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Synaptic Layers (synaptic + layer)
Selected AbstractsBand 4.1 proteins are expressed in the retina and interact with both isoforms of the metabotropic glutamate receptor type 8JOURNAL OF NEUROCHEMISTRY, Issue 6 2008Melanie Rose Abstract The function of the CNS depends on the correct regulation of neurotransmitter receptors by interacting proteins. Here, we screened a retinal cDNA library for proteins interacting with the intracellular C-terminus of the metabotropic glutamate receptor isoform 8a (mGluR8a). The band 4.1B protein binds to the C-termini of mGluR8a and mGluR8b, co-localizes with these glutamate receptors in transfected mammalian cells, facilitates their cell surface expression and inhibits the mGluR8 mediated reduction of intracellular cAMP concentrations. In contrast, no interaction with 4.1B was observed for other mGluRs tested. Amino acids encoded by exons 19 and 20 of 4.1B and a stretch of four basic amino acids present in the mGluR8 C-termini mediate the protein interaction. Besides binding to 4.1B, mGluR8 isoforms interact with 4.1G, 4.1N, and 4.1R. Because band 4.1 transcripts undergo extensive alternative splicing, we analyzed the splicing pattern of interacting regions and detected a 4.1B isoform expressed specifically in the retina. Within this tissue, mGluR8 and 4.1B, 4.1G, 4.1N, and 4.1R show a comparable distribution, being expressed in both synaptic layers and in somata of the ganglion cell layer. In summary, our studies identified band 4.1 proteins as new players for the mGluR8 mediated signal transduction. [source] Expression of neuronal markers, synaptic proteins, and glutamine synthetase in the control and regenerating lizard visual systemTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 19 2010M.M. Romero-Alemán Abstract Spontaneous regrowth of retinal ganglion cell (RGC) axons occurs after optic nerve (ON) transection in the lizard Gallotia galloti. To gain more insight into this event we performed an immunohistochemical study on selected neuron and glial markers, which proved useful for analyzing the axonal regrowth process in different regeneration models. In the control lizards, RGCs were beta-III tubulin- (Tuj1) and HuCD-positive. The vesicular glutamate transporter-1 (VGLUT1) preferentially stained RGCs and glial somata rather than synaptic layers. In contrast, SV2 and vesicular GABA/glycine transporter (VGAT) labeling was restricted to both plexiform layers. Strikingly, the strong expression of glutamine synthetase (GS) in both Müller glia processes and macroglial somata revealed a high glutamate metabolism along the visual system. Upregulation of Tuj1 and HuCD in the surviving RGCs was observed at all the timepoints studied (1, 3, 6, 9, and 12 months postlesion). The significant rise of Tuj1 in the optic nerve head and optic tract (OTr) by 1 and 6 months postlesion, respectively, suggests an increase of the beta-III tubulin transport and incorporation into newly formed axons. Persistent Tuj1+ and SV2+ puncta and swellings were abnormally observed in putative degenerating/dystrophic fibers. Unexpectedly, neuron-like cells of obscure significance were identified in the control and regenerating ON-OTr. We conclude that: 1) the persistent upregulation of Tuj1 and HuCD favors the long-lasting axonal regrowth process; 2) the latter succeeded despite the ectopia and dystrophy of some regrowing fibers; and 3) maintenance of the glutamate-glutamine cycle contributes to the homeostasis and plasticity of the system. J. Comp. Neurol. 518:4067,4087, 2010. © 2010 Wiley-Liss, Inc. [source] Drebrin A is a postsynaptic protein that localizes in vivo to the submembranous surface of dendritic sites forming excitatory synapsesTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 4 2005Chiye Aoki Abstract Drebrin A is a neuron-specific, actin binding protein. Evidence to date is from in vitro studies, consistently supporting the involvement of drebrin A in spinogenesis and synaptogenesis. We sought to determine whether drebrin A arrives at the plasma membrane of neurons, in vivo, in time to orchestrate spinogenesis and synaptogenesis. To this end, a new antibody was used to locate drebrin A in relation to electron microscopically imaged synapses during early postnatal days. Western blotting showed that drebrin A emerges at postnatal day (PNd) 6 and becomes progressively more associated with F-actin in the pellet fraction. Light microscopy showed high concentrations of drebrin A in the synaptic layers of the hippocampus and cortex. Electron microscopy revealed that drebrin A in these regions is located exclusively in dendrites both neonatally and in adulthood. In adulthood, nearly all of the synaptic drebrin A is within spines forming asymmetric excitatory synapses, verified by ,-aminobutyric acid (GABA) negativity. At PNd7, patches of drebrin A immunoreactivity were discretely localized to the submembranous surfaces of dendrites forming slight protrusions,protospines. The drebrin A sites exhibited only thin postsynaptic densities and lacked axonal associations or were contacted by axons that contained only a few vesicles. Yet, because of their immunoreactivity to the NR2B subunit of N -methyl- D -aspartate receptors and immunonegativity of axon terminals to GABA, these could be presumed to be nascent, excitatory synapses. Thus, drebrin A may be involved in organizing the dendritic pool of actin for the formation of spines and of axospinous excitatory synapses during early postnatal periods. J. Comp. Neurol. 483:383,402, 2005. © 2005 Wiley-Liss, Inc. [source] Comparisons of structural and functional abnormalities in mouse b-wave mutantsTHE JOURNAL OF PHYSIOLOGY, Issue 18 2008Maureen A. McCall In the most simplistic view, the retinal circuit can be divided into vertical excitatory pathways that use glutamate as their neurotransmitter and lateral inhibitory pathways in the outer and inner synaptic layers that modulate excitation via glycine and GABA. Within the vertical excitatory pathways, the visual signal is initiated in the rod, cone or both photoreceptors, depending on the adaptation state of the retina. This signal is transmitted to the rest of the retina through the bipolar cells, which can be subdivided based on: the photoreceptor that provides their input, their dendritic and axonal morphology, and the polarity of their response evoked by a luminance increment, e.g. depolarizing or hyperpolarizing responses. The polarity of this response is controlled by the type of glutamatergic postsynaptic receptor that is expressed on their dendritic terminals. Hyperpolarizing bipolar cells express AMPA/kainate receptors, whereas depolarizing bipolar cells (DBCs) express the metabotropic glutamate receptor 6 (Grm6). The electroretinogram (ERG) is a non-invasive method used to assess overall retinal function. The initiation of the visual signal in the photoreceptors is reflected in the ERG a-wave and the ensuing depolarization of DBCs in the b-wave. When there is failure of signal transmission from photoreceptors to DBCs or signalling within DBCs, the ERG a-wave is present, while the b-wave is absent or significantly reduced. This ERG phenotype has been found in the human population and is referred to as congenital stationary night blindness. Until recently, it had been assumed that the absence of a b-wave was indicative of a lack of signalling through the On pathway, leaving the Off pathway unaffected. Here we review recent findings that demonstrate that many mouse mutants share a no b-wave ERG phenotype but their retinal morphology and RGC responses differ significantly, suggesting very different effects of the underlying mutations on output from the DBCs to the rest of the retinal circuit. [source] | ||||||||||