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When citing an abstract from the 2018 annual meeting, please use the format below. [Authors]. [Abstract Title]. Program No. XXX.XX. 2018 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2018. Online.

2018 Copyright by the Society for Neuroscience all rights reserved. Permission to republish any

abstract or part of any abstract in any form must be obtained in writing by SfN office prior to publication.

Poster

724. Neural Circuit Development: Molecules and Mechanisms

Location: SDCC Halls B-H

Time: Wednesday, November 7, 2018, 1:00 PM - 5:00 PM

Program #/Poster #: 724.01/A1

Topic: A.06. Synaptogenesis and Activity-Dependent Development

Support: NINDS NS29709 (JLN)

Title: T-type calcium channel bursting in thalamic association pathways precedes sensory pathways and can be activated by GABAergic input during early postnatal development

Authors: *Q. MIAO1, J. L. NOEBELS2

1Bayrlor Col. of Med., Dept. of Neurol., Houston, TX; 2Baylor Col. of Med., Houston, TX

Abstract: Transient-type low-voltage activated calcium channels (T-channels) regulate the intrinsic excitability of thalamic cells and facilitate the genesis of rebound burst firing which enable thalamocortical oscillations and contribute to the modulation of brain states of awareness. The thalamus takes part in sensory, motor and cognitive functions by transmitting information to the cortex via numerous distinct nuclei. These nuclei are divided into two different categories: first order and higher order relays. First order nuclei receive driver input from the periphery or a subcortical source, while high-order nuclei mainly receive descending inputs from the cortex. Precise regulation of T channels is important for healthy thalamocortical processes since abnormal function of T-channels has been implicated in pathological conditions, including epilepsy, neuropathic pain, and sleep disorders. We examined whether different thalamic nuclei develop T-channel expression simultaneously during early development, or whether bursting in these pathways show distinctive stages of maturation? We performed whole-cell recordings in the developing mouse thalamus (postnatal day 3 to 35). We found that across subregions of the lateral thalamus, there is a high-to-low gradient from dorsal to ventral nuclei in the expression of T-channels. Specifically, all laterodorsal thalamic (LD) neurons projecting to associative retrosplenial cortex show a distinctively high expression of T-currents which enable them to fire low-threshold and rebound spikes in as early as one week old C57BL/6 mice. These spikes could be blocked by a T-channel specific blocker, Z944. At this age, a small fraction of neurons in other higher-order nuclei including lateral posterior nucleus (LP), posterior complex (PO) and the dorsal part of medial geniculate complex (dMG) of the thalamus, can fire low-threshold and rebound spikes. In sharp contrast, similar low-threshold and rebound spikes in first-order primary sensory thalamic relay neurons, including visual (lateral geniculate nucleus, LGN), somatosensory (ventral posteromedial nucleus, VPM), and auditory (ventral part of medial geniculate complex, vMG) neurons appeared nearly one week later. Functionally, our preliminary data showed that optogenetic and electrical activations of GABAergic circuit could elicit burst spiking in LD neurons with cell-attached recording. Together, these results indicate that higher-order thalamic relay neurons utilize firing supported by T-channels earlier than those in the primary sensory pathway and could be recruited by GABAergic inputs.

Disclosures: Q. Miao: None. J.L. Noebels: None.

Poster

724. Neural Circuit Development: Molecules and Mechanisms

Location: SDCC Halls B-H

Time: Wednesday, November 7, 2018, 1:00 PM - 5:00 PM

Program #/Poster #: 724.02/A2

Topic: A.06. Synaptogenesis and Activity-Dependent Development

Support: NHMRC Project Grant APP1099709 2016-2019

NHMRC John Cade Fellowship APP1056929 2014-2018

Rebecca L Cooper Medical Research Grant 2017

Title: Rapid modulation of L-type voltage-gated calcium channels during brain development by vitamin D Authors: *H. M. GOOCH, X. CUI, V. ANGGONO, T. H. BURNE, D. EYLES, P. SAH, J.

MCGRATH

Queensland Brain Inst., St Lucia, Australia

Abstract: The secosteroid vitamin D [1,25(OH)2D3] drives genomic changes in the body via classical steroid hormone pathways. While 1,25(OH)2D3 is also known to drive non-genomic effects in some peripheral tissues, most notably the rapid modulation of L-type voltage-gated calcium channels (L-VGCC), its non-genomic effects within the brain remain unexplored. Since accumulating evidence links common L-VGCC genetic variants with neuropsychiatric disorders, and developmental vitamin D deficiency is an established risk factor for schizophrenia, we are investigating the non-genomic effects of 1,25(OH)2D3 on L-VGCCs in the developing brain. Using wide-field calcium imaging and electrophysiology in the prefrontal cortex (PFC), we found that physiological concentrations of 1,25(OH)2D3 (0.1 nM) rapidly enhanced L-VGCC activity in a subset of PFC neurons, termed vitamin D responsive neurons (I-VDRNs).

1,25(OH)2D3 increased activity-dependent somatic cytosolic Ca2+ levels by as much as 250% in

I-Į

Į). Consistent with

this, nucleated patch recordings revealed 1,25(OH)2D3 enhanced high voltage-activated (HVA) Ca2+ channel currents (33 ± 5%, n=5) in a subset of layer 2/3 PFC cells (n=5/21, 24%), suggesting that Ca2+ influx through VGCCs contributed to the increased cytosolic Ca2+ levels observed during imaging. Further, pre-incubation of imaged slices in the L-VGCC channel

ȝ2D3-induced increase in

cytosolic Ca2+ Į%; n=8/675 cells, 1.2%), demonstrating that

1,25(OH)2D3 enhanced L-VGCC activity in a subset of PFC neurons during development.

Interestingly, wide-field Ca2+ imaging also revealed a second subset of PFC neurons that showed decreases in activity-dependent cytosolic Ca2+ levels following bath application of 1,25(OH)2D3 Į-29 ± 3%; n=38/426 cells, 8.9%), termed D-VDRNs. This effect was not dependent on L-Į-22 ± 2%; n=59/675, 8.7%), however pre-incubation with synaptic blockers significantly reduced the proportion of responsive D-Į -26 ± 4; n=26/677 cells, 3.6%), suggesting network effects beyond vitamin D responsive neurons. Since L-VGCC activity is required for developmentally critical processes such as neuronal maturation and gene transcription, these findings suggest a significant role for vitamin D during healthy brain development, and suggests potential consequences for developmental vitamin D deficiency. Disclosures: H.M. Gooch: None. X. Cui: None. V. Anggono: None. T.H. Burne: None. D.

Eyles: None. P. Sah: None. J. McGrath: None.

Poster

724. Neural Circuit Development: Molecules and Mechanisms

Location: SDCC Halls B-H

Time: Wednesday, November 7, 2018, 1:00 PM - 5:00 PM

Program #/Poster #: 724.03/A3

Topic: A.06. Synaptogenesis and Activity-Dependent Development

Support: JPSP KAKENHI JP17K07076

JPSP KAKENHI JP15K15015

JPSP KAKENHI JP25293043

JPSP KAKENHI JP17H04014

Takeda Science Foundation

Title: Axonal branches of layer 2/3 dual projection neurons targeting an ipsilateral distant area extend more rapidly than locally targeting branches in mouse neocortex

Authors: *M. SATO1,2, Y. LIN1, M. DOI1, Y. OKA1,2

1Dept. of Anat. and Neurosci., Osaka Univ. Grad. Sch. of Med., Suita, Japan; 2Div. of

Developmental Neurosci., Osaka Univ. United Grad. Sch. of Child Develop., Suita, Japan Abstract: Direct connections between different cortical areas have been shown to be important for sensorimotor integration. Developmental processes of these connections and their underlying mechanisms, however, have not been fully understood. By using a subtype-specific promoter and our new vector for enhancing sparse labeling of cortical neurons combined with tissue clearing of flat-mounted cortices, we visualized a population of layer 2/3 (L2/3) neurons in the mouse primary somatosensory area (S1) that had axons projecting to the contralateral hemisphere as well as to the ipsilateral hemisphere. We analyzed the processes of their axon projections and found that these neurons first extended the main axonal shaft projecting to the contralateral hemisphere, already crossing the midline before birth. In contrast, collateral branches projecting to the ipsilateral hemisphere emerged around postnatal day 3 at the level of layer 5. Only one among these collateral branches reached the distant areas, such as the primary motor area (M1) and the secondary somatosensory area (S2). Temporal analysis of the branch length suggested that far-reaching branches grew at a higher rate than those projecting to the local targets. This observation raises the possibility that a branch might be selected at a very early stage, if not at the timing of the budding, to target an area distant from the original area of the soma. Disclosures: M. Sato: None. Y. Lin: None. M. Doi: None. Y. Oka: None.

Poster

724. Neural Circuit Development: Molecules and Mechanisms

Location: SDCC Halls B-H

Time: Wednesday, November 7, 2018, 1:00 PM - 5:00 PM

Program #/Poster #: 724.04/A4

Topic: A.06. Synaptogenesis and Activity-Dependent Development Title: Physiological and pathological maturation of cortical neural networks Authors: *S. DOMINGUEZ1, N. GHANI1, G. POUCHELON3, S. COLOMBO2, M. BOLAND1, V. LETTS1, S. PETRI1, W. N. FRANKEL5, D. GOLDSTEIN5, G. J. FISHELL4, G.

BUZSAKI6, D. KHODAGHOLY1, J. GELINAS1

2Inst. for Genomic Med., 1Columbia Univ., New York, NY; 4Neurobio., 3Harvard Med. Sch.,

Boston, MA; 5Columbia Univ. Med. Ctr., New York, NY; 6New York University, Sch. of Med.,

New York, NY

Abstract: y to support cognitive processes, such as perception, attention, and memory, represents a critical evolutionary advancement. Neural networks underlying these processes mature over the course of development, and are influenced by ongoing synaptic activity. Modulation of this synaptic activity early in development has the potential to disrupt normal maturation, but the underlying mechanisms of this impairment remain unclear. Here, we examine the properties of cortical neural networks during physiologic development compared to pharmacologic and genetic conditions that alter the excitatory-inhibitory balance. We perform in vivo neurophysiological recordings from mouse pups aged postnatal day 5 to 14 that are cycling through natural waking and sleep epochs. With the use of the NeuroGrid, a high spatiotemporal resolution surface array, we simultaneously record from multiple cortical regions as determined by post-mortem immunohistochemical analysis. We study the effects of acute changes to GABAergic neurotransmission using pharmacologic agonists and antagonists, as well as chronic alteration of excitation-inhibition in a mouse model of pediatric epileptic encephalopathy (KCNT1). Although neural networks exhibit some common responses to these neuromodulatory alterations, expression of oscillatory activity is modified by postnatal age and prior synaptic experience. These data allow us to better understand the neurophysiologic patterns that characterize normal maturation, and how they can be impacted by aberrant synaptic activity in diseases such as epilepsy. Disclosures: S. Dominguez: None. N. Ghani: None. G. Pouchelon: None. S. Colombo: None. M. Boland: None. V. Letts: None. S. Petri: None. W.N. Frankel: None. D. Goldstein: None. G.J. Fishell: None. G. Buzsaki: None. D. Khodagholy: None. J. Gelinas: None.

Poster

724. Neural Circuit Development: Molecules and Mechanisms

Location: SDCC Halls B-H

Time: Wednesday, November 7, 2018, 1:00 PM - 5:00 PM

Program #/Poster #: 724.05/A5

Topic: A.06. Synaptogenesis and Activity-Dependent Development

Support: EMBO Long-term Fellowship

Postdoc.Mobility Fellowship, Swiss National Fundation

NIH R01 NS081297

Title: Postsynaptic mGluR signaling controls the development of somatostatin interneurons Authors: *G. POUCHELON1, E. FISHER1, R. MACHOLD2, G. FISHELL1

1Harvard Med. Sch., Boston, MA; 2New York Univ., New York, NY

Abstract: Our internal representation of the outside world is created within the neocortex. Inhibitory interneurons (INs) sculpt cortical activity and are thus critical in shaping these representations. During development, the inhibitory circuits that allow for the emergence of cortical function are assembled early during the postnatal period. Activity has been increasingly associated with these developmental processes, however the role and the type of activity in IN development remain largely unexplored. Although Parvalbumin (PV) and Somatostatin (SST)-INs both arise from the same embryonic structure, the medial ganglionic eminence (MGE), they differentiate into two very distinct IN types within the cortex. It seems likely that the afferent activity impinging upon these distinct cells is central to their integration into cortical circuitry. Recent single-cell RNA-seq analyses has revealed that each interneuron subtype expresses a specific set of neurotransmitter receptors, which are potential candidates for activity-dependent controls of their development. Using in vivo monosynaptic rabies tracing at the postnatal developmental stage when INs settle in their cortical position, we discovered that the earliest presynaptic input to SST-INs is glutamatergic and originate from the thalamus. Analyzing glutamatergic receptors expression during postnatal development revealed that the postsynaptic metabotropic glutamatergic receptor

1 (mGluR1) is specifically expressed in SST-INs and continues to be expressed into adulthood.

In addition, we found that mGluR1 is activated by thalamocortical inputs. Therefore we hypothesize that mGluR1 regulates the integration of SST-INs into cortical networks. Using a combination of mouse genetics, rabies monosynaptic tracing and electrophysiology, we discovered that SST-INs show a defect of maturation upon deletion of mGluR1. Together these findings reveal an activity-dependent postsynaptic mechanism for IN-type differentiation and provide a better understanding of cortical inhibitory circuit development. Disclosures: G. Pouchelon: None. E. Fisher: None. R. Machold: None. G. Fishell: None.

Poster

724. Neural Circuit Development: Molecules and Mechanisms

Location: SDCC Halls B-H

Time: Wednesday, November 7, 2018, 1:00 PM - 5:00 PM

Program #/Poster #: 724.06/A6

Topic: A.06. Synaptogenesis and Activity-Dependent Development

Support: NIH Grant R01 NS081297

Title: BDNF shapes the functional maturation of cortical interneurons Authors: *E. FISHER1, G. POUCHELON1, C. MAYER2, R. C. BANDLER3, G. J. FISHELL1

1Neurobio., Harvard Med. Sch., Boston, MA; 2Max Planck Inst. of Neurobio., Munich,

Germany; 3NYU Neurosci. Institute, Langone Med. Ctr., New York, NY Abstract: In the mammalian cerebral cortex, inhibitory interneurons sculpt the flow of excitatory information. This complex task is carried out by a wide variety of interneuron subtypes which play distinct roles in cortical function. Two major classes of interneurons, parvalbumin (PV)+ fast-spiking basket cells and somatostatin (SST)+ Martinotti cells, are both derived from a common embryonic origin yet differentiate into highly specialized cell types. Mechanisms that control the diversification of these cell types and specify their integration into their respective circuits are not well understood. Increasing evidence suggests that this process depends not only on initial genetic determinants of cell fate, but also activity-dependent signals once the interneurons invade the cortex and begin to form synapses. One candidate signaling factor to mediate cortical interneuron maturation and synaptic integration is brain-derived neurotrophic factor (BDNF), which is a neurotrophin critical for the development of several cells types and has been shown to regulate inhibition in the developing cortex. However, the contribution of the BDNF high-affinity receptor TrkB to interneuron development has never been tested. Here, we employ a combination of longitudinal fate-mapping, electrophysiology, and synaptic puncta analysis to demonstrate that TrkB controls the circuit integration of SST and

PV cortical interneurons.

Disclosures: E. Fisher: None. G. Pouchelon: None. C. Mayer: None. R.C. Bandler:

None. G.J. Fishell: None.

Poster

724. Neural Circuit Development: Molecules and Mechanisms

Location: SDCC Halls B-H

Time: Wednesday, November 7, 2018, 1:00 PM - 5:00 PM

Program #/Poster #: 724.07/A7

Topic: A.06. Synaptogenesis and Activity-Dependent Development Title: Early prenatal exposure of rats to homocysteic acid leads to lasting changes in NMDA receptor subunit expression and GABAergic interneuron markers Authors: *A. LUNDERBERG, S. SIMKO, J. ROYER, L. CHASE

Hope Col., Holland, MI

Abstract: Homocysteic acid (HCA), a NMDA receptor agonist, is an endogenous metabolite formed from the oxidation of homocysteine. Since hyperhomocysteinemia is a risk factor for several neuropsychiatric disorders, including bipolar disorder and major depressive disorder (MDD), we previously tested the hypothesis that elevated HCA levels in developing rats may induce the development of behaviors associated with MDD and/or bipolar disorder. Our earlier work demonstrated that exposure of postnatal rats to HCA from P3-21 leads to a mixed depressive/manic phenotype that develops post-puberty. Specifically, HCA treated rats exhibit increased risk-taking behavior, reduced social behavior, novelty-induced hyper-locomotion, anhedonia in the saccharine preference test, and reduced spatial learning in the Morris water maze, consistent with a depressive state with manic tendencies. Therefore, in this study, we focused on examining the effects early postnatal HCA exposure had on glutamatergic and GABAergic markers in the hippocampus and the cortex in the adult rat. We hypothesized that early postnatal HCA exposure would lead to excitotoxicity and loss of NMDA-receptor containing GABAergic interneurons which are hypothesized to play an important role in the pathology associated schizophrenia, bipolar disorder and depressive disorder. However, contrary to our hypothesis, we observed that HCA exposure led to an increase in expression of the GABAergic marker, GAD-67 in the cortex of both male and female rats. This finding suggests that perhaps GABAergic interneurons were not appropriately pruned during the critical period. In addition, we observed that HCA exposure led to a significant increase in the NR2A:NR2B subunit expression ratio in the cortex and the hippocampus of male and female rats, but no changes in NR1 subunit expression. Functionally, this would result in NMDA receptors with faster gating kinetics which may be less susceptible to HCA-induced excitotoxicity. Furthermore, we also found that HCA leads to an increase in the expression of BDNF, a neurotrophic factor important for maintenance of GABAergic interneurons. This finding is consistent with the observation that the relative NR2A subunit expression increases as activation of NR2A-specific receptors is associated with an increase in BDNF release. Collectively, these data suggest that early HCA exposure may lead to a shift in the NR2A:NR2B subunit expression, leading to an increase in BDNF expression and GABAergic interneuron survival during the critical period. This research was supported by the Hope College Neuroscience Program,

Biology Department and Chemistry Department.

Disclosures: A. Lunderberg: None. S. Simko: None. J. Royer: None. L. Chase: None.

Poster

724. Neural Circuit Development: Molecules and Mechanisms

Location: SDCC Halls B-H

Time: Wednesday, November 7, 2018, 1:00 PM - 5:00 PM

Program #/Poster #: 724.08/A8

Topic: A.06. Synaptogenesis and Activity-Dependent Development

Support: NIH Grant MH110438

Title: Mechanistic insights into autocrine an paracrine roles of endothelial GABA in the embryonic forebrain

Authors: Y. CHOI, A. VASUDEVAN

Dept. of Psychiatry, Angiogenesis & Brain development Laboratory, McLean Hosp., Harvard

Med. Sch., Belmont, MA

Abstract: The developing cerebral cortex uses a complex developmental plan involving angiogenesis, neurogenesis and neuronal migration. After establishment of the periventricular vascular gradient by embryonic day 11 (E11), neurons and/or neuronal progenitors from ventricular zones navigate along diverse courses, radially and tangentially, to adopt final laminar positions and integrate into specific brain circuits. Our recent studies have shown that the developing periventricular vascular network exquisitely patterned amidst neurons not only acts as a physical substrate for neuronal migration, but also holds the key to several novel developmental mechanisms and pathways. It highlights the importance of endothelial cell secreted GABA signaling in the embryonic forebrain and establishes novel autonomous links between blood vessels and the origin of neuropsychiatric diseases like epilepsy, autism and schizophrenia. Since a common GABA pathway operates in both endothelial cells and GABAergic neurons of the embryonic telencephalon, it is essential to gain further mechanistic insights by segregating this pathway in individual cell types. Our recently generated Vgat ǻ-Cre or Vgat ECKO (endothelial cell knockout; ECKO) mouse model that blocks GABA release from endothelial cells, serves as a new tool to study how endothelial GABA signaling shapes angiogenesis and neurovascular interactions during prenatal development. Here, we isolated individually periventricular endothelial cells and GABAergic neurons from E15 Vgat ǻ-cre and Vgat fl/fl telencephalon and characterized them further by using molecular (RNA seq) and cellular techniques. Our results reveal that the endothelial GABA signaling pathway influences angiogenesis related genes and specific processes like tight junction formation, vascular sprouting and migration. It also shows how components of the neuronal GABA pathway, for instance receptor mediated signaling and transcription factors are affected in the absence of endothelial GABA release. Taken together, our findings delineate the close relationship between vascular and nervous systems that begin early in embryogenesis establishing their future interactions and interdependence.

Disclosures: Y. Choi: None. A. Vasudevan: None.

Poster

724. Neural Circuit Development: Molecules and Mechanisms

Location: SDCC Halls B-H

Time: Wednesday, November 7, 2018, 1:00 PM - 5:00 PM

Program #/Poster #: 724.09/A9

Topic: A.06. Synaptogenesis and Activity-Dependent Development

Support: FCT - DFA - SFRH/BD/128869/2017

Title: Towards molecular connectomics: Proteomic dissection of a specific hippocampal synapse type Authors: *N. APÓSTOLO1,2, S. N. SMUKOWSKI4, V. RYBAKIN3, K. M. VENNEKENS1,2, S. PORTEGIES5, N. V. GOUNKO1,2,6, J. N. SAVAS4, J. DE WIT1,2

1VIB Ctr. for the Biol. of Dis., Leuven, Belgium; 2Dept. of Neurosci., 3REGA Inst. - Dept. of

Microbiology and Immunol., KU Leuven, Leuven, Belgium; 4Dept. of Neurol., Northwestern University, Feinberg Sch. of Med., Chicago, IL; 5Cell Biology, Fac. of Sci., Utrecht Univ., Utrecht, Netherlands; 6VIB Bio Imaging Core, Leuven, Belgium Abstract: Neural circuits in the brain communicate through diverse types of synapses. Synapses between different types of neurons can vary widely in their structural and functional properties, and this diversity is required for proper circuit function. Cell adhesion molecules play important roles in synapse development, as they connect pre- and postsynaptic cells and recruit the molecular machinery necessary for synaptic function. However, their potential role in specifying distinct synapse types is still largely unexplored. Single-cell sequencing studies have shown that different neuronal cell types express distinct combinations of adhesion molecules, but whether the structural and functional diversity of different synapse types is reflected in unique adhesion molecule compositions is not known. Typically, the molecular composition of synapses is studied in bulk synaptosome preparations containing many different synapse types. Therefore, the establishment of new methods to elucidate the molecular properties of distinct synapse types is crucial for understanding the molecular basis of synaptic connectivity, function and plasticity. Here, I developed a new method to profile the proteome of a specific hippocampal synapse type, the mossy fiber-CA3 (MF-CA3) synapse, by combining biochemical fractionation, live-labeling for a synapse-specific surface marker, Fluorescence Activated Synaptosome Sorting (FASS) and liquid chromatography-tandem mass spectrometry (LC-MS/MS). Proteomic analysis reveals that several dozen adhesion molecules are specifically enriched at this synapse. To reveal protein- protein interaction networks within these enriched molecules I am performing a small, unbiased oligomerization-based screen to detect extracellular interactions between individually expressed recombinant extracellular domains. The ultimate goal is to map multiple surface protein complexes at an individual synapse type, the MF-CA3 synapse, and analyze the consequences of synaptic loss of validated adhesion molecules on MF-CA3 synapse structure, function, and plasticity. Disclosures: N. Apóstolo: None. S.N. Smukowski: None. V. Rybakin: None. K.M. Vennekens: None. S. Portegies: None. N.V. Gounko: None. J.N. Savas: None. J. De Wit: None.

Poster

724. Neural Circuit Development: Molecules and Mechanisms

Location: SDCC Halls B-H

Time: Wednesday, November 7, 2018, 1:00 PM - 5:00 PM

Program #/Poster #: 724.10/A10

Topic: A.06. Synaptogenesis and Activity-Dependent Development

Support: CIHR Grant

Title: Patterning of cerebellar inhibitory interneurons by the gamma-Protocadherins

Authors: *W. X. WANG1,2, J. L. LEFEBVRE1,2

1Neurosciences and Mental Hlth., Hosp. for Sick Children Res. Inst., Toronto, ON, Canada;

2Dept. of Mol. Genet., Univ. of Toronto, Toronto, ON, Canada

Abstract: The developmental events that orchestrate neural circuit formation are dependent on coordinated interactions of neurons with their local environment. Central to these interactions are cell-surface receptors and adhesion molecules, whose concerted actions allow for remarkable specificity in neuronal cell numbers, distributions, and connectivity patterns. Among these are the clustered Protocadherins, which have emerged as key regulators due to their immensequotesdbs_dbs46.pdfusesText_46

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