Cation Cl− cotransporters in the dendrites of goldfish bipolar cells

Li, Baoqin; Shen, Wen‐Hui

doi:10.1097/wnr.0b013e3280ba49b0

Cited by 5 publications

(7 citation statements)

References 15 publications

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“…The effect seems to be expressed over a wide range of stimulus intensities. This suggestion is not consistent with the proposed opposite action of GABA on the dendrites of ON and OFF bipolar cells in goldfish (Li & Shen, 2007) and mammalian (Vardi et al, 2000) retina. The authors cited suggest that GABA inputs in the distal retina might excite ON bipolar cells, but inhibit OFF bipolar cells, because their dendrites express different types of cation chloride cotransporters.…”

Section: Discussioncontrasting

confidence: 52%

Effects of picrotoxin on light adapted frog electroretinogram are not due entirely to its action in proximal retina

Popova

2014

Vision Research

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In order to evaluate the site of action of picrotoxin (antagonist of ionotropic GABA receptors) on the electroretinographic (ERG) b- and d-waves, in this study we compared its effects on the intensity-response function of the ERG waves in intact light adapted frog eyecup preparations with its effects in eyecups, where the activity of proximal neurons was blocked by 1 mMN-methyl-d-aspartate (MNDA). Picrotoxin markedly enhanced the b- and d-wave amplitude and slowed the time course of the responses at all stimulus intensities in the intact eyecups. Perfusion with NMDA alone caused significant enhancement of the b-wave amplitude and diminution of the d-wave amplitude without altering their time course in the entire intensity range. When picrotoxin was applied in combination with NMDA, an enhancement of the b-wave amplitude and slowing of its time course were observed at all stimulus intensities. The increase of the b-wave amplitude was significantly higher than that seen in NMDA group. Combined application of picrotoxin and NMDA caused an enhancement of the d-wave amplitude at the lower stimulus intensities and its diminution at the higher ones, while the d-wave time course was delayed over the entire intensity range. The results obtained indicate that a part of picrotoxin effects on the amplitude and time course of the photopic ERG b- and d-waves are due to its action in the distal frog retina.

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Section: Discussioncontrasting

confidence: 52%

Effects of picrotoxin on light adapted frog electroretinogram are not due entirely to its action in proximal retina

Popova

2014

Vision Research

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“…pNKCC1, when present in the plasma membrane, is responsible for Cl − and cation uptake (Flemmer et al 2002; Gamba, 2005). In previous studies, we showed that the R5 antibody is specific for pNKCC1, enabling us to detect and label pNKCC1 in amphibian, goldfish and mouse retinas by Western blotting and immunolabelling (Li & Shen, 2007; Li et al 2008; Shen et al 2008), and Fig. 1 shows an example of the Western results for the R5 antibody against pNKCC1 proteins in the samples from mouse brain, mouse retina and tiger salamander retina.…”

Section: Resultsmentioning

confidence: 96%

“…In mature neurons, expression of NKCC1 tends to be reduced, but is still expressed at relatively high levels on sensory neurons within some areas of the CNS (Delpire et al 1999; Restrepo, 2005; Li et al 2008; Delpire & Austin, 2010). Both NKCC1 and NKCC2 have been detected in the vertebrate retina (Gavrikov et al 2006; Zhang et al 2006; Dmitriev et al 2007; Li & Shen, 2007; Li et al 2008), although their cellular distribution and functional roles vary among species. In chick retina, for example, NKCC1 is expressed on the apical dendrites of retinal pigment epithelium cells, and its activity has been linked to the control of ocular growth (Crewther et al 2008).…”

Section: Introductionmentioning

confidence: 99%

“…Interestingly, there is convincing evidence that NKCC1 is preferentially expressed in the distal synaptic layer within photoreceptor terminals and their second‐order neurons, i.e. horizontal cells and some of the dendrites of rod‐bipolar cells (Zhang et al 2006; Li & Shen 2007; Li et al 2008; Shen et al 2008). However, despite the presence of NKCC1 at these sites, and its contribution to the local E Cl in these neurons (Thoreson et al 2003; Thoreson & Bryson, 2004; Shen, 2005), the effect of NKCC1 on synaptic transmission in the distal retina is largely unknown.…”

Section: Introductionmentioning

confidence: 99%

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Regulation of synaptic transmission at the photoreceptor terminal: a novel role for the cation–chloride co‐transporter NKCC1

Shen

Purpura

et al. 2012

The Journal of Physiology

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Key points• The Cl − uptake cotransporter, Na + -K + -2Cl − type 1 (NKCC1), is expressed in the distal synaptic layer of the vertebrate retina, where photoreceptor terminals contact the dendrites of horizontal and bipolar cells.• Light adaptation, dopamine and a D1 receptor agonist increased the expression levels of phosphorylated NKCC1, the active form of the transporter inserted in the cell membrane.• Pharmacological blockage of NKCC1 with bumetanide increased the rod-and cone-mediated excitatory postsynaptic currents in horizontal cells.• Inhibiting NKCC1 increased exocytotic membrane capacitance, intracellular Ca 2+ levels, and voltage-dependent Ca 2+ channel currents in both rod and cone terminals, all of which are associated with increased transmitter release.• This study describes a new function of NKCC1, specifically the suppression of transmitter release at the photoreceptor terminals, a process that serves to prevent the depletion of glutamate and protect retinal neurons from its putative cytotoxic effects.Abstract The Na + -K + -2Cl − co-transporter type 1 (NKCC1) is localized primarily throughout the outer plexiform layer (OPL) of the distal retina, a synaptic lamina that is comprised of the axon terminals of photoreceptors and the dendrites of horizontal and bipolar cells. Although known to play a key role in development, signal transmission and the gating of sensory signals in other regions of the retina and in the CNS, the contribution of NKCC1 to synaptic transmission within the OPL is largely unknown. In the present study, we investigated the function of NKCC1 at the photoreceptor-horizontal cell synapse by recording the electrical responses of photoreceptors and horizontal cells before and after blocking the activity of the transporter with bumetanide (BMN). Because NKCC1 co-transports 1 Na + , 1 K + and 2 Cl − , it is electroneutral and its activation had little effect on membrane conductance. However, recordings from postsynaptic horizontal cells revealed that inhibiting NKCC1 with BMN greatly increased glutamate release from both rod and cone terminals. In addition, we found that NKCC1 directly regulates Ca 2+ -dependent exocytosis at the photoreceptor synapse, raising the possibility that NKCC1 serves to suppress bulk release of glutamate vesicles from photoreceptor terminals in the dark and at light offset. Interestingly, NKCC1 gene and protein expressions were upregulated by light, which we attribute to the light-induced release of dopamine acting on D1-like receptors. In sum, our study reveals a new role for NKCC1 in the regulation of synaptic transmission in photoreceptors.

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“…Thus expression of NKCC in neurons and neuronal regions might be an underlying a mechanism for a glycine evoked depolarization in the CNS. Immunocytochemical studies have revealed that NKCC is expressed in HCs and On-bipolar dendrites in the outer retinas of adult animals, but the expression does not present in the inner retinal neurons [17][18][19]. Clearly glycine may produce different responses in the inner and outer retinal neurons due to different E Cl in the neurons.…”

Section: Introductionmentioning

confidence: 96%

Glycine input induces the synaptic facilitation in salamander rod photoreceptors

Shen

Jiang

2008

J Biomed Sci

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Glycinergic synapses in photoreceptors are made by centrifugal feedback neurons in the network, but the function of the synapses is largely unknown. Here we report that glycinergic input enhances photoreceptor synapses in amphibian retinas. Using specific antibodies against a glycine transporter (GlyT2) and glycine receptor beta subunit, we identified the morphology of glycinergic input in photoreceptor terminals. Electrophysiological recordings indicated that 10 muM glycine depolarized rods and activated voltage-gated Ca(2+) channels in the neurons. The effects facilitated glutamate vesicle release in photoreceptors, meanwhile increased the spontaneous excitatory postsynaptic currents in Off-bipolar cells. Endogenous glycine feedback also enhanced glutamate transmission in photoreceptors. Additionally, inhibition of a Cl(-) uptake transporter NKCC1 with bumetanid effectively eliminated glycine-evoked a weak depolarization in rods, suggesting that NKCC1 maintains a high Cl(-) level in rods, which causes to depolarize in responding to glycine input. This study reveals a new function of glycine in retinal synaptic transmission.

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Cation Cl− cotransporters in the dendrites of goldfish bipolar cells

Cited by 5 publications

References 15 publications

Effects of picrotoxin on light adapted frog electroretinogram are not due entirely to its action in proximal retina

Effects of picrotoxin on light adapted frog electroretinogram are not due entirely to its action in proximal retina

Regulation of synaptic transmission at the photoreceptor terminal: a novel role for the cation–chloride co‐transporter NKCC1

Glycine input induces the synaptic facilitation in salamander rod photoreceptors

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