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Data and codes for https://doi.org/10.1080/17421772.2023.2214600

The oculomotor delayed-response (ODR) task is a common experimental paradigm of working memory (WM) study, in which a monkey must fixate its gaze on the center of a screen and, following a brief cue that flashes on the screen, keep fixating for several more seconds before shifting its gaze to the location where the cue flashed. Consequently, in the delay period between the cue and the response the monkey must maintain a memory of cue location. Electrophysiological recordings from the prefrontal area of the cortex (PFC) revealed neurons that display selective persistent activity: their firing rate change induced by the cue persists through delay period, but only in response to a confined range of cue locations. This suggests that the representation of the cue is maintained in the network by a change in network activity profile. In this work, we study a network of rate-model neurons that is capable of preserving information about a past input, owing to structured connectivity and nonlinearities in the neuronal transfer function (TFs). Particularly, we focus on the acceleration of the TF close to firing threshold and the concavity around TF saturation. Any memory mechanism which exploits TF saturation means that some neurons must fire close to their saturation rates; with our model, however, we show that a certain relation between the excitatory and inhibitory neurons' TFs can cause an effective saturation in the network without forcing the neurons into the saturating parts of their TFs. In addition, this mechanism enables the erasure of memory at the end of the delay by a global excitatory signal. Finally, we demonstrate the mechanism in a model network of spiking neurons which describes with more detail the oscillatory dynamics in the state transition due to the interaction of membrane and synaptic time constants which is neglected in the rate model., Comment: 45 pages, 13 figures

A new angles-only initial relative orbit determination (IROD) algorithm is derived using three line-of-sight observations. This algorithm accomplishes this by taking a Singular Value Decomposition of a 6x6 matrix to arrive at an approximate initial relative orbit determination solution. This involves the approximate solution of 6 polynomial equations in 6 unknowns. An iterative improvement algorithm is also derived that provides the exact solution, to numerical precision, of the 6 polynomial equations in 6 unknowns. The initial relative orbit algorithm is also expanded for more than three line-of-sight observations with an iterative improvement algorithm for more than three line-of-sight observations. The algorithm is tested for a range of relative motion cases in low earth orbit and geosynchronous orbit, with and without the inclusion of J2 perturbations and with camera measurement errors. The performance of the IROD algorithm is evaluated for these cases and show that the tool is most accurate at low inclinations and eccentricities. Results are also presented that show the importance of including J2 perturbations when modelling the relative orbital motion for accurate IROD estimates. This research was funded in part by the Air Force Research Lab, Albuquerque, NM.

PurposePostnatal lead exposure produces rod-selective and Bax-mediated apoptosis, decreased scotopic electroretinograms (ERGs), and scotopic and mesopic vision deficits in humans and/or experimental animals. Rod, but not cone, inner segment mitochondria were considered the primary site of action. However, photoreceptor synaptic mitochondria were not examined. Thus, our experiments investigated the structural and functional effects of environmentally relevant postnatal lead exposure on rod spherule and cone pedicle mitochondria and whether Bcl-xL overexpression provided neuroprotection.MethodsC57BL/6N mice pups were exposed to lead only during lactation via dams drinking water containing lead acetate. The blood [Pb] at weaning was 20.6±4.7 µg/dl, which decreased to the control value by 2 months. To assess synaptic mitochondrial structural differences and vulnerability to lead exposure, wild-type and transgenic mice overexpressing Bcl-xL in photoreceptors were used. Electron microscopy, three-dimensional electron tomography, and retinal and photoreceptor synaptic terminal oxygen consumption (QO(2)) studies were conducted in adult control, Bcl-xL, lead, and Bcl-xL/lead mice.ResultsThe spherule and pedicle mitochondria in lead-treated mice were swollen, and the cristae structure was markedly changed. In the lead-treated mice, the mitochondrial cristae surface area and volume (abundance: measure correlated with ATP (ATP) synthesis) were decreased in the spherules and increased in the pedicles. Pedicles also had an increased number of crista segments per volume. In the lead-treated mice, the number of segments/crista and fraction of cristae with multiple segments (branching) similarly increased in spherule and pedicle mitochondria. Lead-induced remodeling of spherule mitochondria produced smaller cristae with more branching, whereas pedicle mitochondria had larger cristae with more branching and increased crista junction (CJ) diameter. Lead decreased dark- and light-adapted photoreceptor and dark-adapted photoreceptor synaptic terminal QO(2). Bcl-xL partially blocked many of the lead-induced alterations relative to controls. However, spherules still had partially decreased abundance, whereas pedicles still had increased branching, increased crista segments per volume, and increased crista junction diameter. Moreover, photoreceptor and synaptic QO(2) were only partially recovered.ConclusionsThese findings reveal cellular and compartmental specific differences in the structure and vulnerability of rod and cone inner segment and synaptic mitochondria to postnatal lead exposure. Spherule and pedicle mitochondria in lead-exposed mice displayed complex and distinguishing patterns of cristae and matrix damage and remodeling consistent with studies showing that synaptic mitochondria are more sensitive to Ca(2+) overload, oxidative stress, and ATP loss than non-synaptic mitochondria. The lead-induced decreases in QO(2) likely resulted from the decreased spherule cristae abundance and smaller cristae, perhaps due to Bax-mediated effects as they occurred in apoptotic rod inner segments. The increase in pedicle cristae abundance and CJ diameter could have resulted from increased Drp1-mediated fission, as small mitochondrial fragments were observed. The mechanisms of Bcl-xL-mediated remodeling might occur via interaction with formation of CJ protein 1 (Fcj1), whereas the partial protection of synaptic QO(2) might result from the enhanced efficiency of energy metabolism via Bcl-xL's direct interaction with the F1F0 ATP synthase and/or regulation of cellular redox status. These lead-induced alterations in photoreceptor synaptic terminal mitochondria likely underlie the persistent scotopic and mesopic deficits in lead-exposed children, workers, and experimental animals. Our findings stress the clinical and scientific importance of examining synaptic dysfunction following injury or disease during development, and developing therapeutic treatments that prevent synaptic degeneration in retinal and neurodegenerative disorders even when apoptosis is blocked.

Català: El projecte consisteix en crear una eina didàctica que permeti simular diferents conceptes relacionats amb el funcionament dels Sistemes Operatius. Es tracta d'oferir als usuaris una aplicació que els ajudi a entendre (o explicar) tots aquests conceptes que d'altra manera hom només s'hi pot apropar de manera purament teòrica. L'aplicació presenta els sistemes de gestió de processos, gestió de memòria, gestió de disc i gestió d'arxius, permet escollir els paràmetres més rellevants dels diferents sistemes, consultar els valors resultants i generar simulacions autònomes que mostren a l'usuari de manera visual els processos que hi tenen lloc.