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Neuroprotection
Published in Glenn J. Jaffe, Paul Ashton, P. Andrew Pearson, Intraocular Drug Delivery, 2006
Dennis W. Rickman, Melissa J. Mahoney
Under scotopic conditions, mammalian visual processing is dominated by a circuit classically thought to involve only rod photoreceptors, a unique class of rod bipolar cells and ganglion cells. However, it is now clear from the observations of a number of investigators (89–91) that a distinctive, inhibitory interneuron, the AII amacrine cell, is interposed between the rod bipolar cell and ganglion cell. A role has been established for BDNF in the phenotypic differentiation of AII amacrine cells and, thus, the development of the neural pathway underlying scotopic visual processing (67,92,93). Furthermore, the network of AII amacrine cells is modulated by dopaminergic innervation from a population of sparsely distributed, wide-field amacrine cells (94–96). This cell, in the proximal inner nuclear layer (INL), is labeled with antibodies to tyrosine hydroxylase (TH), the rate-limiting enzyme in dopamine biosynthesis. Dendrites of the dopaminergic amacrine cell contribute to a moderately dense plexus in the inner plexiform layer (IPL) where they form “ring-like” structures surrounding the somata and initial dendrites of the AII amacrine cells are sites of synaptic contact (97). Generally, at scotopic light levels, the AII s are interconnected via gap junctions in sublamina a of the IPL, enhancing the overall sensitivity of the rod signaling pathway. In response to increased light levels, dopamine is released, uncoupling gap junctions and reducing the overall sensitivity of the rod pathway. Development of the dopaminergic amacrine cell also has been shown to be dependent on BDNF (98). In retinas from BDNF knockout mice there is a reduced number of TH-containing somata, and the density of the dopaminergic plexus in the IPL is greatly reduced, as compared to the wild type. Conversely, intraocular injection of BDNF in the normal retina results in precocious sprouting of dopaminergic processes throughout the IPL (87). These demonstrated roles for neurotrophins in the development and maintenance of the inner retinal circuitry are consistent with the well-documented role of neurotrophin-mediated survival following transient ischemia (99–102).
Fine structure of the human retina defined by confocal microscopic immunohistochemistry
Published in British Journal of Biomedical Science, 2021
The advanced understanding of the mammalian retina is crucial in the investigation and treatment of ophthalmological disease, and study of the mammalian eye has provided insight [1–3]. Although these studies are informative, human tissues are becoming widely available, providing the opportunity to study the morphology and function of the retina in our own species, which is commonly characterized using cell markers that label specific neurons or glia [4]. Despite similarities in retinal anatomy between humans and other animal species, cell marker immunoreactivity varies between species. For example, antibodies to parvalbumin have been reported to stain AII amacrine cells in both the rat and rabbit retina [5], but in humans, strong immunoreactivity was observed in horizontal cells [6], and calretinin is a suitable marker for AII amacrine cells in the human retina [7]. These data call for a comprehensive study into their potential value in the study of the human eye.
Advances in understanding the mechanisms of retinal degenerations
Published in Clinical and Experimental Optometry, 2020
In contrast, the localisation of P2X receptors in rod mediated pathways are more complex. The neural pathway important for mediating scotopic vision involves rod photoreceptors communicating with rod bipolar cells that in turn pass information to two highly specific amacrine cell types called AII and A17 amacrine cells.200422,23 The AII amacrine cells then pass scotopic information to ganglion cells by communicating with ON and OFF cone bipolar cells.200422,23 A critical step in shaping vision processing in the scotopic pathway is the modulation that occurs between rod bipolar cells and AII and A17 amacrine cells. An example of the synapse between a rod bipolar cell and an A17 and AII amacrine cell is shown in Figure 1B. Importantly, A17 amacrine cells which release the inhibitory neurotransmitter GABA, feedback directly onto rod bipolar cell terminals via reciprocal synapses to shape signalling by rod bipolar cells.24
Nystagmus with pendular low amplitude, high frequency components (PLAHF) in association with retinal disease
Published in Strabismus, 2020
Ping Wang, Pan Ya, Deshun Li, Shuangjun Lv, Dongsheng Yang
Some experimental results also support the opinion the PLAHF waveforms are related to retinal disorders. According to smooth pursuit and fixation ocular motor system (OMS) model (by Dell’ Osso LF), pendular waveforms are generated by pursuit-system (PS) and connected to sensory deficits, and due to gain/delay problem in feedback loop from retina to neural integrator.4 Dual jerk waveforms may be due to instability of fixation in smooth pursuit process. Retina signal pathways obstruction in any synapses will prolong the visual feedback, and if signal processing delay beyond 100 ms might cause oscillations. Effect of electronically delaying visual feedback by 480 ms in normal subject will develop high frequency oscillation. Severe delay will lead to high frequency and low amplitude oscillation.5 Simonsz et al. found that high frequency and low amplitude pendular waveforms were noted in cCSNB and iCSNB patients. It may be induced by rod signals travel via the rod ON-bipolar cell via AII amacrine cells to cone ON – and OFF-bipolar cells synapses defective.6,7