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Long-term potentiation (LTP) in the hippocampus is the most studied form of synaptic plasticity. Temporal integration of synaptic inputs is essential in synaptic plasticity and is assumed to be achieved through Ca signaling in neurons and astroglia. However, whether these two cell types play different roles in LTP remain unknown. Here, we found that through the integration of synaptic inputs, astrocyte inositol triphosphate (IP) receptor type 2 (IPR2)-dependent Ca signaling was critical for late-phase LTP (L-LTP) but not early-phase LTP (E-LTP). Moreover, this process was mediated by astrocyte-derived brain-derived neurotrophic factor (BDNF). In contrast, neuron-derived BDNF was critical for both E-LTP and L-LTP. Importantly, the dynamic differences in BDNF secretion play a role in modulating distinct forms of LTP. Moreover, astrocyte- and neuron-derived BDNF exhibited different roles in memory. These observations enriched our knowledge of LTP and memory at the cellular level and implied distinct roles of astrocytes and neurons in information integration.
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http://dx.doi.org/10.1038/s41380-021-01332-6 | DOI Listing |
Stroke
September 2025
Brain Language Laboratory, Freie Universität Berlin, Germany (A.-T.P.J., M.R.O., A.S., F.P.).
Background: Intensive language-action therapy treats language deficits and depressive symptoms in chronic poststroke aphasia, yet the underlying neural mechanisms remain underexplored. Long-range temporal correlations (LRTCs) in blood oxygenation level-dependent signals indicate persistence in brain activity patterns and may relate to learning and levels of depression. This observational study investigates blood oxygenation level-dependent LRTC changes alongside therapy-induced language and mood improvements in perisylvian and domain-general brain areas.
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September 2025
Faculty of Science and Engineering, Waseda University, Shinjuku, Tokyo, Japan.
Neuronal networks in animal brains are considered to realize specific filter functions through the precise configuration of synaptic weights, which are autonomously regulated without external supervision. In this study, we employ a single Hodgkin-Huxley-type neuron with autapses as a minimum model to computationally investigate how spike-timing-dependent plasticity (STDP) adjusts synaptic weights through recurrent feedback. The results show that the weights undergo oscillatory potentiation or depression with respect to autaptic delay and high-frequency stimulation.
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September 2025
Neuroscience Institute, National Research Council (CNR), Pisa, Italy.
Neural circuits sculpt their structure and modify the strength of their connections to effectively adapt to the external stimuli throughout life. In response to practice and experience, the brain learns to distinguish previously undetectable stimulus features recurring in the external environment. The unconscious acquisition of improved perceptual abilities falls into a form of implicit learning known as perceptual learning.
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September 2025
Department of Mechano-Informatics, Graduate School of Information Science and Technology, The University of Tokyo, Tokyo, Japan.
Introduction: Understanding how neural networks process complex patterns of information is crucial for advancing both neuroscience and artificial intelligence. To investigate fundamental principles of neural computation, we examined whether dissociated neuronal cultures, one of the most primitive living neural networks, exhibit regularity sensitivity beyond mere stimulus-specific adaptation and deviance detection.
Methods: We recorded activity to oddball electrical stimulation paradigms from dissociated rat cortical neurons cultured on high-resolution CMOS microelectrode arrays.
Adv Sci (Weinh)
September 2025
State Key Laboratory of Advanced Medical Materials and Devices, Medical College, Tianjin University, Tianjin, 300072, China.
Recent breakthroughs in tumor biology have redefined the tumor microenvironment as a dynamic ecosystem in which the nervous system has emerged as a pivotal regulator of oncogenesis. In addition to their classical developmental roles, neural‒tumor interactions orchestrate a sophisticated network that drives cancer initiation, stemness maintenance, metabolic reprogramming, and therapeutic evasion. This crosstalk operates through multimodal mechanisms, including paracrine signaling, electrophysiological interactions, and structural innervation guided by axon-derived guidance molecules.
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