The central nervous system sends a neural impulse through an efferent nerve system toward muscles to drive movement. In an electronically artificial neural system, the electronic neural devices and interconnections prevent achieving highly connected and long-distance artificial impulse transmission and exhibit a narrow bandwidth. Here we design and demonstrate light-emitting memristors (LEMs) for the realization of an optoelectronic artificial efferent nerve, in which the LEM combines the functions of a light receiver, a light emitter, and an optoelectronic synapse in a single device. The optical signal from the pre-LEM (presynaptic membrane) acts as the input signal for the post-LEM (postsynaptic membrane), leading to one-to-many transmission, dynamic adjustable transmission, and light-trained synaptic plasticity, thus removing the physical limitation in artificially electronic neural systems. Furthermore, we construct an optoelectronic artificial efferent nerve with LEMs to control manipulators intelligently. These results promote the construction of an artificial optoelectronic nerve for further development of sensorimotor functionalities.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1021/acs.nanolett.1c01482 | DOI Listing |
Life Sci Alliance
April 2025
Telethon Institute of Genetics and Medicine, TIGEM, Pozzuoli, Italy
Protein aggregates in motoneurons, a pathological hallmark of amyotrophic lateral sclerosis, have been suggested to play a key pathogenetic role. ALS8, characterized by ER-associated inclusions, is caused by a heterozygous mutation in VAPB, which acts at multiple membrane contact sites between the ER and almost all other organelles. The link between protein aggregation and cellular dysfunction is unclear.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Institute of Biomedicine of Seville (IBiS), Virgen del Rocío University Hospital/CSIC/University of Seville, 41013 Seville, Spain.
The ubiquitin proteasome system (UPS) is implicated in protein homeostasis. One of the proteins involved in this system is HERC1 E3 ubiquitin ligase, which was associated with several processes including the normal development and neurotransmission at the neuromuscular junction (NMJ), autophagy in projection neurons, myelination of the peripheral nervous system, among others. The tambaleante (tbl) mouse model carries the spontaneous mutation Gly483Glu substitution in the HERC1 E3 protein.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Department of Neurobiology, Harvard Medical School, Boston, MA 02115.
The sense of hearing originates in the cochlea, which detects sounds across dynamic sensory environments. Like other peripheral organs, the cochlea is subjected to environmental insults, including loud, damage-inducing sounds. In response to internal and external stimuli, the central nervous system directly modulates cochlear function through olivocochlear neurons (OCNs), which are located in the brainstem and innervate the cochlear sensory epithelium.
View Article and Find Full Text PDFSci Rep
January 2025
Institute for Antiviral Research, Department of Animal, Dairy, and Veterinary Sciences, Utah State University, Logan, UT, 84321-5600, USA.
Zika virus (ZIKV) causes a variety of peripheral and central nervous system complications leading to neurological symptoms such as limb weakness. We used a mouse model to identify candidate genes potentially involved in causation or recovery from ZIKV-induced acute flaccid paralysis. Using Zikv and Chat chromogenic and fluorescence in situ RNA hybridization, electron microscopy, immunohistochemistry, and ZIKV RT-qPCR, we determined that some paralyzed mice had infected motor neurons, but motor neurons are not reduced in number and the infection was not present in all paralyzed mice; hence infection of motor neurons were not strongly correlated with paralysis.
View Article and Find Full Text PDFExp Brain Res
January 2025
Dept. of Neurosurgery, Upstate Medical University, 750 E. Adams St, Syracuse, NY, 13210, USA.
Transcranial magnetic stimulation (TMS) has been used for many years to study the pathophysiology of amyotrophic lateral sclerosis (ALS). Based on single- or dual-pulse TMS and EMG and/or single motor unit (MU) recordings, many groups have described a loss of central inhibition as an early marker of ALS dysfunction, reflecting a state of cortical 'hyperexcitability'. This conclusion is not without its detractors, however, leading us to reexamine this issue using 4-pulse TMS, shown previously to be more effective for testing central motor pathway functional integrity.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!