Recently, neuromorphic sensors, which convert analogue signals to spiking frequencies, have been reported for neurorobotics. In bio-inspired systems these sensors are connected to the main neural unit to perform post-processing of the sensor data. The performance of spiking neural networks has been improved using optical synapses, which offer parallel communications between the distanced neural areas but are sensitive to the intensity variations of the optical signal. For systems with several neuromorphic sensors, which are connected optically to the main unit, the use of optical synapses is not an advantage. To address this, in this paper we propose and experimentally verify optical axons with synapses activated optically using digital signals. The synaptic weights are encoded by the energy of the stimuli, which are then optically transmitted independently. We show that the optical intensity fluctuations and link's misalignment result in delay in activation of the synapses. For the proposed optical axon, we have demonstrated line of sight transmission over a maximum link length of 190 cm with a delay of 8 μs. Furthermore, we show the axon delay as a function of the illuminance using a fitted model for which the root mean square error (RMS) similarity is 0.95.
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http://dx.doi.org/10.3390/s20216119 | DOI Listing |
Autophagy Rep
November 2023
Department of Ophthalmology & Pathology, Duke University, Durham, NC, 27705, USA.
Glaucoma encompasses a spectrum of disorders characterized by the chronic degeneration of retinal ganglion cell (RGC) axons and the progressive loss of RGCs, resulting in visual impairment. In this study, we investigated the effect of autophagy deficiency on two glaucoma hypertensive models, the DBA/2J spontaneous glaucoma model, and the TGFβ2 (transforming growth factor β2) chronic ocular hypertensive model. For this, we used the and DBA/2J- mice, this latter generated in our laboratory via CRISPR/Cas9 technology, which display impaired autophagy.
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December 2024
Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, Faculty of Brain Sciences, University College London, London, UK.
Background: Cognitive decline in multiple sclerosis (MS) is associated with neuro-axonal loss, quantifiable by optical coherence tomography (OCT). Associations between OCT measures and cognition in relapsing-remitting MS (RRMS) remain incompletely investigated, particularly the added value of OCT when combined with magnetic resonance imaging (MRI). We investigated the contributions of OCT and MRI while applying stringent criteria to control for subclinical optic neuropathy.
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December 2024
Center for Neurological Restoration, Neurological Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH, 44195, USA.
Rapid Eye Movement (REM) sleep behavior disorder (RBD) affects nearly half of Parkinson's disease (PD) patients. However, the structural heterogeneity within the brainstem, which regulates REM sleep, remains largely unexplored in PD. Our objective was to identify distinct PD subtypes based on microstructural characteristics in the brainstem and examine their associations with the severity of RBD.
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December 2024
Key Laboratory of Organ Regeneration and Reconstruction, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Regeneration of injured central nervous system (CNS) axons is highly restricted, leading to permanent neurological deficits. The myristoylated alanine-rich C-kinase substrate (MARCKS) is a membrane-associated protein kinase C (PKC) substrate ubiquitously expressed in eukaryotic cells, plays critical roles in development, brain plasticity, and tissues regeneration. However, little is known about the role of Marcks in CNS axon regeneration.
View Article and Find Full Text PDFTrends Pharmacol Sci
December 2024
State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Sun Yat-sen University, Guangzhou 510060, China. Electronic address:
The optic nerve, comprising axons from retinal ganglion cells (RGCs), is a component of the central nervous system (CNS) that generally exhibits a limited regeneration capacity following injury in mature mammals, resulting in permanent vision loss. Here, we summarize recent advances in interventions targeting cell-intrinsic and cell-extrinsic mechanisms to enhance RGC axon regeneration. Additionally, we summarize strategies for guiding the reconnection of regenerating axons with brain visual targets, aiming to restore partial visual function.
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