Neuronal cell death is both a vital component of the embryo-genesis of the nervous system and forms the basis of all neurodegenerative diseases. This overview explores the fundamental mechanisms underlying neuronal cell death at a cellular and molecular level. The significance of the mode of neuronal death is compared with respect to physiological (developmental) and pathological neuronal loss.
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| http://dx.doi.org/10.1007/BF02815216 | DOI Listing |
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Purpose: We aimed to investigate the role of gallic acid treatment on spinal cord tissues after spinal cord injury (SCI) and its relationship with endoplasmic reticulum (ER) stress by histochemical, immunohistochemical, and in-silico techniques.
Methods: Thirty female Wistar albino rats were divided into three groups: sham, SCI, and SCI+gallic acid. SCI was induced by dropping a 15-g weight onto the exposed T10-T11 spinal cord segment.
Central amygdala NPBWR1 neurons facilitate social novelty seeking and new social interactions.
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January 2025
International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan.
The formation of new social interactions is vital for social animals, but the underlying neural mechanisms remain poorly understood. We identified CeA neurons, a population in central amygdala expressing neuropeptide B/W receptor-1 (NPBWR1), that play a critical role in these interactions. CeA neurons were activated during encounters with unfamiliar, but not with familiar, mice.
View Article and Find Full Text PDFEnvironmental temperature dictates the developmental pace of poikilothermic animals. In , slower development at lower temperatures results in higher brain connectivity, but the generality of such scaling across temperatures and brain regions and its impact on function are unclear. Here, we show that brain connectivity scales continuously across temperatures, in agreement with a first-principle model that postulates different metabolic constraints for the growth of the brain and the organism.
View Article and Find Full Text PDFOpioidergic activation of the descending pain inhibitory system underlies placebo analgesia.
Sci Adv
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Laboratory for Biofunction Dynamics Imaging, RIKEN Center for Biosystems Dynamics Research, 6-7-3 Minatojima-Minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan.
Placebo analgesia is caused by inactive treatment, implicating endogenous brain function involvement. However, the neurobiological basis remains unclear. In this study, we found that μ-opioid signals in the medial prefrontal cortex (mPFC) activate the descending pain inhibitory system to initiate placebo analgesia in neuropathic pain rats.
View Article and Find Full Text PDFA nanoparticle-based wireless deep brain stimulation system that reverses Parkinson's disease.
Sci Adv
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New Cornerstone Science Laboratory, CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety & CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology of China, Beijing 100190, China.
Deep brain stimulation technology enables the neural modulation with precise spatial control but requires permanent implantation of conduits. Here, we describe a photothermal wireless deep brain stimulation nanosystem capable of eliminating α-synuclein aggregates and restoring degenerated dopamine neurons in the substantia nigra to treat Parkinson's disease. This nanosystem (ATB NPs) consists of gold nanoshell, an antibody against the heat-sensitive transient receptor potential vanilloid family member 1 (TRPV1), and β-synuclein (β-syn) peptides with a near infrared-responsive linker.
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