Neurons amacrine cells

Neurohormones like ACTH and a-MSH have been located in the amacrine cells of the IPL.121 The first 24 amino acids of ACTH are phylogenetically well preserved and responsible for its biological activity. ACTH plays a role in the restoration of neuronal function after CNS lesions122 and has receptors widely distributed throughout the brain. Since it can inhibit IFN-y production of macrophages and T-helper cells, it could possibly inhibit phagocytosis by microglia. 

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. 

A fully developed retina consists of six neuron types and the Muller glial cells as shown in this schematic representation. A, Amacrine cells B, bipolar cells C, cone photoreceptor cells G, ganglion cells H, horizontal cells I, interplexiform cells M, Muller cells PE, pigment epithelium R, rod photoreceptor cell INL, inner nuclear layer IPL, inner plexiform layer ONL, outer nuclear layer Ph, photoreceptors RPE, RPE (Reproduced with permission from the publishers of Sharma and Ehinger, 2003)... 

NOS is found in certain amacrine cells in the retina (Sharma et al., 1997 Sharma et al., 2001). NOS produces NO, and the interaction of NO with the superoxide radical is imphcated in normal neuronal metabolism as well as neurodegeneration. 

NO is an important neuromodulator in the retina, and is implicated in many physiological processes (Goldstein et al., 1996). NO is synthesized from arginine via the action of nitric oxide synthase (NOS). Three distinct isoforms of NOS have been identified. Neuronal NOS (nNOS) and endothelial NOS (eNOS) are Ca -dependent. nNOS is constitutively expressed by certain types of amacrine cells in the retina. These cells often have long projections in the irmerplexiform layer (Sharma et al., 1997 Sharma et al., 2001). eNOS is expressed by the endothelial cells of blood vessels (Cheon et al., 2003). iNOS is Ca -independent and expressed in Muller and RPE cells in response to certain stimuli (Lopez-Costa et al., 1997). Activation of the NMDA receptor leads to an increase in intracellular calcium levels, which can induce expression of, and activate NOS isoforms, either directly (nNOS) or via the activation of calcium-dependent protein kinase C (PKC) (Lipton, 1999) (O Figure 3-6). 

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 mGluRl mRNA was observed with moderate intensity in the large majority of neurons in the ganglion cell layer, suggesting that both ganglion cells and a subset of amacrine cells expressed mGluRl mRNA moderate expression was also seen in some putative amacrine cells with cell bodies in the inner third of the inner nuclear layer (Hartveit et al., 1995). 

Although GLT has only been detected in astroglial cells in the normal and mature nervous system [with the exception of retina where bipolar cells and amacrine cells normally express GLT protein (Rauen et al., 1996)], this does not mean that neurons never express GLT. Several populations of neurons express GLT during the development of the nervous system (see Section 4.6), but the neuronal expression is transient and disappears on maturation. GLT has also been frequently observed in cultured neurons (Brooks-Kayal et al., 1998 Mennerick et al., 1998 Meaney et al., 1998 Stanimirovic et al., 1999 Plachez et al., 2000). In newborn piglets, GLT may also appear in neurons after hypoxia-ischemia (Martin et al., 1997) showing that the cellular expression can potentially change. 

The retina extends forward to the sclera as a globe-shaped wineglass almost external to the skull. That part of the sclera devoid of retina is the pars planar, which is used as an access point for injection or for close delivery to the iris and ciliary body (ICB). When stripped from its basement membrane and opened out, the collapsed retina is a circular disk approximately 42 mm in diameter and 0.5 mm in thickness. The organization of the retina is based on a three-neuron chain (photoreceptor cell-bipolar cell-ganglion cell) and accompanying cells (horizontal, amacrine, and Muller cells)... 

The smaller amount of neurons driven by the more numerous cones points to a complex wiring of these receptors located in the second layer of the retina. The inner nuclear layer connects the photoreceptors with the ganglion cells and consists of bipolar, amacrinal, and horizontal cells. Bipolar cells can be divided into ON and OFF bipolars. The OFF bipolar cells inhibit the release of neurotransmitters after a photon triggered increase in electrical potential whereas the ON bipolar cells stimulate the release of neurotransmitters. This allows the visual system to build differential signals already in the first processing stage (see Fig. 5). 

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