Retinal amacrine cells

Figure 2.2 The retina consists of three layers. Retinal ganglion cells are located at the top followed by a layer of bipolar cells and receptors at the bottom. Light has to pass through the top two layers to reach the light-sensitive sensors. Information then travels upward from the receptors to the bipolar cells and on to the retinal ganglion cells. Information is also exchanged laterally through amacrine and horizontal cells. (Retina illustration from LifeART Collection Images 1989-2001 by Lippincott Williams Wilkins, used by permission from SmartDraw.com.

Keywords Amacrine cell Bipolar cell Cone Fovea Horizontal cell Muller cells Photoreceptor Retina Retinal ganglion cell Rod... 

Figure 11.2. The five major retinal cell types (photoreceptors, bipolai cells, horizontal cells, amacrine cells, and ganglion cells) and tlieir synaptic connections.

Dopaminergic amacrine cells with widespread dendritic arborizations increase release of dopamine in response to increases in global illumination. Dopamine diffuses throughout the retina to influence cells as far away as the RPE. The increased release of dopamine by light modifies cell function to opdmize retinal responses in daylight (Witkovsky, 2004). 

Reichenbach et al., 1994b Sharma and Ehinger, 1997b) the same sequence of cytogenesis is found. There are no estimates as to how many amacrine cells are produced in the early phase and how many in the late phase of proliferation. In species in which the retinal development takes place over a short period of time (Xenopus), there is overlapping in the birth dates of cells, whereas species in which retinal development is extended (monkeys), birthdays are more sharply demarcated. As discussed earUer, the birth order of retinal neurons is conserved during the evolution and reflects the evolutionary sequence of retinal neurons. 

The ganglion cell layer, which along with the retinal ganglion cells also contains amacrine cells so-called displaced amacrine cells. 

IL-1 and tumor necrosis factor (TNF) are proinflammatory cytokines. They are produced in response to adverse stimuli. Each cytokine exists as two well-characterized isoforms IL-lot and IL-1P, and TNF-ot and TNF-p, respectively. There is strong evidence for the involvement of IL-1P and TNF ot in the pathogenesis of experimental brain ischemia (Hallenbeck, 2002 Patel et al., 2003). In the retina, transient ischemia causes upregulation of TNF-ot (Fontaine et al., 2002). In the early phase of reperfusion, TNF-ot is primarily upregulated in ganglion cells, amacrine cells, and Muller cells. There is no consensus about the overall efiect of TNF-ot on retinal cell viability. There is an indication that activation of TNF receptor 2 is neuroprotective, whereas activation of TNF receptor 1 augments neuronal death. 

In the rat retina, expression of mGluR4 mRNA was observed in the cell bodies in the ganglion cell layer these were presumed to be the retinal ganglion cells (Akazawa et al., 1994 Hartveit et al., 1995) and displaced amacrine cells (Hartveit et al., 1995). Expression was reported further in amacrine cells in the inner part of the inner nuclear layer (Hartveit et al., 1995). 

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