postsynaptic mechanisms. In saline-treated rats, CRF<jats:sub>1</jats:sub>and CRF<jats:sub>2</jats:sub>coupled predominantly to protein kinase A signaling pathways, whereas after cocaine withdrawal, protein kinase C activity was more prominent and likely contributed to the CRF<jats:sub>2</jats:sub>-mediated presynaptic facilitation. Neither CRF nor Ucn I altered monosynaptic GABA<jats:sub>A</jats:sub>-mediated IPSCs before or after chronic cocaine administration, suggesting that loss of GABA<jats:sub>A</jats:sub>-mediated inhibition could not account for the facilitation. This switch in polarity of Ucn I-mediated neuromodulation, from a negative to positive regulation of excitatory glutamatergic transmission after chronic cocaine administration, could generate an imbalance in the brain reward circuitry associated with the LSMLN.</jats:p> Chronic Cocaine Administration Switches Corticotropin-Releasing Factor<sub>2</sub>Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum The Journal of Neuroscience |
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| title |
Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum |
| title_unstemmed |
Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum |
| title_full |
Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum |
| title_fullStr |
Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum |
| title_full_unstemmed |
Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum |
| title_short |
Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum |
| title_sort |
chronic cocaine administration switches corticotropin-releasing factor<sub>2</sub>receptor-mediated depression to facilitation of glutamatergic transmission in the lateral septum |
| topic |
General Neuroscience |
| url |
http://dx.doi.org/10.1523/jneurosci.4196-04.2005 |
| publishDate |
2005 |
| physical |
577-583 |
| description |
<jats:p>Corticotropin-releasing factor (CRF) and urocortin (Ucn I) are endogenous members among a family of CRF-related peptides that activate two different and synaptically localized G-protein-coupled receptors, CRF<jats:sub>1</jats:sub>and CRF<jats:sub>2</jats:sub>. These peptides and their receptors have been implicated in stress responses and stress with cocaine abuse.</jats:p><jats:p>In this study, we observed significant alterations in excitatory transmission and CRF-related peptide regulation of excitatory transmission in the lateral septum mediolateral nucleus (LSMLN) after chronic cocaine administration. In brain slice recordings from the LSMLN of control (saline-treated) rats, glutamatergic synaptic transmission was facilitated by activation of CRF<jats:sub>1</jats:sub>receptors with CRF but was depressed after activation of CRF<jats:sub>2</jats:sub>receptors with Ucn I. After acute withdrawal from a chronic cocaine administration regimen, CRF<jats:sub>1</jats:sub>activation remained facilitatory, but CRF<jats:sub>2</jats:sub>activation facilitated rather than depressed LSMLN EPSCs. These alterations in CRF<jats:sub>2</jats:sub>effects occurred through both presynaptic and postsynaptic mechanisms. In saline-treated rats, CRF<jats:sub>1</jats:sub>and CRF<jats:sub>2</jats:sub>coupled predominantly to protein kinase A signaling pathways, whereas after cocaine withdrawal, protein kinase C activity was more prominent and likely contributed to the CRF<jats:sub>2</jats:sub>-mediated presynaptic facilitation. Neither CRF nor Ucn I altered monosynaptic GABA<jats:sub>A</jats:sub>-mediated IPSCs before or after chronic cocaine administration, suggesting that loss of GABA<jats:sub>A</jats:sub>-mediated inhibition could not account for the facilitation. This switch in polarity of Ucn I-mediated neuromodulation, from a negative to positive regulation of excitatory glutamatergic transmission after chronic cocaine administration, could generate an imbalance in the brain reward circuitry associated with the LSMLN.</jats:p> |
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| description | <jats:p>Corticotropin-releasing factor (CRF) and urocortin (Ucn I) are endogenous members among a family of CRF-related peptides that activate two different and synaptically localized G-protein-coupled receptors, CRF<jats:sub>1</jats:sub>and CRF<jats:sub>2</jats:sub>. These peptides and their receptors have been implicated in stress responses and stress with cocaine abuse.</jats:p><jats:p>In this study, we observed significant alterations in excitatory transmission and CRF-related peptide regulation of excitatory transmission in the lateral septum mediolateral nucleus (LSMLN) after chronic cocaine administration. In brain slice recordings from the LSMLN of control (saline-treated) rats, glutamatergic synaptic transmission was facilitated by activation of CRF<jats:sub>1</jats:sub>receptors with CRF but was depressed after activation of CRF<jats:sub>2</jats:sub>receptors with Ucn I. After acute withdrawal from a chronic cocaine administration regimen, CRF<jats:sub>1</jats:sub>activation remained facilitatory, but CRF<jats:sub>2</jats:sub>activation facilitated rather than depressed LSMLN EPSCs. These alterations in CRF<jats:sub>2</jats:sub>effects occurred through both presynaptic and postsynaptic mechanisms. In saline-treated rats, CRF<jats:sub>1</jats:sub>and CRF<jats:sub>2</jats:sub>coupled predominantly to protein kinase A signaling pathways, whereas after cocaine withdrawal, protein kinase C activity was more prominent and likely contributed to the CRF<jats:sub>2</jats:sub>-mediated presynaptic facilitation. Neither CRF nor Ucn I altered monosynaptic GABA<jats:sub>A</jats:sub>-mediated IPSCs before or after chronic cocaine administration, suggesting that loss of GABA<jats:sub>A</jats:sub>-mediated inhibition could not account for the facilitation. This switch in polarity of Ucn I-mediated neuromodulation, from a negative to positive regulation of excitatory glutamatergic transmission after chronic cocaine administration, could generate an imbalance in the brain reward circuitry associated with the LSMLN.</jats:p> |
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| imprint_str_mv | Society for Neuroscience, 2005 |
| institution | DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4 |
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| spelling | Liu, Jie Yu, Baojian Orozco-Cabal, Luis Grigoriadis, Dimitri E. Rivier, Jean Vale, Wylie W. Shinnick-Gallagher, Patricia Gallagher, Joel P. 0270-6474 1529-2401 Society for Neuroscience General Neuroscience http://dx.doi.org/10.1523/jneurosci.4196-04.2005 <jats:p>Corticotropin-releasing factor (CRF) and urocortin (Ucn I) are endogenous members among a family of CRF-related peptides that activate two different and synaptically localized G-protein-coupled receptors, CRF<jats:sub>1</jats:sub>and CRF<jats:sub>2</jats:sub>. These peptides and their receptors have been implicated in stress responses and stress with cocaine abuse.</jats:p><jats:p>In this study, we observed significant alterations in excitatory transmission and CRF-related peptide regulation of excitatory transmission in the lateral septum mediolateral nucleus (LSMLN) after chronic cocaine administration. In brain slice recordings from the LSMLN of control (saline-treated) rats, glutamatergic synaptic transmission was facilitated by activation of CRF<jats:sub>1</jats:sub>receptors with CRF but was depressed after activation of CRF<jats:sub>2</jats:sub>receptors with Ucn I. After acute withdrawal from a chronic cocaine administration regimen, CRF<jats:sub>1</jats:sub>activation remained facilitatory, but CRF<jats:sub>2</jats:sub>activation facilitated rather than depressed LSMLN EPSCs. These alterations in CRF<jats:sub>2</jats:sub>effects occurred through both presynaptic and postsynaptic mechanisms. In saline-treated rats, CRF<jats:sub>1</jats:sub>and CRF<jats:sub>2</jats:sub>coupled predominantly to protein kinase A signaling pathways, whereas after cocaine withdrawal, protein kinase C activity was more prominent and likely contributed to the CRF<jats:sub>2</jats:sub>-mediated presynaptic facilitation. Neither CRF nor Ucn I altered monosynaptic GABA<jats:sub>A</jats:sub>-mediated IPSCs before or after chronic cocaine administration, suggesting that loss of GABA<jats:sub>A</jats:sub>-mediated inhibition could not account for the facilitation. This switch in polarity of Ucn I-mediated neuromodulation, from a negative to positive regulation of excitatory glutamatergic transmission after chronic cocaine administration, could generate an imbalance in the brain reward circuitry associated with the LSMLN.</jats:p> Chronic Cocaine Administration Switches Corticotropin-Releasing Factor<sub>2</sub>Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum The Journal of Neuroscience |
| spellingShingle | Liu, Jie, Yu, Baojian, Orozco-Cabal, Luis, Grigoriadis, Dimitri E., Rivier, Jean, Vale, Wylie W., Shinnick-Gallagher, Patricia, Gallagher, Joel P., The Journal of Neuroscience, Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum, General Neuroscience |
| title | Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum |
| title_full | Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum |
| title_fullStr | Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum |
| title_full_unstemmed | Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum |
| title_short | Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum |
| title_sort | chronic cocaine administration switches corticotropin-releasing factor<sub>2</sub>receptor-mediated depression to facilitation of glutamatergic transmission in the lateral septum |
| title_unstemmed | Chronic Cocaine Administration Switches Corticotropin-Releasing Factor2Receptor-Mediated Depression to Facilitation of Glutamatergic Transmission in the Lateral Septum |
| topic | General Neuroscience |
| url | http://dx.doi.org/10.1523/jneurosci.4196-04.2005 |