Topic
Nervous system
About: Nervous system is a research topic. Over the lifetime, 16729 publications have been published within this topic receiving 847181 citations.
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TL;DR: Vesicular acetylcholine transporter immunoreactivity was particularly useful for identification of parasympathetic intrinsic ganglia, and their terminal fields, in heart, uterus, and other peripheral organs receiving parASYmpathetic innervation.
314 citations
TL;DR: It is demonstrated that syntaxin plays a key role in nonneuronal secretion and is absolutely required for evoked neurotransmission.
313 citations
TL;DR: It is reported that peripheral nerve injury triggered long-term changes in excitatory synaptic transmission in layer II/III neurons within the anterior cingulate cortex (ACC) and that AC1 is critical for such long- term changes.
Abstract: Neuropathic pain is caused by a primary lesion or dysfunction in the nervous system. Investigations have mainly focused on the spinal mechanisms of neuropathic pain, and less is known about cortical changes in neuropathic pain. Here, we report that peripheral nerve injury triggered long-term changes in excitatory synaptic transmission in layer II/III neurons within the anterior cingulate cortex (ACC). Both the presynaptic release probability of glutamate and postsynaptic glutamate AMPA receptor-mediated responses were enhanced after injury using the mouse peripheral nerve injury model. Western blot showed upregulated phosphorylation of GluR1 in the ACC after nerve injury. Finally, we found that both presynaptic and postsynaptic changes after nerve injury were absent in genetic mice lacking calcium-stimulated adenylyl cyclase 1 (AC1). Our studies therefore provide direct integrative evidence for both long-term presynaptic and postsynaptic changes in cortical synapses after nerve injury, and that AC1 is critical for such long-term changes. AC1 thus may serve as a potential therapeutic target for treating neuropathic pain.
312 citations
TL;DR: Current work has demonstrated that oligodendrocytes transfer exosomes to neurons as a result of neurotransmitter signaling suggesting that these vesicles may mediate glial support of neurons.
Abstract: In the nervous system, glia cells maintain homeostasis, synthesize myelin, provide metabolic support, and participate in immune defense. The communication between glia and neurons is essential to synchronize these diverse functions with brain activity. Evidence is accumulating that secreted extracellular vesicles (EVs), such as exosomes and shedding microvesicles, are key players in intercellular signaling. The cells of the nervous system secrete EVs, which potentially carry protein and RNA cargo from one cell to another. After delivery, the cargo has the ability to modify the target cell phenotype. Here, we review the recent advances in understanding the role of EV secretion by astrocytes, microglia, and oligodendrocytes in the central nervous system. Current work has demonstrated that oligodendrocytes transfer exosomes to neurons as a result of neurotransmitter signaling suggesting that these vesicles may mediate glial support of neurons.
311 citations
TL;DR: It is demonstrated that upregulation of glial TNF-&agr; is associated with the expression of the p55 receptor on adjacent neurons, which may be related to the pathogenesis of neuropathic pain.
Abstract: Objectives The purpose of the current study was to evaluate changes in tumor necrosis factor-alpha (TNF-alpha ) and TNF-alpha receptor 1 (p55 receptor) using double fluorescent immunohistochemistry in glial and neural cells in the dorsal root ganglion and spinal cord after sciatic nerve injury in mice. SUMMARY OF BACKGROUND DATA.: TNF-alpha is a primary mediator of the inflammatory response and is primarily synthesized and released in the nervous system by macrophages and Schwann cells following peripheral nerve injury. TNF-alpha is also released from astrocytes and microglia in the central nervous system, where it plays a crucial role in the pathophysiology of injury. Methods Sixteen female mice were used. Under anesthesia, the left sciatic nerve was crushed. At 3, 5, and 14 days after surgery, the spinal cord at the level of L5 and the left L5 DRG were removed and processed for immunohistochemistry. Tissue sections were double stained with antibodies to either glial fibrillary acidic protein (GFAP; marker for astrocytes or satellite cells) or NeuN (marker for neurons), and TNF or p55 receptor. RESULTS.: In the dorsal root ganglion, GFAP-immunoreactive (IR) satellite cells became evident after injury and were also immunoreactive for both TNF-alpha and p55 receptor. Dorsal root ganglion neurons expressed p55 receptor after injury. TNF-alpha and GFAP-IR satellite cells surrounded p55-IR neurons. Furthermore, the number of GFAP-IR astrocytes dramatically increased in the spinal cord after nerve injury, and some astrocytes were also TNF-alpha -IR and p55 receptor-IR. TNF-alpha -1R astrocytes were seen around p55 receptor-IR neurons. Conclusions These data demonstrate that upregulation of glial TNF-alpha is associated with the expression of the p55 receptor on adjacent neurons. This association may have induced the expression of several cytokines and immediate early genes in dorsal root ganglion and spinal cord neurons via the TNF signaling pathway. These findings may be related to the pathogenesis of neuropathic pain.
311 citations