Involvement of nitric oxide in the elimination of a transient retinotectal projection in development.

The adult pattern of axonal connections from the eye to the brain arises during development through the refinement of a roughly ordered set of connections. In the chick visual system, refinement normally results in the loss of the ipsilateral retinotectal connections. Inhibition of nitric oxide synthesis reduced the loss of these transient connections. Because nitric oxide is expressed by tectal cells with which retinal axons connect and because reduction of nitric oxide synthesis by tectal cells resulted in a change in the connections of retinal axons, nitric oxide probably serves as a messenger from tectal cells back to retinal axons during development.

[1]  M. Stryker,et al.  Prenatal tetrodotoxin infusion blocks segregation of retinogeniculate afferents. , 1988, Science.

[2]  E. Debski,et al.  N-methyl-D-aspartate receptor antagonist desegregates eye-specific stripes. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[3]  G. Böhme,et al.  Possible involvement of nitric oxide in long-term potentiation. , 1991, European journal of pharmacology.

[4]  L. Nowak,et al.  Magnesium gates glutamate-activated channels in mouse central neurones , 1984, Nature.

[5]  E. Kandel,et al.  Nitric oxide and carbon monoxide produce activity-dependent long-term synaptic enhancement in hippocampus. , 1993, Science.

[6]  V. Hamburger,et al.  A series of normal stages in the development of the chick embryo. 1951. , 2012, Developmental dynamics : an official publication of the American Association of Anatomists.

[7]  W M Cowan,et al.  The development and restriction of the ipsilateral retinofugal projection in the chick. , 1983, Brain research.

[8]  H. Nakamura,et al.  Disturbance of refinement of retinotectal projection in chick embryos by tetrodotoxin and grayanotoxin. , 1990, Brain research. Developmental brain research.

[9]  G. Edelman,et al.  The NO hypothesis: possible effects of a short-lived, rapidly diffusible signal in the development and function of the nervous system. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[10]  M. Constantine-Paton,et al.  Patterned activity, synaptic convergence, and the NMDA receptor in developing visual pathways. , 1990, Annual review of neuroscience.

[11]  S. Snyder,et al.  Nitric oxide synthase: irreversible inhibition by L-NG-nitroarginine in brain in vitro and in vivo. , 1991, Biochemical and biophysical research communications.

[12]  S. Snyder,et al.  Nitric oxide synthase and neuronal NADPH diaphorase are identical in brain and peripheral tissues. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[13]  S. Thanos,et al.  Development of the transient ipsilateral retinotectal projection in the chick embryo: A numerical flourescence‐microscopic analysis , 1984, The Journal of comparative neurology.

[14]  C. Williams,et al.  Correlation of nitric oxide synthase expression with changing patterns of axonal projections in the developing visual system , 1994, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[15]  J. Sandell,et al.  NADPH diaphorase cells in the mammalian inner retina , 1985, The Journal of comparative neurology.

[16]  P. Greengard,et al.  Calcium/calmodulin-dependent protein kinase II increases glutamate and noradrenaline release from synaptosomes , 1990, Nature.

[17]  L. Maffei,et al.  Spontaneous impulse activity of rat retinal ganglion cells in prenatal life. , 1988, Science.

[18]  M. Constantine-Paton,et al.  N-methyl-D-aspartate receptor antagonists disrupt the formation of a mammalian neural map. , 1992, Proceedings of the National Academy of Sciences of the United States of America.

[19]  Hollis T. Cline,et al.  NMDA receptor antagonists disrupt the retinotectal topographic map , 1989, Neuron.

[20]  S. Snyder,et al.  Nitric oxide mediates glutamate-linked enhancement of cGMP levels in the cerebellum. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[21]  K. Johnson,et al.  Nitric oxide induces neurotransmitter release from hippocampal slices. , 1992, European journal of pharmacology.

[22]  D. Madison,et al.  A requirement for the intercellular messenger nitric oxide in long-term potentiation. , 1991, Science.

[23]  George L. Wilcox,et al.  The role of nitric oxide in hippocampal long-term potentiation , 1992, Neuron.

[24]  P G Nelson,et al.  Effects of patterned electrical activity on neurite outgrowth from mouse sensory neurons , 1990, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[25]  M. Sur,et al.  Disruption of retinogeniculate afferent segregation by antagonists to NMDA receptors , 1991, Nature.

[26]  L. Maffei,et al.  Correlation in the discharges of neighboring rat retinal ganglion cells during prenatal life. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[27]  S. Snyder,et al.  Isolation of nitric oxide synthetase, a calmodulin-requiring enzyme. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[28]  E. Nagata,et al.  Inhibition of nitric oxide synthesis induces a significant reduction in local cerebral blood flow in the rat , 1991, Neuroscience Letters.

[29]  C. Stevens,et al.  Glutamate activates multiple single channel conductances in hippocampal neurons , 1987, Nature.

[30]  M. J. Friedlander,et al.  Role of NO production in NMDA receptor-mediated neurotransmitter release in cerebral cortex. , 1994, Science.

[31]  S. McLoon,et al.  Elimination of the transient ipsilateral retinotectal projection is not solely achieved by cell death in the developing chick , 1991, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[32]  S. Moncada,et al.  Nitric oxide: physiology, pathophysiology, and pharmacology. , 1991, Pharmacological reviews.

[33]  J. Garthwaite,et al.  Endothelium-derived relaxing factor release on activation of NMDA receptors suggests role as intercellular messenger in the brain , 1988, Nature.

[34]  E. Kandel,et al.  Are adult learning mechanisms also used for development? , 1992, Science.

[35]  D. Baylor,et al.  Synchronous bursts of action potentials in ganglion cells of the developing mammalian retina. , 1991, Science.

[36]  S. McLoon,et al.  Alterations in precision of the crossed retinotectal projection during chick development. , 1982, Science.

[37]  M. Mayer,et al.  Voltage-dependent block by Mg2+ of NMDA responses in spinal cord neurones , 1984, Nature.

[38]  J. Connor.  Digital imaging of free calcium changes and of spatial gradients in growing processes in single, mammalian central nervous system cells. , 1986, Proceedings of the National Academy of Sciences of the United States of America.

[39]  C. Shatz.  Impulse activity and the patterning of connections during cns development , 1990, Neuron.

[40]  E. Kandel,et al.  Tests of the roles of two diffusible substances in long-term potentiation: evidence for nitric oxide as a possible early retrograde messenger. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[41]  G. Shepherd,et al.  Retinal ganglion cells express a cGMP-gated cation conductance activatable by nitric oxide donors , 1994, Neuron.