Publications by authors named "Sebnem N Tuncdemir"

5 Publications

  • Page 1 of 1

Early Somatostatin Interneuron Connectivity Mediates the Maturation of Deep Layer Cortical Circuits.

Neuron 2016 Feb;89(3):521-35

NYU Neuroscience Institute and the Department of Neuroscience and Physiology, Smilow Research Center, New York University School of Medicine, 522 First Avenue, New York, NY 10016, USA. Electronic address:

The precise connectivity of somatostatin and parvalbumin cortical interneurons is generated during development. An understanding of how these interneuron classes incorporate into cortical circuitry is incomplete but essential to elucidate the roles they play during maturation. Here, we report that somatostatin interneurons in infragranular layers receive dense but transient innervation from thalamocortical afferents during the first postnatal week. During this period, parvalbumin interneurons and pyramidal neurons within the same layers receive weaker thalamocortical inputs, yet are strongly innervated by somatostatin interneurons. Further, upon disruption of the early (but not late) somatostatin interneuron network, the synaptic maturation of thalamocortical inputs onto parvalbumin interneurons is perturbed. These results suggest that infragranular somatostatin interneurons exhibit a transient early synaptic connectivity that is essential for the establishment of thalamic feedforward inhibition mediated by parvalbumin interneurons.
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http://dx.doi.org/10.1016/j.neuron.2015.11.020DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4861073PMC
February 2016

Sensory inputs control the integration of neurogliaform interneurons into cortical circuits.

Nat Neurosci 2015 Mar 9;18(3):393-401. Epub 2015 Feb 9.

1] NYU Neuroscience Institute, New York Langone Medical Center, New York, New York, USA. [2] Department of Neuroscience and Physiology, New York Langone Medical Center, New York, New York, USA. [3] Department of Neural Science, New York University, New York, New York, USA.

Neuronal microcircuits in the superficial layers of the mammalian cortex provide the substrate for associative cortical computation. Inhibitory interneurons constitute an essential component of the circuitry and are fundamental to the integration of local and long-range information. Here we report that, during early development, superficially positioned Reelin-expressing neurogliaform interneurons in the mouse somatosensory cortex receive afferent innervation from both cortical and thalamic excitatory sources. Attenuation of ascending sensory, but not intracortical, excitation leads to axo-dendritic morphological defects in these interneurons. Moreover, abrogation of the NMDA receptors through which the thalamic inputs signal results in a similar phenotype, as well as in the selective loss of thalamic and a concomitant increase in intracortical connectivity. These results suggest that thalamic inputs are critical in determining the balance between local and long-range connectivity and are fundamental to the proper integration of Reelin-expressing interneurons into nascent cortical circuits.
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http://dx.doi.org/10.1038/nn.3946DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4624196PMC
March 2015

miRNAs are Essential for the Survival and Maturation of Cortical Interneurons.

Cereb Cortex 2015 Jul 22;25(7):1842-57. Epub 2014 Jan 22.

NYU Neuroscience Institute and the Department of Neuroscience and Physiology, Smilow Research Center, New York University School of Medicine, New York, NY 10016, USA Current Address: Department of Neurobiology, Yale University, PO Box 208001, New Haven, CT 06520-8001, USA.

Complex and precisely orchestrated genetic programs contribute to the generation, migration, and maturation of cortical GABAergic interneurons (cIN). Yet, little is known about the signals that mediate the rapid alterations in gene expression that are required for cINs to transit through a series of developmental steps leading to their mature properties in the cortex. Here, we investigated the function of post-transcriptional regulation of gene expression by microRNAs on the development of cIN precursors. We find that conditional removal of the RNAseIII enzyme Dicer reduces the number of cINs in the adult mouse. Dicer is further necessary for the morphological and molecular maturation of cINs. Loss of mature miRNAs affects cINs development by impairing migration and differentiation of this cell type, while leaving proliferation of progenitors unperturbed. These developmental defects closely matched the abnormal expression of molecules involved in apoptosis and neuronal specification. In addition, we identified several miRNAs that are selectively upregulated in the postmitotic cINs, consistent with a role of miRNAs in the post-transcriptional control of the differentiation and apoptotic programs essential for cIN maturation. Thus, our results indicate that cIN progenitors require Dicer-dependent mechanisms to fine-tune the migration and maturation of cINs.
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http://dx.doi.org/10.1093/cercor/bht426DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4459287PMC
July 2015

Oxytocin enhances hippocampal spike transmission by modulating fast-spiking interneurons.

Nature 2013 Aug 4;500(7463):458-62. Epub 2013 Aug 4.

Department of Molecular and Cellular Physiology, 279 Campus Drive, Stanford University School of Medicine, Stanford, California 94305, USA.

Neuromodulatory control by oxytocin is essential to a wide range of social, parental and stress-related behaviours. Autism spectrum disorders (ASD) are associated with deficiencies in oxytocin levels and with genetic alterations of the oxytocin receptor (OXTR). Thirty years ago, Mühlethaler et al. found that oxytocin increases the firing of inhibitory hippocampal neurons, but it remains unclear how elevated inhibition could account for the ability of oxytocin to improve information processing in the brain. Here we describe in mammalian hippocampus a simple yet powerful mechanism by which oxytocin enhances cortical information transfer while simultaneously lowering background activity, thus greatly improving the signal-to-noise ratio. Increased fast-spiking interneuron activity not only suppresses spontaneous pyramidal cell firing, but also enhances the fidelity of spike transmission and sharpens spike timing. Use-dependent depression at the fast-spiking interneuron-pyramidal cell synapse is both necessary and sufficient for the enhanced spike throughput. We show the generality of this novel circuit mechanism by activation of fast-spiking interneurons with cholecystokinin or channelrhodopsin-2. This provides insight into how a diffusely delivered neuromodulator can improve the performance of neural circuitry that requires synapse specificity and millisecond precision.
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http://dx.doi.org/10.1038/nature12330DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5283693PMC
August 2013

Neural circuits look forward.

Proc Natl Acad Sci U S A 2011 Sep 13;108(39):16137-8. Epub 2011 Sep 13.

New York University Neuroscience Institute, Department of Cell Biology and Neural Science, New York University School of Medicine, New York, NY 10016, USA.

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http://dx.doi.org/10.1073/pnas.1112842108DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3182682PMC
September 2011