The CSF-contacting nucleus regulates learning and memory through synaptic connections with the hippocampus

Li, Qing; Liu, He; Zhang, Licai; Zhang, Hongxing; Zhou, Fang

doi:10.1016/j.neulet.2020.134972

Cited by 2 publications

(2 citation statements)

References 21 publications

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“…The Li Qing team used the cholera toxin subunit (CB)-saporin (SAP) into the lateral ventricle of rats to exclusively damage the CSF-cNs. As a result, learning and memory abilities in animals decreased significantly after the destruction of CSF-cNs (Li et al, 2020). We have demonstrated that the brain is with acidosis after TBI in the Current Understanding of Secondary Brain Injury After Traumatic Brain Injury section.…”

Section: Intervention Strategies and Clinical Trialsmentioning

confidence: 74%

“…Through the horseradish peroxidase tracing method, it has been confirmed that CSF-cNs project nerve fibers to the dCA1 area and transmit 5-HT to the hippocampus; they can also transport 5-HT from adjacent cells or CSF to hippocampal neurons. When a CSF-cN is impaired, 5-HT transmission decreases, and cognitive function declines (Li et al, 2020).…”

Section: Cerebrospinal Fluid-contacting Neuronsmentioning

confidence: 99%

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Iron Metabolism Disorders for Cognitive Dysfunction After Mild Traumatic Brain Injury

Huang

Feng

et al. 2021

Front. Neurosci.

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Traumatic brain injury (TBI) is one of the most harmful forms of acute brain injury and predicted to be one of the three major neurological diseases that cause neurological disabilities by 2030. A series of secondary injury cascades often cause cognitive dysfunction of TBI patients leading to poor prognosis. However, there are still no effective intervention measures, which drive us to explore new therapeutic targets. In this process, the most part of mild traumatic brain injury (mTBI) is ignored because its initial symptoms seemed not serious. Unfortunately, the ignored mTBI accounts for 80% of the total TBI, and a large part of the patients have long-term cognitive dysfunction. Iron deposition has been observed in mTBI patients and accompanies the whole pathological process. Iron accumulation may affect long-term cognitive dysfunction from three pathways: local injury, iron deposition induces tau phosphorylation, the formation of neurofibrillary tangles; neural cells death; and neural network damage, iron deposition leads to axonal injury by utilizing the iron sensibility of oligodendrocytes. Thus, iron overload and metabolism dysfunction was thought to play a pivotal role in mTBI pathophysiology. Cerebrospinal fluid-contacting neurons (CSF-cNs) located in the ependyma have bidirectional communication function between cerebral–spinal fluid and brain parenchyma, and may participate in the pathway of iron-induced cognitive dysfunction through projected nerve fibers and transmitted factor, such as 5-hydroxytryptamine, etc. The present review provides an overview of the metabolism and function of iron in mTBI, and to seek a potential new treatment target for mTBI with a novel perspective through combined iron and CSF-cNs.

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Section: Intervention Strategies and Clinical Trialsmentioning

confidence: 74%

Section: Cerebrospinal Fluid-contacting Neuronsmentioning

confidence: 99%

Iron Metabolism Disorders for Cognitive Dysfunction After Mild Traumatic Brain Injury

Huang

Feng

et al. 2021

Front. Neurosci.

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The recent research progress in neurobiological characteristics and pain regulation of the cerebrospinal fluid-contacting nucleus

Wei,

Liu,

Zhou

et al. 2024

APS

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The ependymal epithelium forms the cerebrospinal fluid barrier, separating the brain and spinal cord from the cerebrospinal fluid. However, in specific regions of the central nervous system, there are neurons that directly interface with the cerebrospinal fluid, including neuronal bodies, dendrites, or axons, This constitutes what is referred to as the "cerebrospinal fluid contacting neurons system (CSF-CNS)". The research team led by Professor Zhang has successfully utilized cholera toxin subunit B coupled horseradish peroxidase complex (CB-HRP) to selectively label the specialized neuron system that interfaces with cerebrospinal fluid, pioneeringly designating it as the "cerebrospinal fluid-contacting nucleus", commonly referred to as the "CSF-contacting nucleus". For the first time, the discovery of the CSF-contacting nucleus provides compelling morphological evidence for the existence of a distinct neural structure within the brain parenchyma that establishes a connection with the cerebrospinal fluid, thereby suggesting its potential significance in facilitating material and information exchange between the brain parenchyma and cerebrospinal fluid. After conducting a comprehensive series of studies on the morphological structure, material expression, gene analysis and functional aspects of the CSF-contacting nucleus in rodents and non-human primates, it has been revealed that there are fibrous connections between the CSF-contacting nucleus and the cerebral cortex and subcortical nuclei being involved in the regulatory mechanisms of pain, cognition, learning and memory, emotion, addiction, stress and anxiety responses, visceral activity, olfaction, vision processing and perception, auditory processing, perception, motor control and coordination, homeostasis regulation including maintenance of body energy and fluid balance, as well as the control of sleep–wake cycles and synchronization of biological rhythms. Current experiments have confirmed that the CSF-contacting nucleus is related to pain, morphine dependence and withdrawal, learning and memory, as well as stress. This present article offers a comprehensive review of the neurobiological characteristics and recent advancements in pain regulation of the CSF-contacting nucleus. The aim is to provide novel insights into the investigation of pain regulation within bidirectional regulatory pathway between the brain and cerebrospinal fluid, with a specific focus on elucidating the role of the CSF-contacting nucleus as a bridge structure. Additionally, the objective of this research is to propose innovative strategies for pain management and associated disorders in the future.

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The CSF-contacting nucleus regulates learning and memory through synaptic connections with the hippocampus

Cited by 2 publications

References 21 publications

Iron Metabolism Disorders for Cognitive Dysfunction After Mild Traumatic Brain Injury

Iron Metabolism Disorders for Cognitive Dysfunction After Mild Traumatic Brain Injury

The recent research progress in neurobiological characteristics and pain regulation of the cerebrospinal fluid-contacting nucleus

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