Regional specificity of synaptic plasticity deficits in a knock-in mouse model of DYT1 dystonia

DYT1 dystonia is a movement disorder caused by a deletion in the C-terminal of the protein torsinA. It is unclear how torsinA mutation might disrupt cellular processes encoding motor activity, and whether this impairment occurs in specific brain regions. Here, we report a selective impairment of cor...
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Autor*in:	G. Martella [verfasserIn] M. Maltese [verfasserIn] R. Nisticò [verfasserIn] T. Schirinzi [verfasserIn] G. Madeo [verfasserIn] G. Sciamanna [verfasserIn] G. Ponterio [verfasserIn] A. Tassone [verfasserIn] G. Mandolesi [verfasserIn] V. Vanni [verfasserIn] M. Pignatelli [verfasserIn] P. Bonsi [verfasserIn] A. Pisani [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Dystonia Striatum D2 dopamine receptor Long-term depression Long-term potentiation Cholinergic interneurons

Übergeordnetes Werk:	In: Neurobiology of Disease - Elsevier, 2021, 65(2014), Seite 124-132
Übergeordnetes Werk:	volume:65 ; year:2014 ; pages:124-132

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.nbd.2014.01.016

Katalog-ID:	DOAJ056729952

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520			\|a DYT1 dystonia is a movement disorder caused by a deletion in the C-terminal of the protein torsinA. It is unclear how torsinA mutation might disrupt cellular processes encoding motor activity, and whether this impairment occurs in specific brain regions. Here, we report a selective impairment of corticostriatal synaptic plasticity in knock-in mice heterozygous for Δ-torsinA (Tor1a+/Δgag mice) as compared to controls (Tor1a+/+ mice). In striatal spiny neurons from Tor1a+/Δgag mice, high-frequency stimulation failed to induce long-term depression (LTD), whereas long-term potentiation (LTP) exhibited increased amplitude. Of interest, blockade of D2 dopamine receptors (D2Rs) increased LTP in Tor1a+/+ mice to a level comparable to that measured in Tor1a+/Δgag mice and normalized the levels of potentiation across mouse groups. A low-frequency stimulation (LFS) protocol was unable to depotentiate corticostriatal synapses in Tor1a+/Δgag mice. Muscarinic M1 acetylcholine receptor (mAChR) blockade rescued plasticity deficits. Additionally, we found an abnormal responsiveness of cholinergic interneurons to D2R activation, consisting in an excitatory response rather than the expected inhibition, further confirming an imbalance between dopaminergic and cholinergic signaling in the striatum. Conversely, synaptic activity and plasticity in the CA1 hippocampal region were unaltered in Tor1a+/Δgag mice. Importantly, the M1 mAChR-dependent enhancement of hippocampal LTP was unaffected in both genotypes. Similarly, both basic properties of dopaminergic nigral neurons and their responses to D2R activation were normal.These results provide evidence for a regional specificity of the electrophysiological abnormalities observed and demonstrate the reproducibility of such alterations in distinct models of DYT1 dystonia.
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allfields	10.1016/j.nbd.2014.01.016 doi (DE-627)DOAJ056729952 (DE-599)DOAJ2b4ede7036b24ed68c2447fa7ce7403a DE-627 ger DE-627 rakwb eng RC321-571 G. Martella verfasserin aut Regional specificity of synaptic plasticity deficits in a knock-in mouse model of DYT1 dystonia 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier DYT1 dystonia is a movement disorder caused by a deletion in the C-terminal of the protein torsinA. It is unclear how torsinA mutation might disrupt cellular processes encoding motor activity, and whether this impairment occurs in specific brain regions. Here, we report a selective impairment of corticostriatal synaptic plasticity in knock-in mice heterozygous for Δ-torsinA (Tor1a+/Δgag mice) as compared to controls (Tor1a+/+ mice). In striatal spiny neurons from Tor1a+/Δgag mice, high-frequency stimulation failed to induce long-term depression (LTD), whereas long-term potentiation (LTP) exhibited increased amplitude. Of interest, blockade of D2 dopamine receptors (D2Rs) increased LTP in Tor1a+/+ mice to a level comparable to that measured in Tor1a+/Δgag mice and normalized the levels of potentiation across mouse groups. A low-frequency stimulation (LFS) protocol was unable to depotentiate corticostriatal synapses in Tor1a+/Δgag mice. Muscarinic M1 acetylcholine receptor (mAChR) blockade rescued plasticity deficits. Additionally, we found an abnormal responsiveness of cholinergic interneurons to D2R activation, consisting in an excitatory response rather than the expected inhibition, further confirming an imbalance between dopaminergic and cholinergic signaling in the striatum. Conversely, synaptic activity and plasticity in the CA1 hippocampal region were unaltered in Tor1a+/Δgag mice. Importantly, the M1 mAChR-dependent enhancement of hippocampal LTP was unaffected in both genotypes. Similarly, both basic properties of dopaminergic nigral neurons and their responses to D2R activation were normal.These results provide evidence for a regional specificity of the electrophysiological abnormalities observed and demonstrate the reproducibility of such alterations in distinct models of DYT1 dystonia. Dystonia Striatum D2 dopamine receptor Long-term depression Long-term potentiation Cholinergic interneurons Neurosciences. Biological psychiatry. Neuropsychiatry M. Maltese verfasserin aut R. Nisticò verfasserin aut T. Schirinzi verfasserin aut G. Madeo verfasserin aut G. Sciamanna verfasserin aut G. Ponterio verfasserin aut A. Tassone verfasserin aut G. Mandolesi verfasserin aut V. Vanni verfasserin aut M. Pignatelli verfasserin aut P. Bonsi verfasserin aut A. Pisani verfasserin aut In Neurobiology of Disease Elsevier, 2021 65(2014), Seite 124-132 (DE-627)268125414 (DE-600)1471408-5 1095953X nnns volume:65 year:2014 pages:124-132 https://doi.org/10.1016/j.nbd.2014.01.016 kostenfrei https://doaj.org/article/2b4ede7036b24ed68c2447fa7ce7403a kostenfrei http://www.sciencedirect.com/science/article/pii/S0969996114000308 kostenfrei https://doaj.org/toc/1095-953X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_165 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2010 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4700 AR 65 2014 124-132
spelling	10.1016/j.nbd.2014.01.016 doi (DE-627)DOAJ056729952 (DE-599)DOAJ2b4ede7036b24ed68c2447fa7ce7403a DE-627 ger DE-627 rakwb eng RC321-571 G. Martella verfasserin aut Regional specificity of synaptic plasticity deficits in a knock-in mouse model of DYT1 dystonia 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier DYT1 dystonia is a movement disorder caused by a deletion in the C-terminal of the protein torsinA. It is unclear how torsinA mutation might disrupt cellular processes encoding motor activity, and whether this impairment occurs in specific brain regions. Here, we report a selective impairment of corticostriatal synaptic plasticity in knock-in mice heterozygous for Δ-torsinA (Tor1a+/Δgag mice) as compared to controls (Tor1a+/+ mice). In striatal spiny neurons from Tor1a+/Δgag mice, high-frequency stimulation failed to induce long-term depression (LTD), whereas long-term potentiation (LTP) exhibited increased amplitude. Of interest, blockade of D2 dopamine receptors (D2Rs) increased LTP in Tor1a+/+ mice to a level comparable to that measured in Tor1a+/Δgag mice and normalized the levels of potentiation across mouse groups. A low-frequency stimulation (LFS) protocol was unable to depotentiate corticostriatal synapses in Tor1a+/Δgag mice. Muscarinic M1 acetylcholine receptor (mAChR) blockade rescued plasticity deficits. Additionally, we found an abnormal responsiveness of cholinergic interneurons to D2R activation, consisting in an excitatory response rather than the expected inhibition, further confirming an imbalance between dopaminergic and cholinergic signaling in the striatum. Conversely, synaptic activity and plasticity in the CA1 hippocampal region were unaltered in Tor1a+/Δgag mice. Importantly, the M1 mAChR-dependent enhancement of hippocampal LTP was unaffected in both genotypes. Similarly, both basic properties of dopaminergic nigral neurons and their responses to D2R activation were normal.These results provide evidence for a regional specificity of the electrophysiological abnormalities observed and demonstrate the reproducibility of such alterations in distinct models of DYT1 dystonia. Dystonia Striatum D2 dopamine receptor Long-term depression Long-term potentiation Cholinergic interneurons Neurosciences. Biological psychiatry. Neuropsychiatry M. Maltese verfasserin aut R. Nisticò verfasserin aut T. Schirinzi verfasserin aut G. Madeo verfasserin aut G. Sciamanna verfasserin aut G. Ponterio verfasserin aut A. Tassone verfasserin aut G. Mandolesi verfasserin aut V. Vanni verfasserin aut M. Pignatelli verfasserin aut P. Bonsi verfasserin aut A. Pisani verfasserin aut In Neurobiology of Disease Elsevier, 2021 65(2014), Seite 124-132 (DE-627)268125414 (DE-600)1471408-5 1095953X nnns volume:65 year:2014 pages:124-132 https://doi.org/10.1016/j.nbd.2014.01.016 kostenfrei https://doaj.org/article/2b4ede7036b24ed68c2447fa7ce7403a kostenfrei http://www.sciencedirect.com/science/article/pii/S0969996114000308 kostenfrei https://doaj.org/toc/1095-953X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_165 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2010 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4700 AR 65 2014 124-132
allfields_unstemmed	10.1016/j.nbd.2014.01.016 doi (DE-627)DOAJ056729952 (DE-599)DOAJ2b4ede7036b24ed68c2447fa7ce7403a DE-627 ger DE-627 rakwb eng RC321-571 G. Martella verfasserin aut Regional specificity of synaptic plasticity deficits in a knock-in mouse model of DYT1 dystonia 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier DYT1 dystonia is a movement disorder caused by a deletion in the C-terminal of the protein torsinA. It is unclear how torsinA mutation might disrupt cellular processes encoding motor activity, and whether this impairment occurs in specific brain regions. Here, we report a selective impairment of corticostriatal synaptic plasticity in knock-in mice heterozygous for Δ-torsinA (Tor1a+/Δgag mice) as compared to controls (Tor1a+/+ mice). In striatal spiny neurons from Tor1a+/Δgag mice, high-frequency stimulation failed to induce long-term depression (LTD), whereas long-term potentiation (LTP) exhibited increased amplitude. Of interest, blockade of D2 dopamine receptors (D2Rs) increased LTP in Tor1a+/+ mice to a level comparable to that measured in Tor1a+/Δgag mice and normalized the levels of potentiation across mouse groups. A low-frequency stimulation (LFS) protocol was unable to depotentiate corticostriatal synapses in Tor1a+/Δgag mice. Muscarinic M1 acetylcholine receptor (mAChR) blockade rescued plasticity deficits. Additionally, we found an abnormal responsiveness of cholinergic interneurons to D2R activation, consisting in an excitatory response rather than the expected inhibition, further confirming an imbalance between dopaminergic and cholinergic signaling in the striatum. Conversely, synaptic activity and plasticity in the CA1 hippocampal region were unaltered in Tor1a+/Δgag mice. Importantly, the M1 mAChR-dependent enhancement of hippocampal LTP was unaffected in both genotypes. Similarly, both basic properties of dopaminergic nigral neurons and their responses to D2R activation were normal.These results provide evidence for a regional specificity of the electrophysiological abnormalities observed and demonstrate the reproducibility of such alterations in distinct models of DYT1 dystonia. Dystonia Striatum D2 dopamine receptor Long-term depression Long-term potentiation Cholinergic interneurons Neurosciences. Biological psychiatry. Neuropsychiatry M. Maltese verfasserin aut R. Nisticò verfasserin aut T. Schirinzi verfasserin aut G. Madeo verfasserin aut G. Sciamanna verfasserin aut G. Ponterio verfasserin aut A. Tassone verfasserin aut G. Mandolesi verfasserin aut V. Vanni verfasserin aut M. Pignatelli verfasserin aut P. Bonsi verfasserin aut A. Pisani verfasserin aut In Neurobiology of Disease Elsevier, 2021 65(2014), Seite 124-132 (DE-627)268125414 (DE-600)1471408-5 1095953X nnns volume:65 year:2014 pages:124-132 https://doi.org/10.1016/j.nbd.2014.01.016 kostenfrei https://doaj.org/article/2b4ede7036b24ed68c2447fa7ce7403a kostenfrei http://www.sciencedirect.com/science/article/pii/S0969996114000308 kostenfrei https://doaj.org/toc/1095-953X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_165 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2010 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4700 AR 65 2014 124-132
allfieldsGer	10.1016/j.nbd.2014.01.016 doi (DE-627)DOAJ056729952 (DE-599)DOAJ2b4ede7036b24ed68c2447fa7ce7403a DE-627 ger DE-627 rakwb eng RC321-571 G. Martella verfasserin aut Regional specificity of synaptic plasticity deficits in a knock-in mouse model of DYT1 dystonia 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier DYT1 dystonia is a movement disorder caused by a deletion in the C-terminal of the protein torsinA. It is unclear how torsinA mutation might disrupt cellular processes encoding motor activity, and whether this impairment occurs in specific brain regions. Here, we report a selective impairment of corticostriatal synaptic plasticity in knock-in mice heterozygous for Δ-torsinA (Tor1a+/Δgag mice) as compared to controls (Tor1a+/+ mice). In striatal spiny neurons from Tor1a+/Δgag mice, high-frequency stimulation failed to induce long-term depression (LTD), whereas long-term potentiation (LTP) exhibited increased amplitude. Of interest, blockade of D2 dopamine receptors (D2Rs) increased LTP in Tor1a+/+ mice to a level comparable to that measured in Tor1a+/Δgag mice and normalized the levels of potentiation across mouse groups. A low-frequency stimulation (LFS) protocol was unable to depotentiate corticostriatal synapses in Tor1a+/Δgag mice. Muscarinic M1 acetylcholine receptor (mAChR) blockade rescued plasticity deficits. Additionally, we found an abnormal responsiveness of cholinergic interneurons to D2R activation, consisting in an excitatory response rather than the expected inhibition, further confirming an imbalance between dopaminergic and cholinergic signaling in the striatum. Conversely, synaptic activity and plasticity in the CA1 hippocampal region were unaltered in Tor1a+/Δgag mice. Importantly, the M1 mAChR-dependent enhancement of hippocampal LTP was unaffected in both genotypes. Similarly, both basic properties of dopaminergic nigral neurons and their responses to D2R activation were normal.These results provide evidence for a regional specificity of the electrophysiological abnormalities observed and demonstrate the reproducibility of such alterations in distinct models of DYT1 dystonia. Dystonia Striatum D2 dopamine receptor Long-term depression Long-term potentiation Cholinergic interneurons Neurosciences. Biological psychiatry. Neuropsychiatry M. Maltese verfasserin aut R. Nisticò verfasserin aut T. Schirinzi verfasserin aut G. Madeo verfasserin aut G. Sciamanna verfasserin aut G. Ponterio verfasserin aut A. Tassone verfasserin aut G. Mandolesi verfasserin aut V. Vanni verfasserin aut M. Pignatelli verfasserin aut P. Bonsi verfasserin aut A. Pisani verfasserin aut In Neurobiology of Disease Elsevier, 2021 65(2014), Seite 124-132 (DE-627)268125414 (DE-600)1471408-5 1095953X nnns volume:65 year:2014 pages:124-132 https://doi.org/10.1016/j.nbd.2014.01.016 kostenfrei https://doaj.org/article/2b4ede7036b24ed68c2447fa7ce7403a kostenfrei http://www.sciencedirect.com/science/article/pii/S0969996114000308 kostenfrei https://doaj.org/toc/1095-953X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_165 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2010 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4700 AR 65 2014 124-132
allfieldsSound	10.1016/j.nbd.2014.01.016 doi (DE-627)DOAJ056729952 (DE-599)DOAJ2b4ede7036b24ed68c2447fa7ce7403a DE-627 ger DE-627 rakwb eng RC321-571 G. Martella verfasserin aut Regional specificity of synaptic plasticity deficits in a knock-in mouse model of DYT1 dystonia 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier DYT1 dystonia is a movement disorder caused by a deletion in the C-terminal of the protein torsinA. It is unclear how torsinA mutation might disrupt cellular processes encoding motor activity, and whether this impairment occurs in specific brain regions. Here, we report a selective impairment of corticostriatal synaptic plasticity in knock-in mice heterozygous for Δ-torsinA (Tor1a+/Δgag mice) as compared to controls (Tor1a+/+ mice). In striatal spiny neurons from Tor1a+/Δgag mice, high-frequency stimulation failed to induce long-term depression (LTD), whereas long-term potentiation (LTP) exhibited increased amplitude. Of interest, blockade of D2 dopamine receptors (D2Rs) increased LTP in Tor1a+/+ mice to a level comparable to that measured in Tor1a+/Δgag mice and normalized the levels of potentiation across mouse groups. A low-frequency stimulation (LFS) protocol was unable to depotentiate corticostriatal synapses in Tor1a+/Δgag mice. Muscarinic M1 acetylcholine receptor (mAChR) blockade rescued plasticity deficits. Additionally, we found an abnormal responsiveness of cholinergic interneurons to D2R activation, consisting in an excitatory response rather than the expected inhibition, further confirming an imbalance between dopaminergic and cholinergic signaling in the striatum. Conversely, synaptic activity and plasticity in the CA1 hippocampal region were unaltered in Tor1a+/Δgag mice. Importantly, the M1 mAChR-dependent enhancement of hippocampal LTP was unaffected in both genotypes. Similarly, both basic properties of dopaminergic nigral neurons and their responses to D2R activation were normal.These results provide evidence for a regional specificity of the electrophysiological abnormalities observed and demonstrate the reproducibility of such alterations in distinct models of DYT1 dystonia. Dystonia Striatum D2 dopamine receptor Long-term depression Long-term potentiation Cholinergic interneurons Neurosciences. Biological psychiatry. Neuropsychiatry M. Maltese verfasserin aut R. Nisticò verfasserin aut T. Schirinzi verfasserin aut G. Madeo verfasserin aut G. Sciamanna verfasserin aut G. Ponterio verfasserin aut A. Tassone verfasserin aut G. Mandolesi verfasserin aut V. Vanni verfasserin aut M. Pignatelli verfasserin aut P. Bonsi verfasserin aut A. Pisani verfasserin aut In Neurobiology of Disease Elsevier, 2021 65(2014), Seite 124-132 (DE-627)268125414 (DE-600)1471408-5 1095953X nnns volume:65 year:2014 pages:124-132 https://doi.org/10.1016/j.nbd.2014.01.016 kostenfrei https://doaj.org/article/2b4ede7036b24ed68c2447fa7ce7403a kostenfrei http://www.sciencedirect.com/science/article/pii/S0969996114000308 kostenfrei https://doaj.org/toc/1095-953X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_165 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2010 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4700 AR 65 2014 124-132
language	English
source	In Neurobiology of Disease 65(2014), Seite 124-132 volume:65 year:2014 pages:124-132
sourceStr	In Neurobiology of Disease 65(2014), Seite 124-132 volume:65 year:2014 pages:124-132
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Dystonia Striatum D2 dopamine receptor Long-term depression Long-term potentiation Cholinergic interneurons Neurosciences. Biological psychiatry. Neuropsychiatry
isfreeaccess_bool	true
container_title	Neurobiology of Disease
authorswithroles_txt_mv	G. Martella @@aut@@ M. Maltese @@aut@@ R. Nisticò @@aut@@ T. Schirinzi @@aut@@ G. Madeo @@aut@@ G. Sciamanna @@aut@@ G. Ponterio @@aut@@ A. Tassone @@aut@@ G. Mandolesi @@aut@@ V. Vanni @@aut@@ M. Pignatelli @@aut@@ P. Bonsi @@aut@@ A. Pisani @@aut@@
publishDateDaySort_date	2014-01-01T00:00:00Z
hierarchy_top_id	268125414
id	DOAJ056729952
language_de	englisch
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callnumber-first	R - Medicine
author	G. Martella
spellingShingle	G. Martella misc RC321-571 misc Dystonia misc Striatum misc D2 dopamine receptor misc Long-term depression misc Long-term potentiation misc Cholinergic interneurons misc Neurosciences. Biological psychiatry. Neuropsychiatry Regional specificity of synaptic plasticity deficits in a knock-in mouse model of DYT1 dystonia
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topic_title	RC321-571 Regional specificity of synaptic plasticity deficits in a knock-in mouse model of DYT1 dystonia Dystonia Striatum D2 dopamine receptor Long-term depression Long-term potentiation Cholinergic interneurons
topic	misc RC321-571 misc Dystonia misc Striatum misc D2 dopamine receptor misc Long-term depression misc Long-term potentiation misc Cholinergic interneurons misc Neurosciences. Biological psychiatry. Neuropsychiatry
topic_unstemmed	misc RC321-571 misc Dystonia misc Striatum misc D2 dopamine receptor misc Long-term depression misc Long-term potentiation misc Cholinergic interneurons misc Neurosciences. Biological psychiatry. Neuropsychiatry
topic_browse	misc RC321-571 misc Dystonia misc Striatum misc D2 dopamine receptor misc Long-term depression misc Long-term potentiation misc Cholinergic interneurons misc Neurosciences. Biological psychiatry. Neuropsychiatry
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title	Regional specificity of synaptic plasticity deficits in a knock-in mouse model of DYT1 dystonia
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title_full	Regional specificity of synaptic plasticity deficits in a knock-in mouse model of DYT1 dystonia
author_sort	G. Martella
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author_browse	G. Martella M. Maltese R. Nisticò T. Schirinzi G. Madeo G. Sciamanna G. Ponterio A. Tassone G. Mandolesi V. Vanni M. Pignatelli P. Bonsi A. Pisani
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title_sort	regional specificity of synaptic plasticity deficits in a knock-in mouse model of dyt1 dystonia
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title_auth	Regional specificity of synaptic plasticity deficits in a knock-in mouse model of DYT1 dystonia
abstract	DYT1 dystonia is a movement disorder caused by a deletion in the C-terminal of the protein torsinA. It is unclear how torsinA mutation might disrupt cellular processes encoding motor activity, and whether this impairment occurs in specific brain regions. Here, we report a selective impairment of corticostriatal synaptic plasticity in knock-in mice heterozygous for Δ-torsinA (Tor1a+/Δgag mice) as compared to controls (Tor1a+/+ mice). In striatal spiny neurons from Tor1a+/Δgag mice, high-frequency stimulation failed to induce long-term depression (LTD), whereas long-term potentiation (LTP) exhibited increased amplitude. Of interest, blockade of D2 dopamine receptors (D2Rs) increased LTP in Tor1a+/+ mice to a level comparable to that measured in Tor1a+/Δgag mice and normalized the levels of potentiation across mouse groups. A low-frequency stimulation (LFS) protocol was unable to depotentiate corticostriatal synapses in Tor1a+/Δgag mice. Muscarinic M1 acetylcholine receptor (mAChR) blockade rescued plasticity deficits. Additionally, we found an abnormal responsiveness of cholinergic interneurons to D2R activation, consisting in an excitatory response rather than the expected inhibition, further confirming an imbalance between dopaminergic and cholinergic signaling in the striatum. Conversely, synaptic activity and plasticity in the CA1 hippocampal region were unaltered in Tor1a+/Δgag mice. Importantly, the M1 mAChR-dependent enhancement of hippocampal LTP was unaffected in both genotypes. Similarly, both basic properties of dopaminergic nigral neurons and their responses to D2R activation were normal.These results provide evidence for a regional specificity of the electrophysiological abnormalities observed and demonstrate the reproducibility of such alterations in distinct models of DYT1 dystonia.
abstractGer	DYT1 dystonia is a movement disorder caused by a deletion in the C-terminal of the protein torsinA. It is unclear how torsinA mutation might disrupt cellular processes encoding motor activity, and whether this impairment occurs in specific brain regions. Here, we report a selective impairment of corticostriatal synaptic plasticity in knock-in mice heterozygous for Δ-torsinA (Tor1a+/Δgag mice) as compared to controls (Tor1a+/+ mice). In striatal spiny neurons from Tor1a+/Δgag mice, high-frequency stimulation failed to induce long-term depression (LTD), whereas long-term potentiation (LTP) exhibited increased amplitude. Of interest, blockade of D2 dopamine receptors (D2Rs) increased LTP in Tor1a+/+ mice to a level comparable to that measured in Tor1a+/Δgag mice and normalized the levels of potentiation across mouse groups. A low-frequency stimulation (LFS) protocol was unable to depotentiate corticostriatal synapses in Tor1a+/Δgag mice. Muscarinic M1 acetylcholine receptor (mAChR) blockade rescued plasticity deficits. Additionally, we found an abnormal responsiveness of cholinergic interneurons to D2R activation, consisting in an excitatory response rather than the expected inhibition, further confirming an imbalance between dopaminergic and cholinergic signaling in the striatum. Conversely, synaptic activity and plasticity in the CA1 hippocampal region were unaltered in Tor1a+/Δgag mice. Importantly, the M1 mAChR-dependent enhancement of hippocampal LTP was unaffected in both genotypes. Similarly, both basic properties of dopaminergic nigral neurons and their responses to D2R activation were normal.These results provide evidence for a regional specificity of the electrophysiological abnormalities observed and demonstrate the reproducibility of such alterations in distinct models of DYT1 dystonia.
abstract_unstemmed	DYT1 dystonia is a movement disorder caused by a deletion in the C-terminal of the protein torsinA. It is unclear how torsinA mutation might disrupt cellular processes encoding motor activity, and whether this impairment occurs in specific brain regions. Here, we report a selective impairment of corticostriatal synaptic plasticity in knock-in mice heterozygous for Δ-torsinA (Tor1a+/Δgag mice) as compared to controls (Tor1a+/+ mice). In striatal spiny neurons from Tor1a+/Δgag mice, high-frequency stimulation failed to induce long-term depression (LTD), whereas long-term potentiation (LTP) exhibited increased amplitude. Of interest, blockade of D2 dopamine receptors (D2Rs) increased LTP in Tor1a+/+ mice to a level comparable to that measured in Tor1a+/Δgag mice and normalized the levels of potentiation across mouse groups. A low-frequency stimulation (LFS) protocol was unable to depotentiate corticostriatal synapses in Tor1a+/Δgag mice. Muscarinic M1 acetylcholine receptor (mAChR) blockade rescued plasticity deficits. Additionally, we found an abnormal responsiveness of cholinergic interneurons to D2R activation, consisting in an excitatory response rather than the expected inhibition, further confirming an imbalance between dopaminergic and cholinergic signaling in the striatum. Conversely, synaptic activity and plasticity in the CA1 hippocampal region were unaltered in Tor1a+/Δgag mice. Importantly, the M1 mAChR-dependent enhancement of hippocampal LTP was unaffected in both genotypes. Similarly, both basic properties of dopaminergic nigral neurons and their responses to D2R activation were normal.These results provide evidence for a regional specificity of the electrophysiological abnormalities observed and demonstrate the reproducibility of such alterations in distinct models of DYT1 dystonia.
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title_short	Regional specificity of synaptic plasticity deficits in a knock-in mouse model of DYT1 dystonia
url	https://doi.org/10.1016/j.nbd.2014.01.016 https://doaj.org/article/2b4ede7036b24ed68c2447fa7ce7403a http://www.sciencedirect.com/science/article/pii/S0969996114000308 https://doaj.org/toc/1095-953X
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up_date	2024-07-03T22:32:19.335Z
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fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ056729952</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230501172705.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2014 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.nbd.2014.01.016</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ056729952</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ2b4ede7036b24ed68c2447fa7ce7403a</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC321-571</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">G. Martella</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Regional specificity of synaptic plasticity deficits in a knock-in mouse model of DYT1 dystonia</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2014</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">DYT1 dystonia is a movement disorder caused by a deletion in the C-terminal of the protein torsinA. It is unclear how torsinA mutation might disrupt cellular processes encoding motor activity, and whether this impairment occurs in specific brain regions. Here, we report a selective impairment of corticostriatal synaptic plasticity in knock-in mice heterozygous for Δ-torsinA (Tor1a+/Δgag mice) as compared to controls (Tor1a+/+ mice). In striatal spiny neurons from Tor1a+/Δgag mice, high-frequency stimulation failed to induce long-term depression (LTD), whereas long-term potentiation (LTP) exhibited increased amplitude. Of interest, blockade of D2 dopamine receptors (D2Rs) increased LTP in Tor1a+/+ mice to a level comparable to that measured in Tor1a+/Δgag mice and normalized the levels of potentiation across mouse groups. A low-frequency stimulation (LFS) protocol was unable to depotentiate corticostriatal synapses in Tor1a+/Δgag mice. Muscarinic M1 acetylcholine receptor (mAChR) blockade rescued plasticity deficits. Additionally, we found an abnormal responsiveness of cholinergic interneurons to D2R activation, consisting in an excitatory response rather than the expected inhibition, further confirming an imbalance between dopaminergic and cholinergic signaling in the striatum. Conversely, synaptic activity and plasticity in the CA1 hippocampal region were unaltered in Tor1a+/Δgag mice. Importantly, the M1 mAChR-dependent enhancement of hippocampal LTP was unaffected in both genotypes. Similarly, both basic properties of dopaminergic nigral neurons and their responses to D2R activation were normal.These results provide evidence for a regional specificity of the electrophysiological abnormalities observed and demonstrate the reproducibility of such alterations in distinct models of DYT1 dystonia.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Dystonia</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Striatum</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">D2 dopamine receptor</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Long-term depression</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Long-term potentiation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cholinergic interneurons</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Neurosciences. Biological psychiatry. Neuropsychiatry</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">M. Maltese</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">R. Nisticò</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">T. Schirinzi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">G. Madeo</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">G. Sciamanna</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">G. 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Regional specificity of synaptic plasticity deficits in a knock-in mouse model of DYT1 dystonia

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