Self-organizing Neural Maps: The Retinotectal Map and Mechanisms of Neural Development: From Retina to Tectum

Description

Self-organizing Neural Maps: From Retina to Tectum describes the underlying processes that determine how retinal fibers self-organize into an orderly visual map. The formation of neural maps is a fundamental organizing concept in neurodevelopment that can shed light on developmental mechanisms and the functions of genes elsewhere. The book presents a summary of research in the retinotectal field with an ultimate goal of synthesizing how underlying mechanisms in neural development harmoniously come together to create life. A broad spectrum of neuroscientists and biomedical scientists with differing backgrounds and varied expertise will find this book useful. Front Matter Copyright Preface Acknowledgments Overview and basics of the retinotectal system Overview of the development of circuits Topographic maps in the CNS Stability, reproducibility, and flexibility The mature retinotectal system Advantages of studying the retinotectal system Sperry's chemoaffinity theory Organizational overview of the material References Further reading Early work supports chemoaffinity with one contradictory result Grafted eyes regenerate optic nerves to restore vision Optic nerve regeneration restores original connections even when maladaptive Behavioral evidence of the retinotectal map and its regeneration Regeneration with single axis reversals Embryonic eye rotations and the development of polarization Embryonic tectal rotations with different results Electrophysiological mapping demonstrates regeneration of the map Source of the electrical signals Optical factors influence the map The retinotectal map Anatomical mapping of the retinotectal projection “Compound eyes” demonstrate the inadequacy of rigid chemoaffinity Qualitative models of map formation Rigid chemospecificity Distributed relative preferences Fiber-fiber adhesion by homophilic interactions Fiber-fiber sorting by activity-driven Hebbian synapses Contribution of pathway ordering to map formation Conclusion References The search for chemoaffinity molecules in molecular gradients The monoclonal antibody approach The TOP antigens A gradient of ganglioside The laminin receptor The TRAP antigen Newer versions of the search for gradients and conclusions Culture assays of retinal fiber preferences Early attempts Stripe assays for growth cone-target selection Growth cone collapse as a guidance mechanism Response to artificial gradients Purification, isolation, and cloning: A tale of two factors RGM: The first factor RAGS: The second factor Conclusions The genetic approach finds a similar factor, defines the Eph receptor and ephrin ligand families In situ hybridization for the receptors Eph and ephrin family members and revised nomenclature The mechanism of Eph receptor control of growth cones Simple model of how gradients determine the RT map Conclusions References Plasticity after surgical interventions: Size disparity experiments Size disparity: Compression of the projection onto a half tectum Implications for retinal arbors and numbers of synapses Compression is widespread Reversibility of compression Functional consequences of compression Size disparity: Half-retinal projections expand on tectum A model of arbor expansiveness via competition Implications for retinal arbors and synapses Maps organized without any normal chemoaffinity portion or without normal polarity Expansion in other species Evidence for a change in chemoaffinity markers in both expansion and compression Size disparity: Binocular projections to one tectal lobe Eye-specific exclusion and competition Models and interpretation Compound eyes revisited Tests for retinal markers in compound eyes Tests for tectal developmental changes Tests for retinal “regulation” Embryonic retinal ablations—Unexpected results Clockface model predicts compound eye from a remnant Cell migration following retinal lesions Embryonic retinal lesions in chick Retinal lesions in mammals Genetic manipulation of ganglion cell numbers in mice Theoretical models First models Arrow model—Polarity without positional markers A model without any markers A model with retinal induction of tectal markers Chemoaffinity as a weak force Summary of models Summary References Further reading Growth of the retina and tectum: Implications for the retinotectal map Early morphogenesis of retina and tectum Histogenesis of retina Radiolabeled thymidine technique Visual consequences of continued retinal growth Altered magnification of the image on the retina Shifted location of the receptive field of each ganglion cell Change from aquatic to aerial vision Change of visual behavior with maturity Histogenesis of tectum—Cells added on one end only Shifting connections hypothesis A critical assessment of the hypothesis Retinal growth Tectal growth The projection The attack against shifting connections Evidence for shifting terminals in axonal trajectories Different pattern in chick Summary of shifting connections References Further reading Specification of the retina and tectum Specification of the retina Eye rotation and the time of normal specification Anatomical problems and inconsistencies Revision of amphibian specification Contributions of cells from the optic stalk Conclusions Respecification by other tissues Respecification by intraretinal signaling Bisected eyes Complex compound eyes Pie slice compound eyes Summary of retinal specification Genetic control of expression of NT and DV gradients Overview of TF control of specification in retina and tectum The NT axis of the retina The DV axis of the retina Specification of the tectum Is the tectum recognized by retinal axons? Tectal grafts in the adult demonstrate tectal specification Embryonic tectal rotations and the origins of tectal specification Tectal rotations in Xenopus embryos Embryonic tectal rotations in chick Summary Genetic control of the AP axis in tectum Engrailed and EphA/ephrinA expression in tectum What controls the ML axis in tectum? Summary and conclusions References Development of the visual pathways Morphogenesis of the optic cup and optic stalk Axonal outgrowth: Pathfinding within retina Morphological analysis How much directional information is necessary for the axon to reach the ONH? Blueprint hypothesis: Oriented spaces and structural substrates Blueprint hypothesis: Neural cell adhesion molecule and laminin Blueprint hyposthesis: Growth-inhibiting matrix elements Attraction by Shh gradients: Growth-promoting effects Molecular factors in retinal axon fasciculation EphB receptors selectively affect dorsal axons at the ONH Role of pathfinders and followers Netrin-1 attracts axons into the ONH Growth and order of axons in the optic nerve and tract Fish: Highly ordered organization How ordered is the optic nerve across vertebrate classes? Errant paths at chiasm and corrections during development Reorganization after the chiasm Molecular components promoting growth in the optic stalk Molecular guidance at the optic chiasm: The slit guardrail Molecular guidance at the optic chiasm: HSPG and CSPG Molecular guidance at the optic chiasm: Shh inhibitory effects at chiasm Positive factors at chiasm Summary The ipsilateral RT projection from the ventrotemporal axons in mammals Initial retinotectal projection to tectum Xenopus Fish Chick Rodents General conclusions on initial innervation The contributions of pathway guidance References Further reading Genetic analysis of molecular gradients defining map formation Introduction Genetic analysis of the AP axis of the map: The gradients of EphA in retina and of ephrinA in tectum Knockouts and misexpression show roles for ephrinA2 and A5 (Elf-1 and RAGS) Knockouts and misexpression show roles for retinal EphAs The simple model and the complexity produced by countergradients in retina and tectum Reverse signaling, and its contributions Mechanism of reverse signaling involves neurotrophins Importance of relative vs absolute levels of EphAs and ephrinAs Models based explicitly on all EphA and ephrinA forward and reverse interactions The map reversal problem with the ipsilateral retinotectal projections Conclusions DV axis: The gradients of Eph B receptor family in retina and of ephrinB ligand family in tectum EphB receptor and ephrinB ligand gradients Knockouts and misexpression demonstrate forward attraction Reverse signaling via ephrinB2 also mediates attraction A model of dual (forward and reverse) attraction signaling Wnt signaling for the DV axis in chick Semaphorin3D signaling via neuropilin Conclusions References Activity-driven synaptic stabilization Early studies on nicotinic acetylcholine receptors, α -bungarotoxin, and synapse stabilization Initial suggestion of nicotinic transmission turns out to be strong modulation Effects of local α BTX on the retinotectal map Evidence for glutamatergic transmission and presynaptic cholinergic modulation Nucleus isthmi is the source of cholinergic modulation Alpha7 AChRs and Ca + + entry facilitate NT release Activity-dependent map sharpening via NMDA receptors Role of activity in retinotopic sharpening—Regeneration Blocking activity with tetrodotoxin The role of correlated activity—Strobe experiments The role of NMDA receptors in sharpening Role of activity in retinotopic sharpening—Development Studies in frog and fish Spontaneous activity waves in mammalian retina drive sharpening Interaction with EphA-ephrinA gradient system Conclusions The role of activity in sensory map alignments—Several cases with a common theme The indirect ipsilateral retinotectal projection in frogs Binocular cortical neurons in the mammalian geniculocortical system Formation of congruent corticotectal and retinotectal maps Aligning the auditory with the visual map in the tectum The role of activity in eye specific segregation Segregation in different systems—One mechanism Role for NMDA receptors in frog A transient chick RT ipsilateral projection Mammals—Segregation via activity waves References Further reading Activity: Molecular signaling to growth mechanisms Introduction Dynamic analysis of arbor growth Blocking NMDA receptors increases branch formation and deletion Presence of a synapse stabilizes its branch Branches added near synapses Relative activity regulates arbor size Plasticity mechanisms linked to LTP and LTD The Xenopus retinotectal model of LTP induction LTP can be induced by visual activity and can affect postsynaptic response properties Lisman model of plasticity: NMDAR, cam kinase II, cAMP-dep kinase and phosphatases How is Xenopus LTP maintained or reversed after induction? CamKII and growth control in Xenopus Overexpression of CaMKII activity slows retinal arbor growth Inhibiting CaMKII activity increases retinal arbor growth Growth rates drop with maturation and accumulation of CaMKII in tectal neurons LTP and LTD coupled to retrograde signaling in Xenopus LTP and BDNF effects in Xenopus tectum LTD and NO effects in Xenopus tectum LTP and LTD in mammalian tectum Time course of LTP and LTD in rat tectum Mechanisms of LTP and LTD in rat tectum Relationship of LTP and LTD to activity-dependent retinotopic refinement LTD, retraction, and the NO signal in rodent tectum Evidence linking LTD with NO as the retrograde signal for retraction of the errant collaterals NO signaling for retractions in other visual projections Exempting retinotopic synapses from NO-mediated retraction LTP and BDNF effects in rodent and frog tectum BDNF role in LTP at the presynaptic terminals BDNF—Role in LTP on the postsynaptic side BDNF—Role in LTP at the presynaptic terminals LTP and BDNF interact with ephrinB reverse signaling at presynaptic terminals Summary Homeostatic control of synaptic plasticity and regulation of the sensitive period Homeostatic control of synaptic plasticity by neuroimmune proteins Regulation of the sensitive periods for visual plasticity F-actin-based growth-control mechanisms Relationship to synapse formation and stabilization Wider view—F-actin-based axon growth mechanism Summary of the rho mechanisms BDNF effects on p250 GAP How CAMs stimulate growth in axons AA as a Ca + + stimulated retrograde synaptic signal downstream of NMDARs AA targets presynaptic cPKC β for growth modulation via GAP43 The polarity complex and PI3 kinase control branching Polarity complex PI3 kinase Other branching cues Control of lamination Summary of growth-control mechanisms References Summary of mechanisms generating the retinotectal map Introduction Results so far demonstrate little or no contribution from three types of mechanism Rigid chemoaffinity does not determine the map Connections are not based on the timing of the birth of neurons or their axons’ arrival at tectum Selective fiber-fiber homophilic adhesion for pathway ordering has not been directly demonstrated to contribute to the RT map Four main mechanisms contribute to map formation Molecular gradients along the AP and DV axes Molecular gradients of EphA, ephrinAs provide intratectal guidance along AP axis EphB and ephrinBs guide along the ML axis along with other gradients Pathway ordering contributes to the DV to ML axis of the RT map Activity-driven mechanisms provide fine-scale refinement of the maps Competition: Does it work through activity, through ephrin/Eph interactions or is it independent? Basic differences arose between anamniotes and amniotes necessitating modifications of mechanisms Small vs large tissues at time of initial innervation Sequential vs simultaneous innervation by retinal axons Small vs large errors in retinal fiber branching Activity-driven sharpening using visual experience vs without vision using activity waves Continued plasticity vs closing of developmental sensitive period These rules apply to other visual and nonvisual maps Successful models incorporate fiber-target and fiber-fiber gradient signaling as well as activity mechanisms Contributions of models in testing mechanisms and generating further experiments References Index A B C D E F G H I J L M N O P Q R S T V W X Y Z