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MeSH Review

Amacrine Cells

 
 
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Disease relevance of Amacrine Cells

 

High impact information on Amacrine Cells

 

Chemical compound and disease context of Amacrine Cells

  • NO synthase immunoreactivity and NADPH diaphorase staining are colocalized in the pedunculopontine nucleus with choline acetyltransferase-containing cells and are also colocalized in amacrine cells of the inner nuclear layer and ganglion cells of the retina, myenteric plexus neurons of the intestine, and ganglion cells of the adrenal medulla [10].
  • In other mammals, the light responses of polyaxonal amacrine cells like these and cholinergic amacrine cells have been recorded, and the effects of acetylcholine and cholecystokinin on ganglion cells are known [11].
  • Inhibition of on-centre cells, thus, appears to be mediated by GABA, whereas that of off-centre cells, by glycine regardless of whether the cells are 'sustained' or 'transient'. Possible existence of GABAergic and glycinergic amacrine cells making postsynaptic contact with on-centre and off-centre ganglion cells, respectively, is proposed [12].
  • This differential targeting of ganglion cells and amacrine cells in the OFF vs. ON layers indicates a difference in the role of bipolar cells in the generation of receptive field properties, depending on whether or not they use GABA as well as glutamate for their transmitter [13].
  • In addition to the variable NMDA activation pattern, we found that virtually all ganglion cells (87%) showed NMDA-gated AGB entry, compared with only 58% of amacrine cells [14].
 

Biological context of Amacrine Cells

 

Anatomical context of Amacrine Cells

  • Iontophoretic injection of Lucifer yellow into the labeled cells under microscopic control revealed that the serotonin-accumulating neurons in rabbit retina constitute two morphological types of amacrine cells, termed S1 and S2, whose distal dendrites are stratified at the inner margin of the inner plexiform layer [20].
  • Taken together, our results suggest that connexins are expressed in bipolar cells in a neuronal subtype-specific manner and that cx36/cx36 gap junctions form the heterologous electrical synapses between AII amacrine cells and BPGus-GFP cells [21].
  • Fibroblast growth factor receptor blockade results in almost a 50% loss of photoreceptors and amacrine cells, and a concurrent 3.5-fold increase in Müller glia, suggesting a shift towards a Müller cell fate in the absence of a fibroblast growth factor receptor signal [22].
  • To ascertain the effects of glycine-accumulating bipolar and amacrine cells on the response properties of retinal ganglion cells, in vivo iontophoretic studies were performed in the cat eye [23].
  • Our results indicate the existence of three classes of presumed amacrine cell synaptic terminals: synapsin I+/synapsin II-, synapsin I-/synapsin II+, and synapsin I+/synapsin II+ [24].
 

Associations of Amacrine Cells with chemical compounds

 

Gene context of Amacrine Cells

  • These results indicate that Foxn4 is both necessary and sufficient for commitment to the amacrine cell fate and is nonredundantly required for the genesis of horizontal cells [29].
  • Moreover, we have located cx36 puncta at the axonal terminals of BPGus-GFP cells, and we have found that these BPGus-GFP-associated cx36 puncta always colocalized with AII amacrine cell processes [21].
  • RPGRIP is also expressed in other neurons such as amacrine cells [30].
  • Taken together, our data suggest that Barhl2 may function to specify the identity of glycinergic amacrine cells from competent progenitors during retinogenesis [16].
  • A third element in Pax6 intron 4, when combined with either the P0 or P1 promoter, accurately directs expression in amacrine cells, ciliary body and iris [31].
 

Analytical, diagnostic and therapeutic context of Amacrine Cells

References

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