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UNIVERSITY of CALIFORNIA Los Angeles a Transient Microcircuit Underlying Critical Period Plasticity in the Visual Cortex a Disse

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UNIVERSITY of CALIFORNIA Los Angeles a Transient Microcircuit Underlying Critical Period Plasticity in the Visual Cortex a Disse UNIVERSITY OF CALIFORNIA Los Angeles A transient microcircuit underlying critical period plasticity in the visual cortex A dissertation submitted in partial satisfaction of the requirements for the degree of Doctor of Philosophy in Neuroscience by Courtney Yaeger 2018 © Copyright by Courtney Yaeger 2018 iii ABSTRACT OF THE DISSERTATION A transient microcircuit underlying critical period plasticity in the visual cortex by Courtney Yaeger Doctor of Philosophy in Neuroscience University of California, Los Angeles, 2018 Professor Joshua Trachtenberg, Chair During so-called critical periods of early postnatal life, sensory experience profoundly and permanently sculpts cortical neural circuitry. After critical period closure, experience- dependent plasticity is dramatically limited, and it is not known what differentiates juvenile and adult plasticity mechanisms. At its core, plasticity is a dendritic phenomenon, and in the cortex, plasticity is determined by changes in sensory input and cortical state. Here we show that dendritic and somatic activity in pyramidal neurons is fundamentally different across critical period closure due to the cholinergic engagement of inhibitory circuitry. At the peak of the critical period, acetylcholine released from the basal forebrain directly excites somatostatin-expressing (SST) interneurons. The resultant inhibition of pyramidal cell dendrites and of fast-spiking, parvalbumin-expressing (PV) inhibitory neurons enhances branch-specific dendritic responses and increases somatic spiking within pyramidal neurons. By adulthood, SST cells lose ii cholinergic excitability, and inhibition becomes inverted along the somatodendritic axis, with less SST-mediated dendritic inhibition and more PV-mediated somatic inhibition. When SST cells are optogenetically activated in adult cortex, branch-specific dendritic activity and somatic disinhibition re-emerge. Conversely, suppressing SST cell activity during the critical period prevents the normal development of binocular receptive fields by impairing the experience- dependent maturation of ipsilateral eye inputs. These data reveal a transient circuit through which inhibition and neuromodulation converge to facilitate experience-dependent plasticity by shaping dendritic and somatic activity. iii The dissertation of Courtney Yaeger is approved. Dean Buonomano Peyman Golshani Dario Ringach Larry Zipursky Joshua Trachtenberg, Committee Chair University of California, Los Angeles 2018 iv TABLE OF CONTENTS List of Figures .......................................................................................................................... viii Acknowledgements ................................................................................................................... ix Vita .......................................................................................................................................... xi Chapter 1: Introduction 1.1 Overview ................................................................................................................ 1 1.2 Elevated sensory-dependent plasticity in the developing visual cortex.................... 1 1.3 Inhibition is necessary for critical period plasticity ................................................... 3 1.4 Neuromodulation drives cortical state and plasticity ................................................ 8 1.5 Plasticity as a dendritic phenomenon, influenced by inhibition and modulation ...... 10 1.6 Hypothesis and overview ........................................................................................ 12 1.7 References ............................................................................................................. 13 Chapter 2: Methods 2.1 Animals .................................................................................................................. 23 2.2 Cranial window surgeries ........................................................................................ 23 2.3 Virus injections ....................................................................................................... 24 2.4 Two-photon calcium imaging and visual stimulation ............................................... 25 2.5 Analysis of two-photon imaging data ...................................................................... 26 2.6 In vivo optogenetic manipulations of SST cells or nucleus basalis .......................... 27 2.7 DREADD manipulation of SST cells during development ....................................... 28 2.8 Acute slice preparation ........................................................................................... 29 2.9 Intracellular recording and analysis ......................................................................... 29 2.10 Statistics ............................................................................................................... 30 2.11 References .......................................................................................................... 31 Chapter 3: Investigation of major inhibitory classes across development 3.1 Introduction ............................................................................................................. 32 v 3.2 SST interneurons show an age-dependent shift in cholinergic modulation.............. 33 3.3 VIP interneurons consistently respond to acetylcholine across age ........................ 35 3.4 PV interneurons are differentially inhibited during cholinergic modulation across age ..................................................................................................................................... 36 3.5 Summary and discussion ........................................................................................ 36 3.6 Figures ................................................................................................................... 40 3.7 References ............................................................................................................. 49 Chapter 4: Pyramidal cells are differentially engaged across development 4.1 Introduction ............................................................................................................. 52 4.2 Elevated behavioral state decorrelates dendritic branches at P28 .......................... 53 4.3 P28 somatic responses in pyramidal neurons show increased firing during locomotion .................................................................................................................... 54 4.4 SST-mediated inhibition produces branch-specific decoupling and somatic disinhibition .................................................................................................................. 55 4.5 Summary and discussion ........................................................................................ 56 4.6 Figures ................................................................................................................... 58 4.7 References ............................................................................................................. 65 Chapter 5: SST-mediated inhibition is necessary for binocular matching 5.1 Introduction ............................................................................................................. 68 5.2 Validation of chemogenetic suppression of SST cells ............................................. 68 5.3 Reduction of SST cell activity during the critical period preferentially affects inputs from the ipsilateral eye ................................................................................................. 70 5.4 Suppression of SST cells during the critical period prevents binocular matching .... 71 5.5 Summary and discussion ........................................................................................ 71 5.6 Figures ................................................................................................................... 74 5.7 References ............................................................................................................. 77 vi Chapter 6: Discussion 6.1 Overview of findings ............................................................................................... 79 6.2 Neuromodulation drives unique cortical processing during the critical period .......... 79 6.3 A switch in SST cell activation has broad implications for cortical circuits ............... 81 6.4 Towards a cortical plasticity mechanism ................................................................. 84 6.5 Conclusion .............................................................................................................. 87 6.6 References ............................................................................................................. 88 vii LIST OF FIGURES Figure 1. SST cells lose cholinergic sensitivity after critical period closure. ............................ 40 Supplementary Figure 1. Analysis of ΔF/F during still or run events. ........................... 42 Supplementary Figure 2. Current injection responses for SST, PV, and VIP cells across age and condition. ........................................................................................................ 43 Supplementary Figure 3. Verification of basal forebrain injection sites in representative juvenile and adult mice. ................................................................................................. 45 Figure 2. VIP cells show no age-dependent changes in cholinergic modulation.
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