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Role of fractalkine–CX3CR1 pathway in seizure-induced microglial activation, neurodegeneration, and neuroblast production in the adult rat brain
Evidence is provided for a role of the fractalkine-CX3CR1 signaling pathway in seizure-induced microglial activation and suggests that neuroblast production following seizures may partly occur as a result of microglia activation.
Brain inflammation induces post-synaptic changes during early synapse formation in adult-born hippocampal neurons
- D. Chugh, P. Nilsson, Seyedeh-Atiyeh Afjei, Anahita Bakochi, C. T. Ekdahl
- Biology, MedicineExperimental Neurology
- 1 December 2013
Evidence is provided that adult-born hippocampal neurons alter their inhibitory and excitatory synaptic integration when encountering an LPS-induced brain inflammation during the initial stages of synapse formation.
The Cell Adhesion Molecule Neurofascin Stabilizes Axo-axonic GABAergic Terminals at the Axon Initial Segment*
- M. Kriebel, Jennifer Metzger, +4 authors H. Volkmer
- Biology, MedicineThe Journal of Biological Chemistry
- 16 May 2011
Lentiviral shRNA-mediated knockdown of neurofascin in adult rat brain indicates that neurofASCin regulates the number and size of postsynaptic gephyrin scaffolds, the number of GABAA receptor clusters as well as presynaptic glutamate decarboxylase-positive terminals at the axon initial segment.
Altered Synaptic Properties During Integration of Adult-Born Hippocampal Neurons Following a Seizure Insult
The findings indicate that seizure-induced brain pathology alters the sub-cellular expression of synaptic adhesion molecules and scaffolding proteins related to particularly inhibitory but also excitatory synapses, which may yield functional consequences for the integration of adult-born neurons.
Immune response in the eye following epileptic seizures
- Matilda Ahl, Una Avdic, +4 authors C. T. Ekdahl
- Biology, MedicineJournal of Neuroinflammation
- 27 June 2016
The authors' results are the first evidence that epileptic seizures induce an immune response in the retina, and has a potential to become a novel non-invasive tool for detecting brain inflammation through the eyes.
Nonconvulsive status epilepticus in rats leads to brain pathology
There is no general consensus regarding to what extent nonconvulsive SE (NCSE) is harmful to the brain, which adds uncertainty to stringent treatment regimes.
Muscle contractility dysfunction precedes loss of motor unit connectivity in SOD1(G93A) mice
The longitudinal contractility and connectivity paradigm employed here provides additional insight into the SOD1(G93A) mouse model and suggests that loss of muscle contractility is an early finding that may precede loss of MUs and motor neuron death.
Alterations in Brain Inflammation, Synaptic Proteins, and Adult Hippocampal Neurogenesis during Epileptogenesis in Mice Lacking Synapsin2
- D. Chugh, Idrish Ali, Anahita Bakochi, Elma Bahonjic, Lars Etholm, C. T. Ekdahl
- Biology, MedicinePloS one
- 15 July 2015
Molecular alterations in brain inflammation and excitatory/inhibitory balance that could serve as potential targets for therapeutics and diagnostic biomarkers are reported and indicate an epileptogenic zone from where the generalized seizures in synapsin 2 knockout mice may be initiated or spread.
Physical Activity Reduces Epilepsy Incidence: a Retrospective Cohort Study in Swedish Cross-Country Skiers and an Experimental Study in Seizure-Prone Synapsin II Knockout Mice
The clinical study and the experimental findings in mice indicate that physical activity may prevent or delay the development of epilepsy.
Neuromuscular junction transmission failure is a late phenotype in aging mice
- D. Chugh, C. Iyer, Xueyong Wang, P. Bobbili, M. Rich, W. Arnold
- MedicineNeurobiology of Aging
- 5 November 2019
Reduced muscle excitability may be a potential therapeutic target for improvement of physical function in older adults and improved understanding of age-related neurodegeneration will likely have important implications in designing novel therapeutic interventions specific for different stages of sarcopenia.