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ON Cone Bipolar Cells (on + cone_bipolar_cell)
Selected AbstractsSynaptic contacts between an identified type of ON cone bipolar cell and ganglion cells in the mouse retinaEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2005Bin Lin Abstract We surveyed the potential contacts between an identified type of bipolar cell and retinal ganglion cells in the mouse. By crossing two existing mouse strains (line 357 and line GFP-M), we created a double transgenic strain in which GFP is expressed by all members of a single type of ON cone bipolar cell and a sparse, mixed population of retinal ganglion cells. The GFP-expressing bipolar cells appear to be those termed CB4a of Pignatelli & Strettoi [(2004) J. Comp. Neurol., 476, 254,266] and type 7 of Ghosh et al. [(2004) J. Comp. Neurol., 469, 70,82 and J. Comp. Neurol., 476, 202,203]. The labelled ganglion cells include examples of most or all types of ganglion cells present in the mouse. By studying the juxtaposition of their processes in three dimensions, we could learn which ganglion cell types are potential synaptic targets of the line 357 bipolar cell. Of 12 ganglion cell types observed, 10 types could be definitively ruled out as major synaptic targets of the line 357 bipolar cells. One type of monostratified ganglion cell and one bistratified cell tightly cofasciculate with axon terminals of the line 357 bipolar cells. Double labelling for kinesin II demonstrates colocalization of bipolar cell ribbons at the sites of contact between these two types of ganglion cell and the line 357 bipolar cells. [source] Ret-PCP2 colocalizes with protein kinase C in a subset of primate ON cone bipolar cellsTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 7 2010Pyroja Sulaiman Abstract Purkinje cell protein 2 (PCP2), a member of the family of guanine dissociation inhibitors and a strong interactor with the G-protein subunit G,o, localizes to retinal ON bipolar cells. The retina-specific splice variant of PCP2, Ret-PCP2, accelerates the light response of rod bipolar cells by modulating the mGluR6 transduction cascade. All ON cone bipolar cells express mGluR6 and G,o, but only a subset expresses Ret-PCP2. Here we test the hypothesis that Ret-PCP2 contributes to shaping the various temporal bandwidths of ON cone bipolar cells in monkey retina. We found that the retinal splice variants in monkey and mouse are similar and longer than the cerebellar variants. Ret-PCP2 is strongly expressed by diffuse cone bipolar type 4 cells (DB4; marked with anti-PKC,) and weakly expressed by midget bipolar dendrites (labeled by antibodies against G,o, G,13, or mGluR6). Ret-PCP2 is absent from diffuse cone bipolar type 6 (DB6; marked with anti-CD15) and blue cone bipolar cells (marked with anti-CCK precursor). Thus, cone bipolar cells that terminate in stratum 3 of the inner plexiform layer (DB4) express more Ret-PCP2 than those that terminate in strata 3 + 4 (midget bipolar cells), and these in turn express more than those that terminate in stratum 5 (DB6 and blue cone bipolar cells). This expression pattern approximates the arborization of ganglion cells (GC) with different temporal bandwidths: parasol GCs stratifying near stratum 3 are faster than midget GCs stratifying in strata 3 + 4, and these are probably faster than the sluggish GCs that arborize in stratum 5. J. Comp. Neurol. 518:1098,1112, 2010. © 2009 Wiley-Liss, Inc. [source] Differential output of the high-sensitivity rod photoreceptor: AII amacrine pathwayTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 6 2008Artemis Petrides A population of ON cone bipolar cells is not coupled to AII amacrine cells. Neurobiotin (red) diffusion away from an injected AII amacrine cell (top right) at the level of bipolar cell somas in the inner nuclear layer of the rabbit retina. The somas of all depolarizing bipolar cells were labeled with antisera to G0, (green), and rod bipolars are labeled with antisera to PKC, (blue). G0, -outlined somas without PKC, or Neurobiotin are non-coupled ON cone bipolar cells. J. Comp. Neurol. 507:1653,1662, 2008. © 2008 Wiley-Liss, Inc. [source] Differential output of the high-sensitivity rod photoreceptor: AII amacrine pathwayTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 5 2008Artemis Petrides A population of ON cone bipolar cells is not coupled to AII amacrine cells. Neurobiotin (red) diffusion away from an injected AII amacrine cell (top right) at the level of bipolar cell somas in the inner nuclear layer of the rabbit retina. The somas of all depolarizing bipolar cells were labeled with antisera to G0, (green), and rod bipolars are labeled with antisera to PKC, (blue). G0, -outlined somas without PKC, or Neurobiotin are non-coupled ON cone bipolar cells. J. Comp. Neurol. 507:1653-1662, 2008. © 2008 Wiley-Liss, Inc. [source] Differential output of the high-sensitivity rod photoreceptor: AII amacrine pathwayTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 5 2008Artemis Petrides Abstract In the mammalian retina, the scotopic threshold of ganglion cells is in part dependent on how rod inputs are summed by their presynaptic cone bipolar cells. For ON cone bipolar cells, there are two anatomical routes for rod signals: 1) cone photoreceptors receive inputs via gap junctions with the surrounding, more numerous rods; and 2) ON cone bipolar cells receive highly convergent input via gap junctions with AII amacrine cells, which each receive input from hundreds of rods. Rod-cone coupling is thought to be utilized at higher photon fluxes relative to the AII-ON cone bipolar pathway due to the impedance mismatch of a single small rod driving a larger cone. Furthermore, it is widely held that the convergence of high-gain chemical synapses onto AIIs confers the highest sensitivity to ON cone bipolar cells and ganglion cells. A lack of coupling between one or more types of ON cone bipolar cells and AIIs would obviate this high-sensitivity pathway and explain the existence of ganglion cells with elevated scotopic thresholds. To investigate this possibility, we examined Neurobiotin and glycine diffusion from AIIs to bipolar cells and found that approximately one-fifth of ON cone bipolar cells are not coupled to AIIs. Unlike AII-AII coupling, which changes with ambient background intensity, the fraction of noncoupled ON cone bipolar cells was unaltered by dark or light adaptation. These data suggest that one of five morphologically distinct ON cone bipolar cell types is not coupled to AIIs and suggest that AII-ON cone bipolar coupling is modulated differently from AII-AII coupling. J. Comp. Neurol. 507:1653,1662, 2008. © 2008 Wiley-Liss, Inc. [source] Contribution of voltage-gated sodium channels to the b-wave of the mammalian flash electroretinogramTHE JOURNAL OF PHYSIOLOGY, Issue 10 2008Deb Kumar Mojumder Voltage-gated sodium channels (Nav channels) in retinal neurons are known to contribute to the mammalian flash electroretinogram (ERG) via activity of third-order retinal neurons, i.e. amacrine and ganglion cells. This study investigated the effects of tetrodotoxin (TTX) blockade of Nav channels on the b-wave, an ERG wave that originates mainly from activity of second-order retinal neurons. ERGs were recorded from anaesthetized Brown Norway rats in response to brief full-field flashes presented over a range of stimulus energies, under dark-adapted conditions and in the presence of steady mesopic and photopic backgrounds. Recordings were made before and after intravitreal injection of TTX (,3 ,m) alone, 3,6 weeks after optic nerve transection (ONTx) to induce ganglion cell degeneration, or in combination with an ionotropic glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 200 ,m) to block light-evoked activity of inner retinal, horizontal and OFF bipolar cells, or with the glutamate agonist N -methyl- d -aspartate (NMDA, 100,200 ,m) to reduce light-evoked inner retinal activity. TTX reduced ERG amplitudes measured at fixed times corresponding to b-wave time to peak. Effects of TTX were seen under all background conditions, but were greatest for mesopic backgrounds. In dark-adapted retina, b-wave amplitudes were reduced only when very low stimulus energies affecting the inner retina, or very high stimulus energies were used. Loss of ganglion cells following ONTx did not affect b-wave amplitudes, and injection of TTX in eyes with ONTx reduced b-wave amplitudes by the same amount for each background condition as occurred when ganglion cells were intact, thereby eliminating a ganglion cell role in the TTX effects. Isolation of cone-driven responses by presenting test flashes after cessation of a rod-saturating conditioning flash indicated that the TTX effects were primarily on cone circuits contributing to the mixed rod,cone ERG. NMDA significantly reduced only the additional effects of TTX on the mixed rod,cone ERG observed under mesopic conditions, implicating inner retinal involvement in those effects. After pharmacological blockade with CNQX, TTX still reduced b-wave amplitudes in cone-isolated ERGs indicating Nav channels in ON cone bipolar cells themselves augment b-wave amplitude and sensitivity. This augmentation was largest under dark-adapted conditions, and decreased with increasing background illumination, indicating effects of background illumination on Nav channel function. These findings indicate that activation of Nav channels in ON cone bipolar cells affects the b-wave of the rat ERG and must be considered when analysing results of ERG studies of retinal function. [source] |