NMDARs hypofunction in parvalbumin-expressing interneurons alters oscillations and sensory tuning in mouse primary visual cortex

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dc.contributor.advisor Busse, Laura (Prof. Dr.)
dc.contributor.author Fiorini, Matilde
dc.date.accessioned 2018-11-09T08:30:36Z
dc.date.available 2018-11-09T08:30:36Z
dc.date.issued 2020-10-15
dc.identifier.other 1735650072 de_DE
dc.identifier.uri http://hdl.handle.net/10900/84727
dc.identifier.uri http://nbn-resolving.de/urn:nbn:de:bsz:21-dspace-847277 de_DE
dc.identifier.uri http://dx.doi.org/10.15496/publikation-26117
dc.description.abstract Sensory information transmission crucially depends on a correct interplay between synaptic excitation and synaptic inhibition. In this dynamic balance observed in neural circuits, inhibition is thought to be critical to achieve network stability and gate information processing; however, how inhibition itself contributes to the selectivity and sensitivity of neuronal responses to sensory stimuli is still, currently, a matter of intense debate. Furthermore, there is little evidence about the cellular mechanisms that might underlie such shaping of responses by inhibitory interneurons in vivo. In primary visual cortex (V1), for instance, parvalbumin-positive (PV+) inhibitory interneurons control network oscillations, set the gain of sensory responses, and contribute to spatial integration. Interestingly, these aspects of visual processing are often disturbed in several neuropsychiatric disorders, amongst them schizophrenia, where one hypothesis proposes that hypofunctioning NMDA-glutamate receptors (NMDAR) might cause deficient excitatory drive to PV+ interneurons. However, little is known on how genetic modifications specifically causing NMDAR hypofunction in PV+ interneurons, can affect neural responses to visual stimuli. To test how NMDAR hypofunction in PV+ interneurons affects V1 network and visual tuning properties, I compared extracellular activity between control and transgenic mice lacking NMDAR-mediated glutamatergic excitation of PV+ neurons. I found frequency-specific alterations of visual cortex oscillatory power, and enhanced contrast sensitivity and stronger surround suppression in V1 putative pyramidal cells. Importantly, network oscillations and contrast processing were unaltered in the dorsolateral geniculate nucleus (dLGN) of the thalamus, indicating that the observed disruptions of V1 activity are mediated by changes in cortical networks. I conclude that reduced glutamatergic excitation of cortical PV+ interneurons plays a critical role in visual information processing, as it is sufficient to alter V1 rhythms and tuning properties; this is also consistent with the structural and functional alterations previously observed in visual cortex of schizophrenia patients, and further supports the involvement of PV+ interneurons hypofunctionality in the disease etiology. en
dc.language.iso en de_DE
dc.publisher Universität Tübingen de_DE
dc.rights ubt-podno de_DE
dc.rights.uri http://tobias-lib.uni-tuebingen.de/doku/lic_ohne_pod.php?la=de de_DE
dc.rights.uri http://tobias-lib.uni-tuebingen.de/doku/lic_ohne_pod.php?la=en en
dc.subject.classification Neuropsychologie de_DE
dc.subject.classification Kognitionswissenschaft de_DE
dc.subject.ddc 500 de_DE
dc.subject.ddc 610 de_DE
dc.subject.other mouse visual cortex en
dc.subject.other Kognitive Neurowissenschaft de_DE
dc.title NMDARs hypofunction in parvalbumin-expressing interneurons alters oscillations and sensory tuning in mouse primary visual cortex en
dc.type PhDThesis de_DE
dcterms.dateAccepted 2018-08-01
utue.publikation.fachbereich Graduiertenkollegs de_DE
utue.publikation.fakultaet 4 Medizinische Fakultät de_DE


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