pilocarpine mouse model

The main features of temporal lobe epilepsy (TLE) are:

  • Epileptic foci in the limbic system
  • An “initial precipitating injury”
  • The so-called “latent period”
  • The presence of hippocampal sclerosis leading to reorganization of neuronal networks

Many of these characteristics can be reproduced in rodents by systemic injection of pilocarpine.

In this animal model, status epilepticus is followed by a latent period and later by the appearance of spontaneous recurrent seizures.

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Regenerative therapy

Stem cells from adult tissues were considered for a long time as promising tools for regenerative therapy of neurological diseases, including spinal cord injuries (SCI).

Researchers at GIGA have investigated the impact of pure populations of mesenchymal stem cells (MSCs) and neural crest stem cells (NCSCs) isolated from adult bone marrow in a mouse model of spinal cord injury.

They observed that both cell types induced motor recovery in mice, and modified the inflammatory reaction in the lesion site.

Their preliminary results suggest that both cell types have beneficial effects in experimental SCI.

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Role of elongator complex

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the brain and spinal cord. The cause of multiple sclerosis is unknown. It’s considered an autoimmune disease whereby the immune system malfunction destroys myelin. Among others, one strategy to treat MS is to stimulate the recruitment and the activation of resident oligodendrocyte precursor cells (OPCs) to differentiate them into functional myelinating cells.

In this context, researchers at GIGA are studying the role of the Elongator complex in the adult CNS demyelination and demyelination processes.

Their preliminary obtained results suggest that Elongator could play a role in the differentiation of OPCs and act as a negative regulator of the demyelination.

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Model of Dicer depletion in the otocyst

Previous studies have demonstrated the importance of Dicer during early cochlear development.

To extend this investigation to the establishment and differentiation of the prosensory domain, researchers at GIGA crossed Dicerflox/flox mice with FoxG1Cre/+ mice to generate embryos (i.e., FoxG1:Dicer-cKO) with an early (E8.5) depletion of Dicer in the otocyst.

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Ototoxic drug-treated animal

Typically, the cochlear effects of ototoxic drugs are studied in the guinea pig, which is the most common animal model used in hearing research.

In this model, guinea pigs receive an intrapritoneal injection of either Knamycin during 7 days or Cisplatin during 10 days.

Cisplatin- and aminoglycoside-induced ototoxicity is known to be mediated via injury to several terminally differentiated cellular targets in the cochlea, including the marginal and intermediate cells of the stria vascular.

To quantitatively assess hearing loss in toxic drug-treated animals, the Auditory Brainstem Responses (ABR) are measured weekly.

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Guinea pigs deafened by aminoglycoside

Guinea pigs deafened by aminoglycoside are a model of neuronal degeneration secondary to hair cell destruction in the organ of Corti.

In this model, the left ear is operated on and the right ear is used as control (untreated ear, no operations). Each left bulla is opened under sterile conditions through a retro-auricular approach. The cochlea is exposed ventrally and opened using a 26 gauge needle. A catheter is inserted and connected to an electrical Hamilton syringe pump. The aminoglycoside gentamicin is administered at a concentration of 50 mg/ml for the cochlear lesion (25 ml of gentamicin in 5 min). Using the same cochlear opening, a catheter inserted and connected to a subcutaneous osmotic pump filled with products to be tested and dissolved in artificial perilymph solution.

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Cells regeneration

Researchers at GIGA have demonstrated that mammalian hair cells can be directly generated from supporting cells by inhibition of ephrin-B2 signaling.
Using either ephrin-B2 conditional knockout mice, shRNA-mediated gene silencing or soluble inhibitors, they found that downregulation of ephrin-B2 signalling at embryonic stages results in supporting cell translocation into hair cell layers and subsequent switch in cell phenotype from supporting cell to hair cell.

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Role of ELP3

Elp3 lysine acetyl-transferase, the catalytic subunit of the Elongator complex, has been assigned multiple roles in gene transcription, DNA methylation and protein translation efficiency.

Given the importance of acetylation homeostasis in controlling developmental processes together with recent reports implicating Elp3 in cortical neurogenesis, researchers at GIGA investigated its role during inner ear formation.

Using different knock-out mouse models, they have shown that Elp3 enzyme is crucial for neuronal survival in the spiral ganglion and in the vestibule and that it ensures a correct innervation pattern in the developing inner ear. In the absence of Elp3, a drastic increase in the number of apoptotic neurons particularly during the early stages of development (between E12.5 and E14.5). Postnatally, the neurons remaining in Elp3cKO cochleae seem to establish synaptic contacts with the sensory cells but show obvious signs of cell damage.

Furthermore, they identified a severe hearing loss in Elp3cKO mice through Auditory Brainstem Response.

Taken together, these data support a role for Elp3 in hearing and balance and point out an important role for acetylation homeostasis during inner ear formation.

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[18F]SV2A – early diagnosis

In a transgenic mouse model, overexpressing human α–syn under the mThy1 promotor (Parkinson mouse model), researchers have proved that the new SV2A-radioligand developed at CRC is a valid biomarker to study the loss of synaptic terminals appearing before the occurrence of behavioral disturbances.

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[18F]FMT – evaluation of dopaminergic dysfunction

Researchers at CRC have evaluated the feasibility of in vivo PET study using 6-[18F]fluoro-m-tyrosine (6-[18F]FMT) on lesioned rats with 6-hydroxydopamine (6-OHDA), a rat model of Parkinson’s disease (PD).

The (6-[18F]FMT) is an effective PET tracer to evaluate DA terminals integrity and L-aromatic amino acid decarboxylase (AAAD) metabolic pathway.

Using this PET tracer, they were able to quantify loss of DA presynaptic function in unilaterally 6-OHDA lesioned rats.

Researchers are currently investigating this tracer in a longitudinal way to monitor the progression of dopaminergic dysfunction in more moderate and gradual preclinical PD models.

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