scholarly journals Ionotropic glutamate receptors of amacrine cells of the mouse retina

2006 ◽  
Vol 23 (1) ◽  
pp. 79-90 ◽  
Author(s):  
OLIVIA N. DUMITRESCU ◽  
DARIO A. PROTTI ◽  
SRIPARNA MAJUMDAR ◽  
HANNS ULRICH ZEILHOFER ◽  
HEINZ WÄSSLE
Keyword(s):  
Nmda Receptors ◽  
Glutamate Receptors ◽  
Amacrine Cell ◽  
Fluorescent Protein ◽  
Lucifer Yellow ◽  
Amacrine Cells ◽  
Ionotropic Glutamate Receptors ◽  
Mouse Retina ◽  
Wide Field ◽  
Transgenic Mouse Line

The mammalian retina contains approximately 30 different morphological types of amacrine cells, receiving glutamatergic input from bipolar cells. In this study, we combined electrophysiological and pharmacological techniques in order to study the glutamate receptors expressed by different types of amacrine cells. Whole-cell currents were recorded from amacrine cells in vertical slices of the mouse retina. During the recordings the cells were filled with Lucifer Yellow/Neurobiotin allowing classification as wide-field or narrow-field amacrine cells. Amacrine cell recordings were also carried out in a transgenic mouse line whose glycinergic amacrine cells express enhanced green fluorescent protein (EGFP). Agonist-induced currents were elicited by exogenous application of NMDA, AMPA, and kainate (KA) while holding cells at −75 mV. Using a variety of specific agonists and antagonists (NBQX, AP5, cyclothiazide, GYKI 52466, GYKI 53655, SYM 2081) responses mediated by AMPA, KA, and NMDA receptors could be dissected. All cells (n= 300) showed prominent responses to non-NMDA agonists. Some cells expressed AMPA receptors exclusively and some cells expressed KA receptors exclusively. In the majority of cells both receptor types could be identified. NMDA receptors were observed in about 75% of the wide-field amacrine cells and in less than half of the narrow-field amacrine cells. Our results confirm that different amacrine cell types express distinct sets of ionotropic glutamate receptors, which may be critical in conferring their unique temporal responses to this diverse neuronal class.

Neural interactions mediating the detection of motion in the retina of the tiger salamander

1988 ◽  
Vol 1 (3) ◽  
pp. 317-329 ◽  
Author(s):  
Frank Werblin ◽  
Greg Maguire ◽  
Peter Lukasiewicz ◽  
Scott Eliasof ◽  
Samuel M. Wu
Keyword(s):  
Time Course ◽  
Amacrine Cell ◽  
Lucifer Yellow ◽  
Amacrine Cells ◽  
Cell Types ◽  
Lateral Spread ◽  
Wide Field ◽  
Inner Plexiform Layer ◽  
Local Populations ◽  
Transient Activity

AbstractThe neural circuitry underlying movement detection was inferred from studies of amacrine cells under whole-cell patch clamp in retinal slices. Cells were identified by Lucifer yellow staining. Synaptic inputs were driven by “puffing“ transmitter substances at the dendrites of presynaptic cells. Spatial sensitivity profiles for amacrine cells were measured by puffing transmitter substances along the lateral spread of their processes. Synaptic pathways were separated and identified with appropriate pre- and postsynaptic pharmacological blocking agents.Two distinct amacrine cell types were found: one with narrow spread of processes that sustained excitatory synaptic current, the other with very wide spread of processes that transient excitatory synaptic currents. The transient currents found only in the wide-field amacrine cell were formed presynaptically at GABAB receptors. They could be blocked with baclofen, a GABAB agonist, and their time course was extended by AVA, a GABAB antagonist. Baclofen and AVA had no direct affect upon the wide-field amacrine cell, but picrotoxin blocked a separate, direct GABA input to this cell.The narrow-field amacrine cell was shown to be GABAergic by counterstaining with anti-GABA antiserum after it was filled with Lucifer yellow. Its narrow, spatial profile and sustained synaptic input are properties that closely match those of the GABAergic antagonistic signal that forms transient activity (described above), suggesting that the narrow-field amacrine cell itself is the source of the GABAergic interaction mediating transient activity in the inner plexiform layer (IPL). Other work has shown a GABAB sensitivity at some bipolar terminals, suggesting a population of bipolars as the probable site of interaction mediating transient action.The results suggest that two local populations of amacrine cell types (sustained and transient) interact with the two populations of bipolar cell types (transient forming and nontransient forming). These interactions underlie the formation of the change-detecting subunits. We suggest that local populations of these subunits converge to form the receptive fields of movement-detecting ganglion cells.

Ionotropic Glutamate Receptors - Focus on Non-NMDA Receptors

1995 ◽  
Vol 76 (5) ◽  
pp. 312-319 ◽  
Author(s):  
Marianne Jørgensen ◽  
Charlotte K. Tygesen ◽  
Peter Høngaard Andersen
Keyword(s):  
Nmda Receptors ◽  
Glutamate Receptors ◽  
Ionotropic Glutamate Receptors

Amacrine-to-amacrine cell inhibition: Spatiotemporal properties of GABA and glycine pathways

2011 ◽  
Vol 28 (3) ◽  
pp. 193-204 ◽  
Author(s):  
XIN CHEN ◽  
HAIN ANN HSUEH ◽  
FRANK S. WERBLIN
Keyword(s):  
Amacrine Cell ◽  
Ganglion Cells ◽  
Amacrine Cells ◽  
Peak Level ◽  
Wide Field ◽  
Gabaergic Inhibition ◽  
Onset Latency ◽  
Temporal Properties ◽  
Glycinergic Inhibition ◽  
Cell Inhibition

AbstractWe measured the spatial and temporal properties of GABAergic and glycinergic inhibition to amacrine cells in the whole-mount rabbit retina. The amacrine cells were parsed into two morphological classes: narrow-field cells with processes spreading less than 200 μm and wide-field cells with processes extending more than 300 μm. The inhibition was also parsed into two types: sustained glycine and transient GABA. Narrow-field amacrine cells receive 1) very transient GABAergic inhibition with a fast onset latency of 140 ± 16 ms decaying to 30% of the peak level within 208 ± 27 ms elicited broadly over a lateral distance of up to 1500 μm and 2) sustained glycinergic inhibition with a medium onset latency of 286 ± 23 ms that was elicited over a spatial area often broader than the processes of the narrow-field amacrine cells. Wide-field amacrine cells received sustained glycinergic inhibition but no broad transient GABAergic inhibition. Surprisingly, neither of these amacrine cell classes received sustained local GABAergic inhibition, commonly found in an earlier study of ganglion cells.

scholarly journals Disinhibitory recruitment of NMDA receptor pathways in retina

2014 ◽  
Vol 112 (1) ◽  
pp. 193-203 ◽  
Author(s):  
Santhosh Sethuramanujam ◽  
Malcolm M. Slaughter
Keyword(s):  
Nmda Receptor ◽  
Glutamate Receptors ◽  
Presynaptic Inhibition ◽  
Amacrine Cell ◽  
Glutamate Release ◽  
Relative Strength ◽  
Bipolar Cells ◽  
Ionotropic Glutamate Receptors ◽  
Nmdar Activation ◽  
On And Off Pathways

Glutamate release at bipolar to ganglion cell synapses activates NMDA and AMPA/kainic acid (KA) ionotropic glutamate receptors. Their relative strength determines the output signals of the retina. We found that this balance is tightly regulated by presynaptic inhibition that preferentially suppresses NMDA receptor (NMDAR) activation. In transient ON-OFF neurons, block of GABA and glycine feedback enhanced total NMDAR charge by 35-fold in the ON response and 9-fold in the OFF compared with a 1.7-fold enhancement of AMPA/KA receptors. Blocking only glycine receptors enhanced the NMDAR excitatory postsynaptic current 10-fold in the ON and 2-fold in the OFF pathway. Blocking GABAA or GABAC receptors (GABACRs or GABAARs) produced small changes in total NMDAR charge. When both GABAARs and GABACRs were blocked, the total NMDAR charge increased ninefold in the ON and fivefold in the OFF pathway. This exposed a strong GABACR feedback to bipolar cells that was suppressed by serial amacrine cell synapses mediated by GABAARs. The results indicate that NMDAR currents are large but latent, held in check by dual GABA and glycine presynaptic inhibition. One example of this controlled NMDAR activation is the cross talk between ON and OFF pathways. Blocking the ON pathway increased NMDAR relative strength in the OFF pathway. Stimulus prolongation similarly increased the NMDAR relative strength in the OFF response. This NMDAR enhancement was produced by a diminution in GABA and glycine feedback. Thus the retinal network recruits NMDAR pathways through presynaptic disinhibition.

Ionotropic Glutamate Receptors (AMPA, Kainate and NMDA Receptors)

2012 ◽  
pp. 972-972
Author(s):  
Kathryn M. Appleton ◽  
Ian Cushman ◽  
Yuri K. Peterson ◽  
Balachandran Manavalan ◽  
Shaherin Basith ◽  
...  
Keyword(s):  
Nmda Receptors ◽  
Glutamate Receptors ◽  
Ionotropic Glutamate Receptors

Glycine receptors of A-type ganglion cells of the mouse retina

2007 ◽  
Vol 24 (4) ◽  
pp. 471-487 ◽  
Author(s):  
SRIPARNA MAJUMDAR ◽  
LIANE HEINZE ◽  
SILKE HAVERKAMP ◽  
ELENA IVANOVA ◽  
HEINZ WÄSSLE
Keyword(s):  
Fluorescent Protein ◽  
Ganglion Cells ◽  
Glycine Receptor ◽  
Mouse Retina ◽  
Inhibitory Input ◽  
Visual Channel ◽  
Fast Kinetics ◽  
Transgenic Mouse Line ◽  
Green Fluorescent ◽  
Α Subunits

A-type ganglion cells of the mouse retina represent the visual channel that transfers temporal changes of the outside world very fast and with high fidelity. In this study we combined anatomical and physiological methods in order to study the glycinergic, inhibitory input of A-type ganglion cells. Immunocytochemical studies were performed in a transgenic mouse line whose ganglion cells express green fluorescent protein (GFP). The cells were double labeled for GFP and the four α subunits of the glycine receptor (GlyR). It was found that most of the glycinergic input of A-type cells is through fast, α1-expressing synapses. Whole-cell currents were recorded from A-type ganglion cells in retinal whole mounts. The response to exogenous application of glycine and spontaneous inhibitory postsynaptic currents (sIPSCs) were measured. By comparing glycinergic currents recorded in wildtype mice and in mice with specific deletions of GlyRα subunits (Glra1spd-ot,Glra2−/−,Glra3−/−), the subunit composition of GlyRs of A-type ganglion cells could be further defined. Glycinergic sIPSCs of A-type ganglion cells have fast kinetics (decay time constant τ = 3.9 ± 2.5 ms, mean ± SD). Glycinergic sIPSCs recorded inGlra2−/−andGlra3−/−mice did not differ from those of wildtype mice. However, the number of glycinergic sIPSCs was significantly reduced inGlra1spd-otmice and the remaining sIPSCs had slower kinetics than in wildtype mice. The results show that A-type ganglion cells receive preferentially kinetically fast glycinergic inputs, mediated by GlyRs composed of α1 and β subunits.

scholarly journals Regulation of retinal amacrine cell generation by miR-216b and Foxn3

2020 ◽  
Author(s):  
Huanqing Zhang ◽  
Pei Zhuang ◽  
Ryan M. Welchko ◽  
Manhong Dai ◽  
Fan Meng ◽  
...  
Keyword(s):  
Amacrine Cell ◽  
Ectopic Expression ◽  
Cell Formation ◽  
Complex Mixture ◽  
Amacrine Cells ◽  
Retinal Cell ◽  
Mouse Retina ◽  
Mammalian Retina ◽  
Different Types ◽  
Retinal Explants

AbstractThe mammalian retina contains a complex mixture of different types of neurons. We find that the microRNA miR-216b is preferentially expressed in postmitotic retinal amacrine cells in the mouse retina, and expression of miR-216a/b and miR-217 in the retina depend in part on Ptf1a, a transcription factor required for amacrine cell differentiation. Surprisingly, ectopic expression of miR-216b, or the related miR-216a, can direct the formation of additional amacrine cells in the developing retina. In addition, we observe the loss of bipolar neurons in the retina after miR-216b expression. We identify the mRNA for the transcriptional regulator Foxn3 as a retinal target of miR-216b by Argonaute PAR-CLIP and reporter analysis. Inhibition of Foxn3 in the postnatal developing retina by RNAi also increases the formation of amacrine cells and reduces bipolar cell formation, while overexpression of Foxn3 inhibits amacrine cell formation prior to the expression of Ptf1a. Disruption of Foxn3 by CRISPR in embryonic retinal explants also reduces amacrine cell formation. Co-expression of Foxn3 can partially reverse the effects of ectopic miR-216b on retinal cell type formation. Our results identify Foxn3 as a novel regulator of interneuron formation in the developing retina and suggest that miR-216b likely regulates expression of Foxn3 and other genes in amacrine cells.

Sign in / Sign up

Export Citation Format

Share Document