Subunit composition of rat ventral spinal cord GABAA receptors, assessed by single cell RT-multiplex PCR

Neuroreport ◽  
2000 ◽  
Vol 11 (14) ◽  
pp. 3169-3173 ◽  
Author(s):  
Diego Ruano ◽  
Valérie Létang ◽  
Bruno Biton ◽  
Patrick Avenet ◽  
Jesus Benavides ◽  
...  
2019 ◽  
Vol 31 (2) ◽  
pp. 279-284 ◽  
Author(s):  
Ahmed Mansour ◽  
Toshiki Endo ◽  
Tomoo Inoue ◽  
Kenichi Sato ◽  
Hidenori Endo ◽  
...  

The authors report the case of a 78-year-old man with a craniocervical junction epidural arteriovenous fistula who presented with subarachnoid hemorrhage from a ruptured anterior spinal artery (ASA) aneurysm. Because endovascular embolization was difficult, a posterolateral approach was chosen and a novel endoscopic fluorescence imaging system was utilized to clip the aneurysm. The fluorescence imaging system provided clear and magnified views of the ventral spinal cord simultaneously with the endoscope-integrated indocyanine green videoangiography, which helped safely obliterate the ASA aneurysm. With the aid of this novel imaging system, surgeons can appreciate and manipulate complex vascular pathologies of the ventral spinal cord through a posterolateral approach, even when the lesion is closely related to the ASA.


2021 ◽  
Vol 24 (4) ◽  
pp. 572-583 ◽  
Author(s):  
Jacob A. Blum ◽  
Sandy Klemm ◽  
Jennifer L. Shadrach ◽  
Kevin A. Guttenplan ◽  
Lisa Nakayama ◽  
...  

1991 ◽  
Vol 69 (6) ◽  
pp. 877-885 ◽  
Author(s):  
D. Nicholson ◽  
T. D. White ◽  
J. Sawynok

The effects of forskolin, Ro 20-1724, rolipram, and 3-isobutyl-1-methylxanthine (IBMX) on morphine-evoked release of adenosine from dorsal spinal cord synaptosomes were evaluated to examine the potential involvement of cyclic AMP in this action of morphine. Ro 20-1724 (1–100 μM), rolipram (1–100 μM), and forskolin (1–10 μM) increased basal release of adenosine, and at 1 μM inhibited morphine-evoked release of adenosine. Release of adenosine by Ro 20-1724, rolipram, and forskolin was reduced 42–77% in the presence of α, β-methylene ADP and GMP, which inhibits ecto-5′-nucleotidase activity by 81%, indicating that this adenosine originated predominantly as nucleotide(s). Significant amounts of adenosine also were released from the ventral spinal cord by these agents. Ro 20-1724 and rolipram did not significantly alter the uptake of adenosine into synaptosomes. Although Ro 20-1724 and rolipram had only limited effects on the extrasynaptosomal conversion of added cyclic AMP to adenosine, IBMX, a phosphodiesterase inhibitor with a broader spectrum of inhibitory activity for phosphodiesterase isoenzymes, significantly inhibited the conversion of cyclic AMP to adenosine and resulted in recovery of a substantial amount of cyclic AMP. As with the non-xanthine phosphodiesterase inhibitors, IBMX increased basal release of adenosine and reduced morphine-evoked release of adenosine. Adenosine released by IBMX was reduced 70% in the presence of α, β-methylene ADP and GMP, and release from the ventral spinal cord was 61% of that from the dorsal spinal cord. Collectively, these results indicate that forskolin and phosphodiesterase inhibitors release nucleotide(s) which is (are) converted extrasynaptosomally to adenosine. For forskolin, Ro 20-1724, and rolipram, the nucleotide released could be cyclic AMP. Morphine releases adenosine per se, and forskolin and phosphodiesterase inhibitors reduce this release. The lack of increase in the action of morphine with phosphodiesterase inhibitors in particular does not support a role for stimulation of cyclic AMP production by morphine in the release of adenosine. The reduction in morphine-evoked release of adenosine by forskolin and phosphodiesterase inhibitors suggests either (a) that a reduction in cyclic levels by morphine promotes adenosine release, or (b) that cyclic AMP interferes with the release process.Key words: forskolin, Ro 20-1724, 3-isobutyl-1-methylxanthine, cyclic AMP, morphine, adenosine release, spinal cord.


genesis ◽  
2000 ◽  
Vol 27 (1) ◽  
pp. 6-11 ◽  
Author(s):  
Jun Cai ◽  
Xiaohua Xu ◽  
Huliang Yin ◽  
Rachel Wu ◽  
Geoffrey Modderman ◽  
...  

2020 ◽  
Author(s):  
Luipa Khandker ◽  
Marisa A. Jeffries ◽  
Yun-Juan Chang ◽  
Marie L. Mather ◽  
Jennifer N. Bourne ◽  
...  

AbstractBrain and spinal cord oligodendroglia have distinct functional characteristics, and cell autonomous loss of individual genes can result in different regional phenotypes. However, sequencing studies to date have not revealed distinctions between brain and spinal cord oligodendroglia. Using single-cell analysis of oligodendroglia during myelination, we demonstrate that brain and spinal cord precursors are transcriptionally distinct, defined predominantly by cholesterol biosynthesis. We further identify mechanistic target of rapamycin (mTOR) as a major regulator promoting cholesterol biosynthesis in oligodendroglia. Oligodendroglial-specific loss of mTOR compromises cholesterol biosynthesis in both the brain and spinal cord. Importantly, mTOR loss has a greater impact on cholesterol biosynthesis in spinal cord oligodendroglia that corresponds with more pronounced developmental deficits. However, loss of mTOR in brain oligodendroglia ultimately results in oligodendrocyte death, spontaneous demyelination, and impaired axonal function, demonstrating that mTOR is required for myelin maintenance in the adult brain.


2020 ◽  
Author(s):  
Lev Starikov ◽  
Andreas H. Kottmann

AbstractOligodendrocyte precursor cells (OPCs) arise sequentially first from a ventral and then from a dorsal precursor domain at the end of neurogenesis during spinal cord development. Whether the sequential production of OPCs is of physiological significance has not been examined. Here we show that ablating Shh signaling from nascent ventricular zone derivatives and partially from the floor plate results in a severe diminishment of ventral derived OPCs but normal numbers of motor neurons in the postnatal spinal cord. In the absence of ventral vOPCs, dorsal dOPCs populate the entire spinal cord resulting in an increased OPC density in the ventral horns. These OPCs take on an altered morphology, do not participate in the removal of excitatory vGlut1 synapses from injured motor neurons, and exhibit morphological features similar to those found in the vicinity of motor neurons in the SOD1 mouse model of Amyotrophic Lateral Sclerosis (ALS). Our data indicates that vOPCs prevent dOPCs from invading ventral spinal cord laminae and suggests that vOPCs have a unique ability to communicate with injured motor neurons.


2021 ◽  
Author(s):  
Teresa Rayon ◽  
Rory J. Maizels ◽  
Christopher Barrington ◽  
James Briscoe

AbstractThe spinal cord receives input from peripheral sensory neurons and controls motor output by regulating muscle innervating motor neurons. These functions are carried out by neural circuits comprising molecularly and physiologically distinct neuronal subtypes that are generated in a characteristic spatial-temporal arrangement from progenitors in the embryonic neural tube. The systematic mapping of gene expression in mouse embryos has provided insight into the diversity and complexity of cells in the neural tube. For human embryos, however, less information has been available. To address this, we used single cell mRNA sequencing to profile cervical and thoracic regions in four human embryos of Carnegie Stages (CS) CS12, CS14, CS17 and CS19 from Gestational Weeks (W) 4-7. In total we recovered the transcriptomes of 71,219 cells. Analysis of progenitor and neuronal populations from the neural tube, as well as cells of the peripheral nervous system, in dorsal root ganglia adjacent to the neural tube, identified dozens of distinct cell types and facilitated the reconstruction of the differentiation pathways of specific neuronal subtypes. Comparison with existing mouse datasets revealed the overall similarity of mouse and human neural tube development while highlighting specific features that differed between species. These data provide a catalogue of gene expression and cell type identity in the developing neural tube that will support future studies of sensory and motor control systems and can be explored at https://shiny.crick.ac.uk/scviewer/neuraltube/.


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