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Sensory experience regulates cortical inhibition by inducing IGF1 in VIP neurons (2016)

A. R. Mardinly; I. Spiegel; A. Patrizi; E. Centofante; J. E. Bazinet; C. P. Tzeng; C. Mandel-Brehm; D. A. Harmin; H. Adesnik; M. Fagiolini; M. E. Greenberg

Springer Nature

In: Nature

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Publication Date: 2016-03-17

Description: Sensory experience regulates cortical inhibition by inducing IGF1 in VIP neurons Nature 531, 7594 (2016). doi:10.1038/nature17187 Authors: A. R. Mardinly, I. Spiegel, A. Patrizi, E. Centofante, J. E. Bazinet, C. P. Tzeng, C. Mandel-Brehm, D. A. Harmin, H. Adesnik, M. Fagiolini & M. E. Greenberg Inhibitory neurons regulate the adaptation of neural circuits to sensory experience, but the molecular mechanisms by which experience controls the connectivity between different types of inhibitory neuron to regulate cortical plasticity are largely unknown. Here we show that exposure of dark-housed mice to light induces a gene program in cortical vasoactive intestinal peptide (VIP)-expressing neurons that is markedly distinct from that induced in excitatory neurons and other subtypes of inhibitory neuron. We identify Igf1 as one of several activity-regulated genes that are specific to VIP neurons, and demonstrate that IGF1 functions cell-autonomously in VIP neurons to increase inhibitory synaptic input onto these neurons. Our findings further suggest that in cortical VIP neurons, experience-dependent gene transcription regulates visual acuity by activating the expression of IGF1, thus promoting the inhibition of disinhibitory neurons and affecting inhibition onto cortical pyramidal neurons.

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Published by Springer Nature

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Sensory experience regulates cortical inhibition by inducing IGF1 in VIP neurons (2016)

A. R. Mardinly ; I. Spiegel ; A. Patrizi ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 531(7594): 371-5. doi: 10.1038/nature17187.

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Publication Date: 2016-03-10

Description: Inhibitory neurons regulate the adaptation of neural circuits to sensory experience, but the molecular mechanisms by which experience controls the connectivity between different types of inhibitory neuron to regulate cortical plasticity are largely unknown. Here we show that exposure of dark-housed mice to light induces a gene program in cortical vasoactive intestinal peptide (VIP)-expressing neurons that is markedly distinct from that induced in excitatory neurons and other subtypes of inhibitory neuron. We identify Igf1 as one of several activity-regulated genes that are specific to VIP neurons, and demonstrate that IGF1 functions cell-autonomously in VIP neurons to increase inhibitory synaptic input onto these neurons. Our findings further suggest that in cortical VIP neurons, experience-dependent gene transcription regulates visual acuity by activating the expression of IGF1, thus promoting the inhibition of disinhibitory neurons and affecting inhibition onto cortical pyramidal neurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4823817/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4823817/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mardinly, A R -- Spiegel, I -- Patrizi, A -- Centofante, E -- Bazinet, J E -- Tzeng, C P -- Mandel-Brehm, C -- Harmin, D A -- Adesnik, H -- Fagiolini, M -- Greenberg, M E -- P01 NS047572/NS/NINDS NIH HHS/ -- P30 HD018655/HD/NICHD NIH HHS/ -- R01 NS028829/NS/NINDS NIH HHS/ -- R37 NS028829/NS/NINDS NIH HHS/ -- England -- Nature. 2016 Mar 17;531(7594):371-5. doi: 10.1038/nature17187. Epub 2016 Mar 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, University of California Berkeley, 205 Life Sciences Addition, Berkeley, California 94720, USA. ; Department of Neurobiology, Harvard Medical School, 220 Longwood Ave, Boston, Massachusetts 02115, USA. ; FM Kirby Neurobiology Center, Boston Children's Hospital, 3 Blackfan Circle, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26958833" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Female ; Insulin-Like Growth Factor I/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; *Neural Inhibition ; Neural Pathways ; Neuronal Plasticity ; Neurons/cytology/*metabolism/secretion ; Pyramidal Cells/metabolism ; Synapses/metabolism ; Vasoactive Intestinal Peptide/*metabolism ; Vision, Ocular/physiology ; Visual Cortex/*cytology/*physiology

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Published by Nature Publishing Group (NPG)

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Widespread transcription at neuronal activity-regulated enhancers (2010)

T. K. Kim ; M. Hemberg ; J. M. Gray ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 465(7295): 182-7. doi: 10.1038/nature09033.

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Publication Date: 2010-04-16

Description: We used genome-wide sequencing methods to study stimulus-dependent enhancer function in mouse cortical neurons. We identified approximately 12,000 neuronal activity-regulated enhancers that are bound by the general transcriptional co-activator CBP in an activity-dependent manner. A function of CBP at enhancers may be to recruit RNA polymerase II (RNAPII), as we also observed activity-regulated RNAPII binding to thousands of enhancers. Notably, RNAPII at enhancers transcribes bi-directionally a novel class of enhancer RNAs (eRNAs) within enhancer domains defined by the presence of histone H3 monomethylated at lysine 4. The level of eRNA expression at neuronal enhancers positively correlates with the level of messenger RNA synthesis at nearby genes, suggesting that eRNA synthesis occurs specifically at enhancers that are actively engaged in promoting mRNA synthesis. These findings reveal that a widespread mechanism of enhancer activation involves RNAPII binding and eRNA synthesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3020079/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3020079/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Tae-Kyung -- Hemberg, Martin -- Gray, Jesse M -- Costa, Allen M -- Bear, Daniel M -- Wu, Jing -- Harmin, David A -- Laptewicz, Mike -- Barbara-Haley, Kellie -- Kuersten, Scott -- Markenscoff-Papadimitriou, Eirene -- Kuhl, Dietmar -- Bito, Haruhiko -- Worley, Paul F -- Kreiman, Gabriel -- Greenberg, Michael E -- DP2OD006461/OD/NIH HHS/ -- MH-053608/MH/NIMH NIH HHS/ -- NS028829/NS/NINDS NIH HHS/ -- P30 HD018655/HD/NICHD NIH HHS/ -- P30 HD018655-25/HD/NICHD NIH HHS/ -- P30 HD018655-26/HD/NICHD NIH HHS/ -- P30 HD018655-27/HD/NICHD NIH HHS/ -- R01 NS028829/NS/NINDS NIH HHS/ -- R21EY019710/EY/NEI NIH HHS/ -- R37 NS028829/NS/NINDS NIH HHS/ -- R37 NS028829-12/NS/NINDS NIH HHS/ -- R37 NS028829-13/NS/NINDS NIH HHS/ -- R37 NS028829-14/NS/NINDS NIH HHS/ -- R37 NS028829-15/NS/NINDS NIH HHS/ -- R37 NS028829-16/NS/NINDS NIH HHS/ -- R37 NS028829-17/NS/NINDS NIH HHS/ -- England -- Nature. 2010 May 13;465(7295):182-7. doi: 10.1038/nature09033. Epub 2010 Apr 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20393465" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; CREB-Binding Protein/metabolism ; Consensus Sequence/genetics ; Cytoskeletal Proteins/genetics ; Enhancer Elements, Genetic/*genetics ; Gene Expression Regulation/*genetics ; Genes, Reporter ; Genes, fos/genetics ; Histones/metabolism ; Methylation ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/genetics ; Neurons/*metabolism ; RNA Polymerase II/metabolism ; RNA, Untranslated/biosynthesis/genetics ; Transcription, Genetic/*genetics

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Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Published by Nature Publishing Group (NPG)

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Disruption of DNA-methylation-dependent long gene repression in Rett syndrome (2015)

H. W. Gabel ; B. Kinde ; H. Stroud ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 522(7554): 89-93. doi: 10.1038/nature14319.

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Publication Date: 2015-03-13

Description: Disruption of the MECP2 gene leads to Rett syndrome (RTT), a severe neurological disorder with features of autism. MECP2 encodes a methyl-DNA-binding protein that has been proposed to function as a transcriptional repressor, but despite numerous mouse studies examining neuronal gene expression in Mecp2 mutants, no clear model has emerged for how MeCP2 protein regulates transcription. Here we identify a genome-wide length-dependent increase in gene expression in MeCP2 mutant mouse models and human RTT brains. We present evidence that MeCP2 represses gene expression by binding to methylated CA sites within long genes, and that in neurons lacking MeCP2, decreasing the expression of long genes attenuates RTT-associated cellular deficits. In addition, we find that long genes as a population are enriched for neuronal functions and selectively expressed in the brain. These findings suggest that mutations in MeCP2 may cause neurological dysfunction by specifically disrupting long gene expression in the brain.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4480648/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4480648/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gabel, Harrison W -- Kinde, Benyam -- Stroud, Hume -- Gilbert, Caitlin S -- Harmin, David A -- Kastan, Nathaniel R -- Hemberg, Martin -- Ebert, Daniel H -- Greenberg, Michael E -- 1R01NS048276/NS/NINDS NIH HHS/ -- P30 HD018655/HD/NICHD NIH HHS/ -- R01 NS048276/NS/NINDS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- T32GM007753/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Jun 4;522(7554):89-93. doi: 10.1038/nature14319. Epub 2015 Mar 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Department of Ophthalmology, Children's Hospital Boston, Center for Brain Science and Swartz Center for Theoretical Neuroscience, Harvard University, 300 Longwood Avenue, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25762136" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Base Sequence ; Brain/metabolism ; DNA (Cytosine-5-)-Methyltransferase/metabolism ; DNA Methylation/*genetics ; Disease Models, Animal ; Female ; Gene Expression Regulation ; Humans ; Male ; Methyl-CpG-Binding Protein 2/deficiency/*genetics/*metabolism ; Mice ; Molecular Sequence Data ; Mutation/*genetics ; Neurons/metabolism ; Rett Syndrome/*genetics

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Published by Nature Publishing Group (NPG)

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