Open this publication in new window or tab >>Neurosciences Research, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Neurobiology and Psychiatry, Stanford University School of Medicine, Stanford, California 94305, USA.
Neurosciences and 2Ophthalmic Research, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Neurobiology, Stanford University School of Medicine, Stanford, California 94305, USA.
Neurobiology and Psychiatry, Stanford University School of Medicine, Stanford, California 94305, USA.
Neurobiology, Stanford University School of Medicine, Stanford, California 94305, USA.
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Neurobiology and Psychiatry, Stanford University School of Medicine, Stanford, California 94305, USA.
Ophthalmic Research, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA/Research Service, Cleveland VA Medical Center, Cleveland, Ohio 44106, USA.
Ophthalmic Research, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA/Research Service, Cleveland VA Medical Center, Cleveland, Ohio 44106, USA.
Department of Ophthalmology, University of California, San Francisco, San Francisco, California 94143, USA.
Center for Neuroscience, University of California, Davis, California 95616, USA.
Neurosciences Research, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Neurobiology, Stanford University School of Medicine, Stanford, California 94305, USA.
Neurosciences and 2Ophthalmic Research, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
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2006 (English)In: Journal of Neuroscience, ISSN 0270-6474, E-ISSN 1529-2401, Vol. 26, no 23, p. 6269-6281Article in journal (Refereed) Published
Abstract [en]
Neuronal pentraxins (NPs) define a family of proteins that are homologous to C-reactive and acute-phase proteins in the immune system and have been hypothesized to be involved in activity-dependent synaptic plasticity. To investigate the role of NPs in vivo, we generated mice that lack one, two, or all three NPs. NP1/2 knock-out mice exhibited defects in the segregation of eye-specific retinal ganglion cell (RGC) projections to the dorsal lateral geniculate nucleus, a process that involves activity-dependent synapse formation and elimination. Retinas from mice lacking NP1 and NP2 had cholinergically driven waves of activity that occurred at a frequency similar to that of wild-type mice, but several other parameters of retinal activity were altered. RGCs cultured from these mice exhibited a significant delay in functional maturation of glutamatergic synapses. Other developmental processes, such as pathfinding of RGCs at the optic chiasm and hippocampal long-term potentiation and long-term depression, appeared normal in NP-deficient mice. These data indicate that NPs are necessary for early synaptic refinements in the mammalian retina and dorsal lateral geniculate nucleus. We speculate that NPs exert their effects through mechanisms that parallel the known role of short pentraxins outside the CNS.
Keywords
retinogeniculate, neuronal pentraxins, synaptic plasticity, LTP, long-term potentiation, LTD, long-term depression, development, knock-out, retinal ganglion cell
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-51407 (URN)10.1523/JNEUROSCI.4212-05.2006 (DOI)
2009-10-302009-10-302018-07-03Bibliographically approved