In vivo synaptic transmission and morphology in mouse models of Tuberous sclerosis, Fragile X syndrome, Neurofibromatosis type 1 and Costello syndrome.

Defects in the rat sarcoma viral oncogene homolog (Ras)/extracellular-signal-regulated kinase (ERK) and the phosphatidylinositol 3-kinase (PI3K)-mammalian target of rapamycin (mTOR) signaling pathways are responsible for several neurodevelopmental disorders. These disorders are an important cause fo...
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Gespeichert in:

Autor*in:	Tiantian eWang [verfasserIn] Laura eKok [verfasserIn] Rob eWillemsen [verfasserIn] Ype eElgersma [verfasserIn] Gerard eBorst [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2015

Schlagwörter:	Intellectual Disability Synaptic Transmission H-ras short-term plasticity Autism Spectrum Disorders calyx of held

Übergeordnetes Werk:	In: Frontiers in Cellular Neuroscience - Frontiers Media S.A., 2008, 9(2015)
Übergeordnetes Werk:	volume:9 ; year:2015

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fncel.2015.00234

Katalog-ID:	DOAJ009520759

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spelling	10.3389/fncel.2015.00234 doi (DE-627)DOAJ009520759 (DE-599)DOAJ722763f718b242baa7db57571f23f74c DE-627 ger DE-627 rakwb eng RC321-571 Tiantian eWang verfasserin aut In vivo synaptic transmission and morphology in mouse models of Tuberous sclerosis, Fragile X syndrome, Neurofibromatosis type 1 and Costello syndrome. 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Defects in the rat sarcoma viral oncogene homolog (Ras)/extracellular-signal-regulated kinase (ERK) and the phosphatidylinositol 3-kinase (PI3K)-mammalian target of rapamycin (mTOR) signaling pathways are responsible for several neurodevelopmental disorders. These disorders are an important cause for intellectual disability; additional manifestations include autism spectrum disorder, seizures and brain malformations. Changes in synaptic function are thought to underlie the neurological conditions associated with these syndromes. We therefore studied morphology and in vivo synaptic transmission of the calyx of Held synapse, a relay synapse in the medial nucleus of the trapezoid body (MNTB) of the auditory brainstem, in mouse models of Tuberous sclerosis (TSC), Fragile X syndrome (FXS), Neurofibromatosis type 1 (NF1) and Costello syndrome (CS). Calyces from both Tsc1+/- and from Fmr1 knock-out (KO) mice showed increased volume and surface area compared to wild-type (WT) controls. In addition, in Fmr1 KO animals a larger fraction of calyces showed complex morphology. In MNTB principal neurons of Nf1+/- mice the average delay between EPSPs and APs was slightly smaller compared to wild-type controls, which could indicate an increased excitability. Otherwise, no obvious changes in synaptic transmission or short-term plasticity were observed during juxtacellular recordings in any of the four lines. Our results in these four mutants thus indicate that abnormalities of mTOR or Ras signaling do not necessarily result in changes in in vivo synaptic transmission. Intellectual Disability Synaptic Transmission H-ras short-term plasticity Autism Spectrum Disorders calyx of held Neurosciences. Biological psychiatry. Neuropsychiatry Laura eKok verfasserin aut Rob eWillemsen verfasserin aut Ype eElgersma verfasserin aut Ype eElgersma verfasserin aut Gerard eBorst verfasserin aut In Frontiers in Cellular Neuroscience Frontiers Media S.A., 2008 9(2015) (DE-627)579826414 (DE-600)2452963-1 16625102 nnns volume:9 year:2015 https://doi.org/10.3389/fncel.2015.00234 kostenfrei https://doaj.org/article/722763f718b242baa7db57571f23f74c kostenfrei http://journal.frontiersin.org/Journal/10.3389/fncel.2015.00234/full kostenfrei https://doaj.org/toc/1662-5102 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2015
allfields_unstemmed	10.3389/fncel.2015.00234 doi (DE-627)DOAJ009520759 (DE-599)DOAJ722763f718b242baa7db57571f23f74c DE-627 ger DE-627 rakwb eng RC321-571 Tiantian eWang verfasserin aut In vivo synaptic transmission and morphology in mouse models of Tuberous sclerosis, Fragile X syndrome, Neurofibromatosis type 1 and Costello syndrome. 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Defects in the rat sarcoma viral oncogene homolog (Ras)/extracellular-signal-regulated kinase (ERK) and the phosphatidylinositol 3-kinase (PI3K)-mammalian target of rapamycin (mTOR) signaling pathways are responsible for several neurodevelopmental disorders. These disorders are an important cause for intellectual disability; additional manifestations include autism spectrum disorder, seizures and brain malformations. Changes in synaptic function are thought to underlie the neurological conditions associated with these syndromes. We therefore studied morphology and in vivo synaptic transmission of the calyx of Held synapse, a relay synapse in the medial nucleus of the trapezoid body (MNTB) of the auditory brainstem, in mouse models of Tuberous sclerosis (TSC), Fragile X syndrome (FXS), Neurofibromatosis type 1 (NF1) and Costello syndrome (CS). Calyces from both Tsc1+/- and from Fmr1 knock-out (KO) mice showed increased volume and surface area compared to wild-type (WT) controls. In addition, in Fmr1 KO animals a larger fraction of calyces showed complex morphology. In MNTB principal neurons of Nf1+/- mice the average delay between EPSPs and APs was slightly smaller compared to wild-type controls, which could indicate an increased excitability. Otherwise, no obvious changes in synaptic transmission or short-term plasticity were observed during juxtacellular recordings in any of the four lines. Our results in these four mutants thus indicate that abnormalities of mTOR or Ras signaling do not necessarily result in changes in in vivo synaptic transmission. Intellectual Disability Synaptic Transmission H-ras short-term plasticity Autism Spectrum Disorders calyx of held Neurosciences. Biological psychiatry. Neuropsychiatry Laura eKok verfasserin aut Rob eWillemsen verfasserin aut Ype eElgersma verfasserin aut Ype eElgersma verfasserin aut Gerard eBorst verfasserin aut In Frontiers in Cellular Neuroscience Frontiers Media S.A., 2008 9(2015) (DE-627)579826414 (DE-600)2452963-1 16625102 nnns volume:9 year:2015 https://doi.org/10.3389/fncel.2015.00234 kostenfrei https://doaj.org/article/722763f718b242baa7db57571f23f74c kostenfrei http://journal.frontiersin.org/Journal/10.3389/fncel.2015.00234/full kostenfrei https://doaj.org/toc/1662-5102 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2015
allfieldsGer	10.3389/fncel.2015.00234 doi (DE-627)DOAJ009520759 (DE-599)DOAJ722763f718b242baa7db57571f23f74c DE-627 ger DE-627 rakwb eng RC321-571 Tiantian eWang verfasserin aut In vivo synaptic transmission and morphology in mouse models of Tuberous sclerosis, Fragile X syndrome, Neurofibromatosis type 1 and Costello syndrome. 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Defects in the rat sarcoma viral oncogene homolog (Ras)/extracellular-signal-regulated kinase (ERK) and the phosphatidylinositol 3-kinase (PI3K)-mammalian target of rapamycin (mTOR) signaling pathways are responsible for several neurodevelopmental disorders. These disorders are an important cause for intellectual disability; additional manifestations include autism spectrum disorder, seizures and brain malformations. Changes in synaptic function are thought to underlie the neurological conditions associated with these syndromes. We therefore studied morphology and in vivo synaptic transmission of the calyx of Held synapse, a relay synapse in the medial nucleus of the trapezoid body (MNTB) of the auditory brainstem, in mouse models of Tuberous sclerosis (TSC), Fragile X syndrome (FXS), Neurofibromatosis type 1 (NF1) and Costello syndrome (CS). Calyces from both Tsc1+/- and from Fmr1 knock-out (KO) mice showed increased volume and surface area compared to wild-type (WT) controls. In addition, in Fmr1 KO animals a larger fraction of calyces showed complex morphology. In MNTB principal neurons of Nf1+/- mice the average delay between EPSPs and APs was slightly smaller compared to wild-type controls, which could indicate an increased excitability. Otherwise, no obvious changes in synaptic transmission or short-term plasticity were observed during juxtacellular recordings in any of the four lines. Our results in these four mutants thus indicate that abnormalities of mTOR or Ras signaling do not necessarily result in changes in in vivo synaptic transmission. Intellectual Disability Synaptic Transmission H-ras short-term plasticity Autism Spectrum Disorders calyx of held Neurosciences. Biological psychiatry. Neuropsychiatry Laura eKok verfasserin aut Rob eWillemsen verfasserin aut Ype eElgersma verfasserin aut Ype eElgersma verfasserin aut Gerard eBorst verfasserin aut In Frontiers in Cellular Neuroscience Frontiers Media S.A., 2008 9(2015) (DE-627)579826414 (DE-600)2452963-1 16625102 nnns volume:9 year:2015 https://doi.org/10.3389/fncel.2015.00234 kostenfrei https://doaj.org/article/722763f718b242baa7db57571f23f74c kostenfrei http://journal.frontiersin.org/Journal/10.3389/fncel.2015.00234/full kostenfrei https://doaj.org/toc/1662-5102 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2015
allfieldsSound	10.3389/fncel.2015.00234 doi (DE-627)DOAJ009520759 (DE-599)DOAJ722763f718b242baa7db57571f23f74c DE-627 ger DE-627 rakwb eng RC321-571 Tiantian eWang verfasserin aut In vivo synaptic transmission and morphology in mouse models of Tuberous sclerosis, Fragile X syndrome, Neurofibromatosis type 1 and Costello syndrome. 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Defects in the rat sarcoma viral oncogene homolog (Ras)/extracellular-signal-regulated kinase (ERK) and the phosphatidylinositol 3-kinase (PI3K)-mammalian target of rapamycin (mTOR) signaling pathways are responsible for several neurodevelopmental disorders. These disorders are an important cause for intellectual disability; additional manifestations include autism spectrum disorder, seizures and brain malformations. Changes in synaptic function are thought to underlie the neurological conditions associated with these syndromes. We therefore studied morphology and in vivo synaptic transmission of the calyx of Held synapse, a relay synapse in the medial nucleus of the trapezoid body (MNTB) of the auditory brainstem, in mouse models of Tuberous sclerosis (TSC), Fragile X syndrome (FXS), Neurofibromatosis type 1 (NF1) and Costello syndrome (CS). Calyces from both Tsc1+/- and from Fmr1 knock-out (KO) mice showed increased volume and surface area compared to wild-type (WT) controls. In addition, in Fmr1 KO animals a larger fraction of calyces showed complex morphology. In MNTB principal neurons of Nf1+/- mice the average delay between EPSPs and APs was slightly smaller compared to wild-type controls, which could indicate an increased excitability. Otherwise, no obvious changes in synaptic transmission or short-term plasticity were observed during juxtacellular recordings in any of the four lines. Our results in these four mutants thus indicate that abnormalities of mTOR or Ras signaling do not necessarily result in changes in in vivo synaptic transmission. Intellectual Disability Synaptic Transmission H-ras short-term plasticity Autism Spectrum Disorders calyx of held Neurosciences. Biological psychiatry. Neuropsychiatry Laura eKok verfasserin aut Rob eWillemsen verfasserin aut Ype eElgersma verfasserin aut Ype eElgersma verfasserin aut Gerard eBorst verfasserin aut In Frontiers in Cellular Neuroscience Frontiers Media S.A., 2008 9(2015) (DE-627)579826414 (DE-600)2452963-1 16625102 nnns volume:9 year:2015 https://doi.org/10.3389/fncel.2015.00234 kostenfrei https://doaj.org/article/722763f718b242baa7db57571f23f74c kostenfrei http://journal.frontiersin.org/Journal/10.3389/fncel.2015.00234/full kostenfrei https://doaj.org/toc/1662-5102 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2015
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callnumber-first	R - Medicine
author	Tiantian eWang
spellingShingle	Tiantian eWang misc RC321-571 misc Intellectual Disability misc Synaptic Transmission misc H-ras misc short-term plasticity misc Autism Spectrum Disorders misc calyx of held misc Neurosciences. Biological psychiatry. Neuropsychiatry In vivo synaptic transmission and morphology in mouse models of Tuberous sclerosis, Fragile X syndrome, Neurofibromatosis type 1 and Costello syndrome.
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topic_title	RC321-571 In vivo synaptic transmission and morphology in mouse models of Tuberous sclerosis, Fragile X syndrome, Neurofibromatosis type 1 and Costello syndrome Intellectual Disability Synaptic Transmission H-ras short-term plasticity Autism Spectrum Disorders calyx of held
topic	misc RC321-571 misc Intellectual Disability misc Synaptic Transmission misc H-ras misc short-term plasticity misc Autism Spectrum Disorders misc calyx of held misc Neurosciences. Biological psychiatry. Neuropsychiatry
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title	In vivo synaptic transmission and morphology in mouse models of Tuberous sclerosis, Fragile X syndrome, Neurofibromatosis type 1 and Costello syndrome.
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title_full	In vivo synaptic transmission and morphology in mouse models of Tuberous sclerosis, Fragile X syndrome, Neurofibromatosis type 1 and Costello syndrome
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title_sort	in vivo synaptic transmission and morphology in mouse models of tuberous sclerosis, fragile x syndrome, neurofibromatosis type 1 and costello syndrome
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title_auth	In vivo synaptic transmission and morphology in mouse models of Tuberous sclerosis, Fragile X syndrome, Neurofibromatosis type 1 and Costello syndrome.
abstract	Defects in the rat sarcoma viral oncogene homolog (Ras)/extracellular-signal-regulated kinase (ERK) and the phosphatidylinositol 3-kinase (PI3K)-mammalian target of rapamycin (mTOR) signaling pathways are responsible for several neurodevelopmental disorders. These disorders are an important cause for intellectual disability; additional manifestations include autism spectrum disorder, seizures and brain malformations. Changes in synaptic function are thought to underlie the neurological conditions associated with these syndromes. We therefore studied morphology and in vivo synaptic transmission of the calyx of Held synapse, a relay synapse in the medial nucleus of the trapezoid body (MNTB) of the auditory brainstem, in mouse models of Tuberous sclerosis (TSC), Fragile X syndrome (FXS), Neurofibromatosis type 1 (NF1) and Costello syndrome (CS). Calyces from both Tsc1+/- and from Fmr1 knock-out (KO) mice showed increased volume and surface area compared to wild-type (WT) controls. In addition, in Fmr1 KO animals a larger fraction of calyces showed complex morphology. In MNTB principal neurons of Nf1+/- mice the average delay between EPSPs and APs was slightly smaller compared to wild-type controls, which could indicate an increased excitability. Otherwise, no obvious changes in synaptic transmission or short-term plasticity were observed during juxtacellular recordings in any of the four lines. Our results in these four mutants thus indicate that abnormalities of mTOR or Ras signaling do not necessarily result in changes in in vivo synaptic transmission.
abstractGer	Defects in the rat sarcoma viral oncogene homolog (Ras)/extracellular-signal-regulated kinase (ERK) and the phosphatidylinositol 3-kinase (PI3K)-mammalian target of rapamycin (mTOR) signaling pathways are responsible for several neurodevelopmental disorders. These disorders are an important cause for intellectual disability; additional manifestations include autism spectrum disorder, seizures and brain malformations. Changes in synaptic function are thought to underlie the neurological conditions associated with these syndromes. We therefore studied morphology and in vivo synaptic transmission of the calyx of Held synapse, a relay synapse in the medial nucleus of the trapezoid body (MNTB) of the auditory brainstem, in mouse models of Tuberous sclerosis (TSC), Fragile X syndrome (FXS), Neurofibromatosis type 1 (NF1) and Costello syndrome (CS). Calyces from both Tsc1+/- and from Fmr1 knock-out (KO) mice showed increased volume and surface area compared to wild-type (WT) controls. In addition, in Fmr1 KO animals a larger fraction of calyces showed complex morphology. In MNTB principal neurons of Nf1+/- mice the average delay between EPSPs and APs was slightly smaller compared to wild-type controls, which could indicate an increased excitability. Otherwise, no obvious changes in synaptic transmission or short-term plasticity were observed during juxtacellular recordings in any of the four lines. Our results in these four mutants thus indicate that abnormalities of mTOR or Ras signaling do not necessarily result in changes in in vivo synaptic transmission.
abstract_unstemmed	Defects in the rat sarcoma viral oncogene homolog (Ras)/extracellular-signal-regulated kinase (ERK) and the phosphatidylinositol 3-kinase (PI3K)-mammalian target of rapamycin (mTOR) signaling pathways are responsible for several neurodevelopmental disorders. These disorders are an important cause for intellectual disability; additional manifestations include autism spectrum disorder, seizures and brain malformations. Changes in synaptic function are thought to underlie the neurological conditions associated with these syndromes. We therefore studied morphology and in vivo synaptic transmission of the calyx of Held synapse, a relay synapse in the medial nucleus of the trapezoid body (MNTB) of the auditory brainstem, in mouse models of Tuberous sclerosis (TSC), Fragile X syndrome (FXS), Neurofibromatosis type 1 (NF1) and Costello syndrome (CS). Calyces from both Tsc1+/- and from Fmr1 knock-out (KO) mice showed increased volume and surface area compared to wild-type (WT) controls. In addition, in Fmr1 KO animals a larger fraction of calyces showed complex morphology. In MNTB principal neurons of Nf1+/- mice the average delay between EPSPs and APs was slightly smaller compared to wild-type controls, which could indicate an increased excitability. Otherwise, no obvious changes in synaptic transmission or short-term plasticity were observed during juxtacellular recordings in any of the four lines. Our results in these four mutants thus indicate that abnormalities of mTOR or Ras signaling do not necessarily result in changes in in vivo synaptic transmission.
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title_short	In vivo synaptic transmission and morphology in mouse models of Tuberous sclerosis, Fragile X syndrome, Neurofibromatosis type 1 and Costello syndrome.
url	https://doi.org/10.3389/fncel.2015.00234 https://doaj.org/article/722763f718b242baa7db57571f23f74c http://journal.frontiersin.org/Journal/10.3389/fncel.2015.00234/full https://doaj.org/toc/1662-5102
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In vivo synaptic transmission and morphology in mouse models of Tuberous sclerosis, Fragile X syndrome, Neurofibromatosis type 1 and Costello syndrome.

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