Slow progression of sciatic nerve degeneration and regeneration after loose ligation through microglial activation and decreased KCC2 levels in the mouse spinal cord ventral horn

2021 ◽  
Author(s):  
Tsukasa Yafuso ◽  
Yoshinori Kosaka ◽  
Chigusa Shimizu-Okabe ◽  
Nobuhiko Okura ◽  
Shiori Kobayashi ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Sciatic Nerve ◽  
Microglial Activation ◽  
Ventral Horn ◽  
Nerve Degeneration ◽  
Mouse Spinal Cord ◽  
Slow Progression

scholarly journals ERG Conductance Expression Modulates the Excitability of Ventral Horn GABAergic Interneurons That Control Rhythmic Oscillations in the Developing Mouse Spinal Cord

2007 ◽  
Vol 27 (4) ◽  
pp. 919-928 ◽  
Author(s):  
F. Furlan ◽  
G. Taccola ◽  
M. Grandolfo ◽  
L. Guasti ◽  
A. Arcangeli ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Ventral Horn ◽  
Gabaergic Interneurons ◽  
Mouse Spinal Cord

scholarly journals Differential astroglial responses in the spinal cord of rats submitted to a sciatic nerve double crush treated with local injection of cultured Schwann cell suspension or lesioned spinal cord extract: implications on cell therapy for nerve repair

2007 ◽  
Vol 22 (6) ◽  
pp. 485-494 ◽  
Author(s):  
João Gabriel Martins Dallo ◽  
Bernardo Vergara Reichert ◽  
José Benedito Ramos Valladão Júnior ◽  
Camila Silva ◽  
Bianca Aparecida de Luca ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Sciatic Nerve ◽  
Cell Therapy ◽  
Dorsal Horn ◽  
Wound Repair ◽  
Ventral Horn ◽  
Local Injection ◽  
Spinal Cord Dorsal Horn ◽  
Nerve Lesion ◽  
Double Crush

PURPOSE: Reactive astrocytes are implicated in several mechanisms after central or peripheral nervous system lesion, including neuroprotection, neuronal sprouting, neurotransmission and neuropathic pain. Schwann cells (SC), a peripheral glia, also react after nerve lesion favoring wound/repair, fiber outgrowth and neuronal regeneration. We investigated herein whether cell therapy for repair of lesioned sciatic nerve may change the pattern of astroglial activation in the spinal cord ventral or dorsal horn of the rat. METHODS: Injections of a cultured SC suspension or a lesioned spinal cord homogenized extract were made in a reservoir promoted by a contiguous double crush of the rat sciatic nerve. Local injection of phosphate buffered saline (PBS) served as control. One week later, rats were euthanized and spinal cord astrocytes were labeled by immunohistochemistry and quantified by means of quantitative image analysis. RESULTS: In the ipsilateral ventral horn, slight astroglial activations were seen after PBS or SC injections, however, a substantial activation was achieved after cord extract injection in the sciatic nerve reservoir. Moreover, SC suspension and cord extract injections were able to promote astroglial reaction in the spinal cord dorsal horn bilaterally. Conclusion: Spinal cord astrocytes react according to repair processes of axotomized nerve, which may influence the functional outcome. The event should be considered during the neurosurgery strategies.

Activation of NF-κB in the mouse spinal cord following sciatic nerve transection

2005 ◽  
Vol 165 (4) ◽  
pp. 470-477 ◽  
Author(s):  
G. Pollock ◽  
K.R. Pennypacker ◽  
S. Mémet ◽  
A. Israël ◽  
S. Saporta
Keyword(s):  
Spinal Cord ◽  
Sciatic Nerve ◽  
Nerve Transection ◽  
Sciatic Nerve Transection ◽  
Mouse Spinal Cord

scholarly journals Developmental Formation of the GABAergic and Glycinergic Networks in the Mouse Spinal Cord

2022 ◽  
Vol 23 (2) ◽  
pp. 834
Author(s):  
Chigusa Shimizu-Okabe ◽  
Shiori Kobayashi ◽  
Jeongtae Kim ◽  
Yoshinori Kosaka ◽  
Masanobu Sunagawa ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Radial Glia ◽  
Ventricular Zone ◽  
Glycine Receptor ◽  
Ventral Horn ◽  
Gabaergic Neurons ◽  
Inhibitory Neurons ◽  
Gamma Aminobutyric Acid ◽  
Mouse Spinal Cord ◽  
Mature Mouse

Gamma-aminobutyric acid (GABA) and glycine act as inhibitory neurotransmitters. Three types of inhibitory neurons and terminals, GABAergic, GABA/glycine coreleasing, and glycinergic, are orchestrated in the spinal cord neural circuits and play critical roles in regulating pain, locomotive movement, and respiratory rhythms. In this study, we first describe GABAergic and glycinergic transmission and inhibitory networks, consisting of three types of terminals in the mature mouse spinal cord. Second, we describe the developmental formation of GABAergic and glycinergic networks, with a specific focus on the differentiation of neurons, formation of synapses, maturation of removal systems, and changes in their action. GABAergic and glycinergic neurons are derived from the same domains of the ventricular zone. Initially, GABAergic neurons are differentiated, and their axons form synapses. Some of these neurons remain GABAergic in lamina I and II. Many GABAergic neurons convert to a coreleasing state. The coreleasing neurons and terminals remain in the dorsal horn, whereas many ultimately become glycinergic in the ventral horn. During the development of terminals and the transformation from radial glia to astrocytes, GABA and glycine receptor subunit compositions markedly change, removal systems mature, and GABAergic and glycinergic action shifts from excitatory to inhibitory.

scholarly journals Adenosine-mediated modulation of ventral horn interneurons and spinal motoneurons in neonatal mice

2015 ◽  
Vol 114 (4) ◽  
pp. 2305-2315 ◽  
Author(s):  
Emily C. Witts ◽  
Filipe Nascimento ◽  
Gareth B. Miles
Keyword(s):  
Spinal Cord ◽  
Purinergic Signaling ◽  
Presynaptic Receptors ◽  
Ventral Horn ◽  
Cellular Mechanisms ◽  
Mouse Spinal Cord ◽  
Synaptic Inputs ◽  
Adenosine Receptor Antagonist ◽  
Postsynaptic Currents

Neuromodulation allows neural networks to adapt to varying environmental and biomechanical demands. Purinergic signaling is known to be an important modulatory system in many parts of the CNS, including motor control circuitry. We have recently shown that adenosine modulates the output of mammalian spinal locomotor control circuitry (Witts EC, Panetta KM, Miles GB. J Neurophysiol 107: 1925–1934, 2012). Here we investigated the cellular mechanisms underlying this adenosine-mediated modulation. Whole cell patch-clamp recordings were performed on ventral horn interneurons and motoneurons within in vitro mouse spinal cord slice preparations. We found that adenosine hyperpolarized interneurons and reduced the frequency and amplitude of synaptic inputs to interneurons. Both effects were blocked by the A1-type adenosine receptor antagonist DPCPX. Analysis of miniature postsynaptic currents recorded from interneurons revealed that adenosine reduced their frequency but not amplitude, suggesting that adenosine acts on presynaptic receptors to modulate synaptic transmission. In contrast to interneurons, recordings from motoneurons revealed an adenosine-mediated depolarization. The frequency and amplitude of synaptic inputs to motoneurons were again reduced by adenosine, but we saw no effect on miniature postsynaptic currents. Again these effects on motoneurons were blocked by DPCPX. Taken together, these results demonstrate differential effects of adenosine, acting via A1 receptors, in the mouse spinal cord. Adenosine has a general inhibitory action on ventral horn interneurons while potentially maintaining motoneuron excitability. This may allow for adaptation of the locomotor pattern generated by interneuronal networks while helping to ensure the maintenance of overall motor output.

scholarly journals Alterations in mouse spinal cord and sciatic nerve microRNAs after the chronic constriction injury (CCI) model of neuropathic pain

2020 ◽  
Vol 731 ◽  
pp. 135029
Author(s):  
Jenny L. Wilkerson ◽  
Jinmai Jiang ◽  
Jasmine S. Felix ◽  
Julie K. Bray ◽  
Lais da Silva ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Sciatic Nerve ◽  
Chronic Constriction Injury ◽  
Mouse Spinal Cord ◽  
Cci Model

Increased phosphorylated-μ-opioid receptor immunoreactivity in the mouse spinal cord following sciatic nerve ligation

2004 ◽  
Vol 354 (2) ◽  
pp. 148-152 ◽  
Author(s):  
Minoru Narita ◽  
Naoko Kuzumaki ◽  
Masami Suzuki ◽  
Michiko Narita ◽  
Kousei Oe ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Sciatic Nerve ◽  
Opioid Receptor ◽  
Mouse Spinal Cord ◽  
Μ Opioid Receptor

scholarly journals Phosphoglycerate Mutase 1 Prevents Neuronal Death from Ischemic Damage by Reducing Neuroinflammation in the Rabbit Spinal Cord

2020 ◽  
Vol 21 (19) ◽  
pp. 7425
Author(s):  
Hyo Young Jung ◽  
Hyun Jung Kwon ◽  
Woosuk Kim ◽  
Kyu Ri Hahn ◽  
Seung Myung Moon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Inflammatory Cytokines ◽  
Neuronal Death ◽  
Microglial Activation ◽  
Ventral Horn ◽  
Phosphoglycerate Mutase ◽  
Ischemic Damage ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

Phosphoglycerate mutase 1 (PGAM1) is a glycolytic enzyme that increases glycolytic flux in the brain. In the present study, we examined the effects of PGAM1 in conditions of oxidative stress and ischemic damage in motor neuron-like (NSC34) cells and the rabbit spinal cord. A Tat-PGAM1 fusion protein was prepared to allow easy crossing of the blood-brain barrier, and Control-PGAM1 was synthesized without the Tat peptide protein transduction domain. Intracellular delivery of Tat-PGAM1, not Control-PGAM1, was achieved in a time- and concentration-dependent manner. Immunofluorescent staining confirmed the intracellular expression of Tat-PGAM1 in NSC34 cells. Tat-PGAM1, but not Control-PGAM1, significantly alleviated H2O2-induced oxidative stress, neuronal death, mitogen-activated protein kinase, and apoptosis-inducing factor expression in NSC34 cells. After ischemia induction in the spinal cord, Tat-PGAM1 treatment significantly improved ischemia-induced neurological impairments and ameliorated neuronal cell death in the ventral horn of the spinal cord 72 h after ischemia. Tat-PGAM1 treatment significantly mitigated the ischemia-induced increase in malondialdehyde and 8-iso-prostaglandin F2α production in the spinal cord. In addition, Tat-PGAM1, but not Control-PGAM1, significantly decreased microglial activation and secretion of pro-inflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α induced by ischemia in the ventral horn of the spinal cord. These results suggest that Tat-PGAM1 can be used as a therapeutic agent to reduce spinal cord ischemia-induced neuronal damage by lowering the oxidative stress, microglial activation, and secretion of pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α.

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