Satellite-derived variability in chlorophyll, wind stress, sea surface height, and temperature in the northern California Current System

Satellite-derived data provide the temporal means and seasonal and nonseasonal variability of four physical and biological parameters off Oregon and Washington (41°–48.5°N). Eight years of data (1998–2005) are available for surface chlorophyll concentrations, sea surface temperature (SST), and sea surface height, while six years of data (2000–2005) are available for surface wind stress. Strong cross-shelf and alongshore variability is apparent in the temporal mean and seasonal climatology of all four variables. Two latitudinal regions are identified and separated at 44°–46°N, where the coastal ocean experiences a change in the direction of the mean alongshore wind stress, is influenced by topographic features, and has differing exposure to the Columbia River Plume. All these factors may play a part in defining the distinct regimes in the northern and southern regions. Nonseasonal signals account for ∼60–75% of the dynamical variables. An empirical orthogonal function analysis shows stronger intra-annual variability for alongshore wind, coastal SST, and surface chlorophyll, with stronger interannual variability for surface height. Interannual variability can be caused by distant forcing from equatorial and basin-scale changes in circulation, or by more localized changes in regional winds, all of which can be found in the time series. Correlations are mostly as expected for upwelling systems on intra-annual timescales. Correlations of the interannual timescales are complicated by residual quasi-annual signals created by changes in the timing and strength of the seasonal cycles. Examination of the interannual time series, however, provides a convincing picture of the covariability of chlorophyll, surface temperature, and surface height, with some evidence of regional wind forcing

Functional and Structural Plasticity in the Adult Mammalian Retina After Local Photoreceptor Loss

The retina is a thin layer of neural tissue that lines the back of the eye and transforms the visual scene into an electrical signal that is sent to the brain via the optic nerve. The synapse between photoreceptors, the light sensitive neurons, and bipolar cells is the first connection in the retinal circuitry. Loss of photoreceptors during retinal degeneration results in permanent visual loss. Photoreceptor reintroduction has been suggested as a potential approach to sight restoration, but the ability of bipolar cells to establish new functional synapses with photoreceptors is poorly understood. In my work, I investigate if deafferented bipolar cells, i.e. the ones that lost photoreceptors, in the adult mammalian retina can rewire with new photoreceptors. I use focal laser photocoagulation to selectively ablate a small patch of photoreceptors while leaving the rest of the retinal neurons intact. I use electrophysiology recordings of retinal response to visual stimuli to show that the neighboring healthy photoreceptors shift into the ablation zone, thus returning visual sensitivity to the previously deafferented bipolar cells. Furthermore, I use immunohistochemistry to determine if the new synapses of the deafferented bipolar cells are selective for appropriate pre-synaptic partners and investigate the structural mechanisms bipolar cells use to find new partners. I find that deafferented bipolar cells are capable of rewiring correctly with new photoreceptors, but different bipolar cell types use different rewiring strategies. I also find that the new synapses may not be as selective as those in the healthy retina. These findings support the idea that bipolar cells might be able to synapse with reintroduced photoreceptors, thereby restoring vision in patients blinded by retinal degeneration. However, the diversity of responses to deafferentation between bipolar cell types shows that different parallel pathways have access to different plasticity mechanisms, suggesting that they will respond to photoreceptor reintroduction therapies differently. Improving our understanding of the plasticity within the adult retina is important for the success of future vision restoration therapies

Stereotyped Synaptic Connectivity Is Restored during Circuit Repair in the Adult Mammalian Retina

Proper function of the central nervous system (CNS) depends on the specificity of synaptic connections between cells of various types. Cellular and molecular mechanisms responsible for the establishment and refinement of these connections during development are the subject of an active area of research [1-6]. However, it is unknown if the adult mammalian CNS can form new type-selective synapses following neural injury or disease. Here, we assess whether selective synaptic connections can be reestablished after circuit disruption in the adult mammalian retina. The stereotyped circuitry at the first synapse in the retina, as well as the relatively short distances new neurites must travel compared to other areas of the CNS, make the retina well suited to probing for synaptic specificity during circuit reassembly. Selective connections between short-wavelength sensitive cone photoreceptors (S-cones) and S-cone bipolar cells provides the foundation of the primordial blue-yellow vision, common to all mammals [7-18]. We take advantage of the ground squirrel retina, which has a one-to-one S-cone-to-S-cone-bipolar-cell connection, to test if this connectivity can be reestablished following local photoreceptor loss [8, 19]. We find that after in vivo selective photoreceptor ablation, deafferented S-cone bipolar cells expand their dendritic trees. The new dendrites randomly explore the proper synaptic layer, bypass medium-wavelength sensitive cone photoreceptors (M-cones), and selectively synapse with S-cones. However, non-connected dendrites are not pruned back to resemble unperturbed S-cone bipolar cells. We show, for the first time, that circuit repair in the adult mammalian retina can recreate stereotypic selective wiring

Deafferented Adult Rod Bipolar Cells Create New Synapses with Photoreceptors to Restore Vision

Upon degeneration of photoreceptors in the adult retina, interneurons, including bipolar cells, exhibit a plastic response leading to their aberrant rewiring. Photoreceptor reintroduction has been suggested as a potential approach to sight restoration, but the ability of deafferented bipolar cells to establish functional synapses with photoreceptors is poorly understood. Here we use photocoagulation to selectively destroy photoreceptors in adult rabbits while preserving the inner retina. We find that rods and cones shift into the ablation zone over several weeks, reducing the blind spot at scotopic and photopic luminances. During recovery, rod and cone bipolar cells exhibit markedly different responses to deafferentation. Rod bipolar cells extend their dendrites to form new synapses with healthy photoreceptors outside the lesion, thereby restoring visual function in the deafferented retina. Secretagogin-positive cone bipolar cells did not exhibit such obvious dendritic restructuring. These findings are encouraging to the idea of photoreceptor reintroduction for vision restoration in patients blinded by retinal degeneration. At the same time, they draw attention to the postsynaptic side of photoreceptor reintroduction; various bipolar cell types, representing different visual pathways, vary in their response to the photoreceptor loss and in their consequent dendritic restructuring.SIGNIFICANCE STATEMENT Loss of photoreceptors during retinal degeneration results in permanent visual impairment. Strategies for vision restoration based on the reintroduction of photoreceptors inherently rely on the ability of the remaining retinal neurons to correctly synapse with new photoreceptors. We show that deafferented bipolar cells in the adult mammalian retina can reconnect to rods and cones and restore retinal sensitivity at scotopic and photopic luminances. Rod bipolar cells extend their dendrites to form new synapses with healthy rod photoreceptors. These findings support the idea that bipolar cells might be able to synapse with reintroduced photoreceptors, thereby restoring vision in patients blinded by retinal degeneration

Development of Animal Models of Local Retinal Degeneration

PurposeDevelopment of nongenetic animal models of local retinal degeneration is essential for studies of retinal pathologies, such as chronic retinal detachment or age-related macular degeneration. We present two different methods to induce a highly localized retinal degeneration with precise onset time, that can be applied to a broad range of species in laboratory use.MethodsA 30-μm thin polymer sheet was implanted subretinally in wild-type (WT) rats. The effects of chronic retinal separation from the RPE were studied using histology and immunohistochemistry. Another approach is applicable to species with avascular retina, such as rabbits, where the photoreceptors and RPE were thermally ablated over large areas, using a high power scanning laser.ResultsPhotoreceptors above the subretinal implant in rats degenerated over time, with 80% of the outer nuclear layer disappearing within a month, and the rest by 3 months. Similar loss was obtained by selective photocoagulation with a scanning laser. Cells in the inner nuclear layer and ganglion cell layer were preserved in both cases. However, there were signs of rewiring and decrease in the size of the bipolar cell terminals in the damaged areas.ConclusionsBoth methods induce highly reproducible degeneration of photoreceptors over a defined area, with complete preservation of the inner retinal neurons during the 3-month follow-up. They provide a reliable platform for studies of local retinal degeneration and development of therapeutic strategies in a wide variety of species