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Photonic synapses combining photosensitivity and synaptic function can efficiently perceive and memorize visual information, making them crucial for the development of artificial vision systems. However, the development of high-performance photonic synapses with low power consumption and rapid optical erasing ability remains challenging. Here, we propose a photon-modulated charging/discharging mechanism for self-powered photonic synapses. The current hysteresis enables the devices based on CsPbBr/solvent/carbon nitride multilayer architecture to emulate synaptic behaviors, such as excitatory postsynaptic currents, paired-pulse facilitation, and long/short-term memory. Intriguingly, the unique radiation direction-dependent photocurrent endows the photonic synapses with the capability of optical writing and rapid optical erasing. Moreover, the photonic synapses exhibit exceptional performance in contrast enhancement and noise reduction owing to the notable synaptic plasticity. In simulations based on artificial neural network (ANN) algorithms, the pre-processing by our photonic synapses improves the recognition rate of handwritten digit from 11.4% (200 training epochs) to 85% (~60 training epochs). Furthermore, due to the excellent feature extraction and memory capability, an array based on the photonic synapses can imitate facial recognition of human retina without the assistance of ANN.
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http://dx.doi.org/10.34133/research.0526 | DOI Listing |
eNeuro
September 2025
Department of Neurology, Long School of Medicine, University of Texas Health Science Center San Antonio, San Antonio, Texas, USA, 78229.
The corticospinal tract (CST) is essential for forelimb-specific fine motor skills. In rodents, it undergoes extensive structural remodeling across development, injury, and disease states, with major implications for motor function. A vast body of literature, spanning numerous injury models, frequently assesses these projections.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Institute of Neuroscience, Technical University of Munich, Munich 80802, Germany.
Amyloid β (Aβ)-dependent circuit dysfunction in Alzheimer's disease (AD) is determined by a puzzling mix of hyperactive and inactive ("silent") brain neurons. Recent studies identified excessive glutamate accumulation as a key Aβ-dependent determinant of hyperactivity. The cellular mechanisms underlying neuronal silence depend on both Aβ and tau protein pathologies, with an unknown role of Aβ.
View Article and Find Full Text PDFNat Commun
August 2025
Department of Neuroscience, Del Monte Institute for Neuroscience, University of Rochester Medical Center, Rochester, NY, USA.
Adolescence is a sensitive period for frontal cortical development and cognitive maturation, marked by heightened structural plasticity in the dopaminergic (DA) mesofrontal circuit. However, the cellular and molecular mechanisms underlying this plasticity remain unclear. Here, we show that microglia, the brain's innate immune cells, are highly responsive to mesofrontal DA signaling during adolescence.
View Article and Find Full Text PDFACS Appl Mater Interfaces
August 2025
Department of Materials Science and Engineering, National Tsing Hua University, Hsinchu 30013, Taiwan.
Inspired by the human visual system, photonic synapses with photonic sensing and data memorization offer a promising alternative to traditional von Neumann architectures for neuromorphic computing. This study introduces a multifunctional artificial photonic synapse based on solution-processed PEASnI 2D Ruddlesden-Popper perovskite. By modulation of the applied bias voltage, the PEASnI device can switch between two distinct optoelectronic modes.
View Article and Find Full Text PDFJ Neurosci
August 2025
Sanders-Brown Center on Aging, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
While cerebrovascular dysfunction and reactive astrocytosis are extensively characterized hallmarks of Alzheimer's disease (AD) and related dementias, the dynamic relationship between reactive astrocytes and cerebral vessels remains poorly understood. Here, we used jGCaMP8f and two photon microscopy to investigate calcium signaling in multiple astrocyte subcompartments, concurrent with changes in cerebral arteriole activity, in fully awake seven-to-eight-month-old male and female 5xFAD mice, a model for AD-like pathology, and wild-type (WT) littermates. In the absence of movement, spontaneous calcium transients in barrel cortex occurred more frequently in astrocyte somata, processes, and perivascular regions of 5xFAD mice.
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