Noradrenergic synapses and effects of noradrenaline on interneurons in the ventral horn of the cat spinal cord

1977 ◽  
Vol 55 (3) ◽  
pp. 399-412 ◽  
Author(s):  
Larry M. Jordan ◽  
David A. McCrea ◽  
John D. Steeves ◽  
John E. Menzies
Keyword(s):  
Spinal Cord ◽  
Close Contact ◽  
Cell Types ◽  
Muscle Afferents ◽  
Ventral Horn ◽  
Lumbar Spinal Cord ◽  
High Threshold ◽  
Depressant Action ◽  
Motor Nuclei ◽  
Lumbar Spinal

Histochemical and electrophysiological procedures were carried out to determine the cell types in the ventral horn which are in close contact with noradrenergic terminals and to identify the types of neurons in the ventral horn which are influenced by noradrenaline (NA). Fluorescence histochemical studies revealed that noradrenaline-containing fibers rarely form intimate contacts with alpha motoneurons, whereas many small interneurons which are closely invested with fluorescent fibers can be found near the motoneurons. The effects of microiontophoretically applied NA on interneurons were examined in the lateral motor areas of the lumbar spinal cord ventral horn. NA had a substantial depressant action on 43% of cells in chloralose-anesthetized and decerebrate cats; it excited 6% of the cells, and was without effect on the rest. The cells which were depressed by NA could be excited by electrical stimulation of high threshold muscle afferents or skin afferents, and they could be influenced from a variety of exteroceptive and proprioceptive inputs. Owing to considerable convergence on the affected interneurons, no distinct population of NA-sensitive interneurons could be identified. Many of the interneurons strongly depressed by NA were found near the motor nuclei. The hypothesis is presented that inhibitory actions of NA on interneurons in the motor nuclei might explain its hyperpolarizing action on motoneurons.

Changes in serotonin-induced potentials during spinal cord development

1993 ◽  
Vol 69 (4) ◽  
pp. 1338-1349 ◽  
Author(s):  
L. Ziskind-Conhaim ◽  
B. S. Seebach ◽  
B. X. Gao
Keyword(s):  
Spinal Cord ◽  
Direct Action ◽  
Membrane Resistance ◽  
Ventral Horn ◽  
Repetitive Firing ◽  
Lumbar Spinal Cord ◽  
Receptor Subtypes ◽  
Gamma Aminobutyric Acid ◽  
Spinal Neurons ◽  
Lumbar Spinal

1. Motoneuron responses to serotonin (5-hydroxytryptamine, 5-HT), and the growth pattern of 5-HT projections into the ventral horn were studied in the isolated spinal cord of embryonic and neonatal rats. 2. 5-HT projections first appeared in lumbar spinal cord at days 16-17 of gestation (E16-E17) and were localized in the lateral and ventral funiculi. By E18, the projections had grown into the ventral horn, and at 1-2 days after birth they were in close apposition to motoneuron somata. 3. At E16-E17, slow-rising depolarizing potentials of 1-4 mV were recorded intracellularly in lumbar motoneurons in response to bath application of 5-HT. These potentials were not apparent after E18; at that time 5-HT generated long-lasting depolarizations with an average amplitude of 6 mV, and an increase of 11% in membrane resistance. Starting at E18, 5-HT also induced high-frequency fast-rising potentials that were blocked by antagonists of glutamate, gamma-aminobutyric acid, and glycine. 4. Motoneuron responses to 5-HT increased significantly after birth, when 5-HT produced an average depolarization of 19 mV and repetitive firing of action potentials. 5. Tetrodotoxin and high Mg2+ did not reduce the amplitude of the long-lasting depolarizations, which suggested that they were produced by direct action of 5-HT on motoneuron membrane. 6. At all developmental ages, 5-HT reduced the amplitude of dorsal root-evoked potentials. The suppressed responses were neither due to 5-HT-induced depolarization nor the result of a decrease in motoneuron excitability. 7. The pharmacological profile of 5-HT-induced potentials was studied with the use of various agonists and antagonists of 5-HT. The findings indicated that the actions of 5-HT on spinal neurons were mediated via multiple 5-HT receptor subtypes. 8. Our results suggested that 5-HT excited spinal neurons before 5-HT projections grew into the ventral horn. The characteristics of 5-HT-induced potentials changed, however, at the time when the density of 5-HT projections increased in the motor nuclei.

scholarly journals Locomotor Training Increases Synaptic Structure With High NGL-2 Expression After Spinal Cord Hemisection

2019 ◽  
Vol 33 (3) ◽  
pp. 225-231 ◽  
Author(s):  
Kazu Kobayakawa ◽  
Kyleigh Alexis DePetro ◽  
Hui Zhong ◽  
Bau Pham ◽  
Masamitsu Hara ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Motor Neurons ◽  
Ventral Horn ◽  
Lumbar Spinal Cord ◽  
Locomotor Training ◽  
Synaptic Structure ◽  
Cord Injury ◽  
Lumbar Spinal ◽  
Spinal Cord Hemisection ◽  
Activity Dependent

Background. We previously demonstrated that step training leads to reorganization of neuronal networks in the lumbar spinal cord of rodents after a hemisection (HX) injury and step training, including increases excitability of spinally evoked potentials in hindlimb motor neurons. Methods. In this study, we investigated changes in RNA expression and synapse number using RNA-Seq and immunohistochemistry of the lumbar spinal cord 23 days after a mid-thoracic HX in rats with and without post-HX step training. Results. Gene Ontology (GO) term clustering demonstrated that expression levels of 36 synapse-related genes were increased in trained compared with nontrained rats. Many synaptic genes were upregulated in trained rats, but Lrrc4 (coding NGL-2) was the most highly expressed in the lumbar spinal cord caudal to the HX lesion. Trained rats also had a higher number of NGL-2/synaptophysin synaptic puncta in the lumbar ventral horn. Conclusions. Our findings demonstrate clear activity-dependent regulation of synapse-related gene expression post-HX. This effect is consistent with the concept that activity-dependent phenomena can provide a mechanistic drive for epigenetic neuronal group selection in the shaping of the reorganization of synaptic networks to learn the locomotion task being trained after spinal cord injury.

scholarly journals Therapeutic Hypothermia Improves Hind Limb Motor Outcome and Attenuates Oxidative Stress and Neuronal Damage in the Lumbar Spinal Cord Following Cardiac Arrest

Antioxidants ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 38
Author(s):  
Ji Hyeon Ahn ◽  
Tae-Kyeong Lee ◽  
Bora Kim ◽  
Jae-Chul Lee ◽  
Hyun-Jin Tae ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Therapeutic Hypothermia ◽  
Hind Limb ◽  
Neuronal Damage ◽  
Ventral Horn ◽  
Lumbar Spinal Cord ◽  
Neuronal Protection ◽  
Endogenous Antioxidants ◽  
Lumbar Spinal

Hypothermia enhances outcomes of patients after resuscitation after cardiac arrest (CA). However, the underlying mechanism is not fully understood. In this study, we investigated effects of hypothermic therapy on neuronal damage/death, microglial activation, and changes of endogenous antioxidants in the anterior horn in the lumbar spinal cord in a rat model of asphyxial CA (ACA). A total of 77 adult male Sprague–Dawley rats were randomized into five groups: normal, sham ACA plus (+) normothermia, ACA + normothermia, sham ACA + hypothermia, and ACA + hypothermia. ACA was induced for 5 min by injecting vecuronium bromide. Therapeutic hypothermia was applied after return of spontaneous circulation (ROSC) via rapid cooling with isopropyl alcohol wipes, which was maintained at 33 ± 0.5 °C for 4 h. Normothermia groups were maintained at 37 ± 0.2 °C for 4 h. Neuronal protection, microgliosis, oxidative stress, and changes of endogenous antioxidants were evaluated at 12 h, 1 day, and 2 days after ROSC following ACA. ACA resulted in neuronal damage from 12 h after ROSC and evoked obvious degeneration/loss of spinal neurons in the ventral horn at 1 day after ACA, showing motor deficit of the hind limb. In addition, ACA resulted in a gradual increase in microgliosis with time after ACA. Therapeutic hypothermia significantly reduced neuronal loss and attenuated hind limb dysfunction, showing that hypothermia significantly attenuated microgliosis. Furthermore, hypothermia significantly suppressed ACA-induced increases of superoxide anion production and 8-hydroxyguanine expression, and significantly increased superoxide dismutase 1 (SOD1), SOD2, catalase, and glutathione peroxidase. Taken together, hypothermic therapy was found to have a substantial impact on changes in ACA-induced microglia activation, oxidative stress factors, and antioxidant enzymes in the ventral horn of the lumbar spinal cord, which closely correlate with neuronal protection and neurological performance after ACA.

NADPH-diaphorase reactivity and Fos-immunoreactivity within the ventral horn of the lumbar spinal cord of cats submitted to acute muscle inflammation induced by injection of carrageenan

2016 ◽  
Vol 118 (7) ◽  
pp. 659-664
Author(s):  
Vladimir A. Maisky ◽  
Olena P. Mankivska ◽  
Andriy V. Maznychenko ◽  
Oleh V. Vlasenko ◽  
Olexandr V. Dovgan’ ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Ventral Horn ◽  
Nadph Diaphorase ◽  
Lumbar Spinal Cord ◽  
Muscle Inflammation ◽  
Lumbar Spinal

scholarly journals Caudal-rostral progression of alpha motoneurone degeneration in the SOD1G93A mouse model of amyotrophic lateral sclerosis

2020 ◽  
Author(s):  
Alastair J Kirby ◽  
Thomas Palmer ◽  
Richard Mead ◽  
Ronaldo Ichiyama ◽  
Samit Chakrabarty
Keyword(s):  
Spinal Cord ◽  
Cervical Spinal Cord ◽  
Motor Impairment ◽  
Ventral Horn ◽  
Lumbar Spinal Cord ◽  
List Type ◽  
Spatial Trend ◽  
Transgenic Expression ◽  
Spinal Segments ◽  
Lumbar Spinal

AbstractMice with transgenic expression of human SOD1G93A are a widely used model of ALS, with a caudal-rostral progression of motor impairment. Previous studies have quantified the progression of motoneurone (MN) degeneration based on size, even though alpha (α-) and gamma (γ-) MNs overlap in size. Therefore, using molecular markers and synaptic inputs, we quantified the survival of α-MNs and γ-MNs at the lumbar and cervical spinal segments of 3- and 4-month SOD1G93A mice, to investigate whether there is a caudal-rostral progression of MN death. By 3-months, in the cervical and lumbar spinal cord, there was α-MN degeneration with complete γ-MN sparing. At 3-months the cervical spinal cord had more α-MNs per ventral horn than the lumbar spinal cord, in SOD1G93A mice. A similar spatial trend of degeneration was observed in the corticospinal tract, which remained intact in the cervical spinal cord at 3- and 4-months of age. These findings agree with the corticofugal synaptopathy model, that α-MN and CST of the lumbar spinal cord are more susceptible to degeneration in SOD1G93A mice. Hence, there is spatial and temporal caudal-rostral progression of α-MN and CST degeneration in SOD1G93A mice.HighlightsSOD1G93A mice display a caudal-rostral progression of motor impairment.Lumbar spinal cord of SOD1G93A mice has an enhanced susceptibility to degeneration.SOD1G93A mice exhibit a caudal-rostral progression of α-MN and CST degeneration

Transient ischemia-induced changes of excitatory amino acid carrier 1 in the ventral horn of the lumbar spinal cord in rabbits

2007 ◽  
Vol 29 (3) ◽  
pp. 310-316 ◽  
Author(s):  
InKoo Hwang ◽  
Jae-Chul Lee ◽  
Ki-Yeon Yoo ◽  
Jun-Hwi Cho ◽  
Ju-Young Jung ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Amino Acid ◽  
Excitatory Amino Acid ◽  
Ventral Horn ◽  
Lumbar Spinal Cord ◽  
Transient Ischemia ◽  
Lumbar Spinal ◽  
Induced Changes ◽  
Amino Acid Carrier

scholarly journals Integrative genetic analysis of the amyotrophic lateral sclerosis spinal cord implicates glial activation and suggests new risk genes

2021 ◽  
Author(s):  
Jack Humphrey ◽  
Sanan Venkatesh ◽  
Rahat Hasan ◽  
Jake T Herb ◽  
Katia de Paiva Lopes ◽  
...  
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Amyotrophic Lateral Sclerosis ◽  
Motor Neurons ◽  
Cell Types ◽  
Lumbar Spinal Cord ◽  
Gene Expression Response ◽  
Expression Response ◽  
Lumbar Spinal ◽  
Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a progressively fatal neurodegenerative disease affecting motor neurons in the brain and spinal cord. We used 380 post-mortem tissue RNA-seq transcriptomes from 154 ALS cases and 49 control individuals from cervical, thoracic, and lumbar spinal cord segments to investigate the gene expression response to ALS. We observed an increase in microglia and astrocyte expression, accompanied by a decrease in oligodendrocytes. By creating a gene co-expression network in the ALS samples, we identify several activated microglia modules that negatively correlate with retrospective disease duration. We map molecular quantitative trait loci and find several potential ALS risk loci that may act through gene expression or splicing in the spinal cord and assign putative cell-types for FNBP1, ACSL5, SH3RF1 and NFASC. Finally, we outline how repeat expansions that alter splicing of C9orf72 are tagged by common variants, and use this to suggest ATXN3 as a putative risk gene.

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