scholarly journals Dimethyl fumarate improves white matter function following severe hypoperfusion: Involvement of microglia/macrophages and inflammatory mediators

2017 ◽  
Vol 38 (8) ◽  
pp. 1354-1370 ◽  
Author(s):  
Jill H Fowler ◽  
Jamie McQueen ◽  
Philip R Holland ◽  
Yasmina Manso ◽  
Martina Marangoni ◽  
...  
Keyword(s):  
Blood Flow ◽  
White Matter ◽  
Functional Impairment ◽  
Action Potentials ◽  
Dimethyl Fumarate ◽  
Peak Latency ◽  
Cerebral Hypoperfusion ◽  
Bilateral Common Carotid Artery ◽  
Compound Action Potentials ◽  
Compound Action

The brain’s white matter is highly vulnerable to reductions in cerebral blood flow via mechanisms that may involve elevated microgliosis and pro-inflammatory pathways. In the present study, the effects of severe cerebral hypoperfusion were investigated on white matter function and inflammation. Male C57Bl/6J mice underwent bilateral common carotid artery stenosis and white matter function was assessed at seven days with electrophysiology in response to evoked compound action potentials (CAPs) in the corpus callosum. The peak latency of CAPs and axonal refractoriness was increased following hypoperfusion, indicating a marked functional impairment in white matter, which was paralleled by axonal and myelin pathology and increased density and numbers of microglia/macrophages. The functional impairment in peak latency was significantly correlated with increased microglia/macrophages. Dimethyl fumarate (DMF; 100 mg/kg), a drug with anti-inflammatory properties, was found to reduce peak latency but not axonal refractoriness. DMF had no effect on hypoperfusion-induced axonal and myelin pathology. The density of microglia/macrophages was significantly increased in vehicle-treated hypoperfused mice, whereas DMF-treated hypoperfused mice had similar levels to that of sham-treated mice. The study suggests that increased microglia/macrophages following cerebral hypoperfusion contributes to the functional impairment in white matter that may be amenable to modulation by DMF.

Contribution of Fast and Slow Conducting Myelinated Axons to Single-Peak Compound Action Potentials in Rat Spinal Cord White Matter Preparations

2011 ◽  
Vol 105 (2) ◽  
pp. 929-941 ◽  
Author(s):  
Alexander A. Velumian ◽  
Yudi Wan ◽  
Marina Samoilova ◽  
Michael G. Fehlings
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Action Potentials ◽  
Lower Threshold ◽  
Differential Sensitivity ◽  
Single Peak ◽  
Rat Spinal Cord ◽  
Conducting Component ◽  
Compound Action Potentials ◽  
Compound Action

Unlike recordings derived from optic nerve or corpus callosum, compound action potentials (CAPs) recorded from rodent spinal cord white matter (WM) have a characteristic single-peak shape despite the heterogeneity of axonal populations. Using a double sucrose gap technique, we analyzed the CAPs recorded from dorsal, lateral, and ventral WM from mature rat spinal cord. The CAP decay was significantly prolonged with increasing stimulus intensities suggesting a recruitment of higher threshold, slower conducting axons. At 3.5 mm conduction distance, a hidden higher threshold, slower conducting component responsible for prolongation of CAP decay was uncovered in 22 of 25 of dorsal WM strips by analyzing the stimulus-response relationships and a normalization-subtraction procedure. This component had a peak conduction velocity (CV) of 5.0 ± 0.2 (SE) m/s as compared with 9.3 ± 0.5 m/s for the lower threshold peak ( P < 0.0001). Oxygen-glucose deprivation (OGD), along with its known effects on CAP amplitude, significantly ( P < 0.015) shortened the CAP decay. The hidden higher threshold, slower conducting component showed greater sensitivity to OGD compared with the lower threshold, faster conducting component, suggesting a differential sensitivity of axonal populations of spinal cord WM. At longer conduction distances and lower temperatures (9.8 mm, 22–24°C), the slower peak could be directly visualized in CAPs at higher stimulation intensities. A detailed analysis of single-peak CAPs to identify their fast and slow conducting components may be of particular importance for studies of axonal physiology and pathophysiology in small animals where the conduction distance is not sufficiently long to separate the CAP peaks.

Resistance of Gerbil Auditory Function to Reversible Decrease in Cochlear Blood Flow

2017 ◽  
Vol 22 (2) ◽  
pp. 89-95
Author(s):  
Fahd El Afia ◽  
Fabrice Giraudet ◽  
Laurent Gilain ◽  
Thierry Mom ◽  
Paul Avan
Keyword(s):  
Blood Flow ◽  
Action Potentials ◽  
Round Window ◽  
Mongolian Gerbils ◽  
Neural Responses ◽  
Cochlear Function ◽  
Cochlear Blood Flow ◽  
Compound Action Potentials ◽  
Cochlear Microphonic Potential ◽  
Compound Action

The objective was to design in gerbils a model of reversible decrease in cochlear blood flow (CBF) and analyze its influence on cochlear function. In Mongolian gerbils injected with ferromagnetic microbeads, a magnet placed near the porus acusticus allowed CBF to be manipulated. The cochlear microphonic potential (CM) from the basal cochlea was monitored by a round-window electrode. In 13 of the 20 successfully injected gerbils, stable CBF reduction was obtained for 11.5 min on average. The CM was affected only when CBF fell to less than 60% of its baseline, yet remained >40% of its initial level in about 2/3 of such cases. After CBF restoration, CM recovery was fast and usually complete. Reduced CM came with a 35- to 45-dB threshold elevation of neural responses determined by compound action potentials. This method allowing reversible changes of CBF confirms the robustness of cochlear function to decreased CBF. It can be used to study whether a hypovascularized cochlea is abnormally sensitive to stress.

Stretch of mammalian nerve in vitro: Effect on compound action potentials

2000 ◽  
Vol 5 (4) ◽  
pp. 227-235 ◽  
Author(s):  
Sidney Ochs ◽  
Rahman Pourmand ◽  
Kenan Si ◽  
Richard N. Friedman
Keyword(s):  
Action Potentials ◽  
Compound Action Potentials ◽  
Vitro Effect ◽  
Mammalian Nerve ◽  
Compound Action

scholarly journals Site of cochlear stimulation and its effect on electrically evoked compound action potentials using the MED-EL standard electrode array

2009 ◽  
Vol 8 (1) ◽  
pp. 40 ◽  
Author(s):  
Stefan Brill ◽  
Joachim Müller ◽  
Rudolf Hagen ◽  
Alexander Möltner ◽  
Steffi-Johanna Brockmeier ◽  
...  
Keyword(s):  
Action Potentials ◽  
Electrode Array ◽  
Compound Action Potentials ◽  
Compound Action

Using Evoked Compound Action Potentials to Assess Activation of Electrodes and Predict C-Levels in the Tempo+ Cochlear Implant Speech Processor

2010 ◽  
Vol 31 (1) ◽  
pp. 134-145 ◽  
Author(s):  
Isaac Alvarez ◽  
Angel de la Torre ◽  
Manuel Sainz ◽  
Cristina Roldán ◽  
Hansjoerg Schoesser ◽  
...  
Keyword(s):  
Cochlear Implant ◽  
Action Potentials ◽  
Speech Processor ◽  
Compound Action Potentials ◽  
Compound Action

Synaptic transmission in the chronically decentralized middle cervical and stellate ganglia of the dog

1983 ◽  
Vol 61 (10) ◽  
pp. 1149-1155 ◽  
Author(s):  
J. A. Armour
Keyword(s):  
Central Nervous System ◽  
Action Potentials ◽  
Autonomic Nerves ◽  
Autonomic Ganglia ◽  
Afferent Nerves ◽  
Stellate Ganglia ◽  
Compound Action Potentials ◽  
The Central Nervous System ◽  
Compound Action ◽  
Stimulation Of

Afferent stimulation of one thoracic cardiopulmonary nerve generated compound action potentials in the efferent axons of other ipsilateral cardiopulmonary nerves in dogs, 14 days after their thoracic autonomic ganglia had been decentralized. The compound action potentials were influenced by the frequency of activation and (in 5 of 12 dogs) by pharmacological autonomic blocking agents (hexamethonium, atropine, phentolamine, and propranolol). Moreover, they were abolished transiently when chymotrypsin was injected locally into the ganglia, and extendedly when manganese was injected. Thus, synapses that can be activated by stimulation of afferent nerves exist in chronically decentralized thoracic autonomic nerves and ganglia. It is proposed that regulation of the heart and lungs occurs in part via thoracic autonomic neural elements independent of the central nervous system.

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