Thalamocortical-auditory network alterations following cuprizone-induced demyelination

Autor: Ali Gorji, Nikoo Ghaffarian, Sven G. Meuth, Thomas Budde, Kerstin Göbel, Masoud Mesgari, Manuela Cerina, Erwin-Josef Speckmann
Rok vydání: 2016
Předmět:
0301 basic medicine
Auditory Pathways
Monoamine Oxidase Inhibitors
Patch-Clamp Techniques
Time Factors
Immunology
Biophysics
Action Potentials
Neurotransmission
Biology
In Vitro Techniques
Auditory cortex
03 medical and health sciences
Cellular and Molecular Neuroscience
Cuprizone
Mice
0302 clinical medicine
Thalamus
Neuroplasticity
medicine
Premovement neuronal activity
Animals
Remyelination
Myelin Proteolipid Protein
Auditory Cortex
Neurons
Neuronal activity
General Neuroscience
Multiple sclerosis
Research
Long-term potentiation
Synaptic Potentials
medicine.disease
Electric Stimulation
Mice
Inbred C57BL
Disease Models
Animal
030104 developmental biology
medicine.anatomical_structure
Neurology
Excitatory postsynaptic potential
Internal capsule
Neuroscience
030217 neurology & neurosurgery
Demyelinating Diseases
Zdroj: Journal of Neuroinflammation
ISSN: 1742-2094
Popis: Background Demyelination and remyelination are common pathological processes in many neurological disorders, including multiple sclerosis (MS). Clinical evidence suggests extensive involvement of the thalamocortical (TC) system in patients suffering from MS. Methods Using murine brain slices of the primary auditory cortex, we investigated the functional consequences of cuprizone-induced de- and remyelination on neuronal activity and auditory TC synaptic transmission in vitro. Results Our results revealed an impact of myelin loss and restoration on intrinsic cellular firing patterns, synaptic transmission, and neuronal plasticity in layer 3 and 4 neurons of the auditory TC network. While there was a complex hyper- and depolarizing shift of the resting membrane potential, spontaneous and induced action potential firing was reduced during demyelination and early remyelination. In addition, excitatory postsynaptic potential amplitudes were decreased and induction of LTP was reduced during demyelination. Conclusions These data indicate that demyelination-induced impairment of neurons and network activity within the TC system may underlie clinical symptoms observed in demyelinating diseases, corroborating human findings that disease progression is significantly correlated with microstructural tissue damage of the TC system. Further investigation into focal inflammation-induced demyelination models ex vivo and in vivo are needed to understand the functional implication of local and remote lesion formation on TC network activity in MS.
Databáze: OpenAIRE
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