104 research outputs found
Microelectrode arrays in combination with in vitro models of spinal cord injury as tools to investigate pathological changes in network activity: facts and promises
No full textMicroelectrode arrays (MEAs) represent an important tool to study the basic characteristics of spinal networks that control locomotion in physiological conditions. Fundamental properties of this neuronal rhythmicity like burst origin, propagation, coordination and resilience can, thus, be investigated at multiple sites within a certain spinal topography and neighbouring circuits. A novel challenge will be to apply this technology to unveil the mechanisms underlying pathological processes evoked by spinal cord injury. To achieve this goal, it is necessary to fully identify spinal networks that make up the locomotor central pattern generator (CPG) and to understand their operational rules. In this review, the use of isolated spinal cord preparations from rodents, or organotypic spinal slice cultures is discussed to study rhythmic activity. In particular, this review surveys our recently developed in vitro models of spinal cord injury by evoking excitotoxic (or even hypoxic/dysmetabolic) damage to spinal networks and assessing their impact on rhythmic activity and cell survival. These pathological processes which evolve via different cell death mechanisms are discussed as a paradigm to apply MEA recording for detailed mapping of the functional damage and its time-dependent evolution. © 2013 Mladinic and Nistri
Dynamic expression of ATF3 as a novel tool to study activation and migration of endogenous spinal stem cells and their role in neural repair
No full textKainate-mediated excitotoxicity induces neuronal death in the rat spinal cord in vitro via a PARP-1 dependent cell death pathway (parthanatos)
No full textThe differential intracellular expression of the novel marker ATF-3 characterizes the quiescent or activated state of endogenous spinal stem cells: a tool to study neurorepair?
No full textWorldwide, spinal cord injury (SCI) remains a major cause of disability with serious consequences in terms of personal and social costs [1]. Thus, important issues are how to protect the spinal cord to limit its initial damage, how to repair a lesion, and how to facilitate recovery by exploiting surviving tissue. These needs are currently unmet because our knowledge of the detailed structure of the neuronal networks responsible for human locomotion is scanty and our control over the mechanisms involved in neuronal death and regeneration is very limited. The molecular mechanisms underlying neuronal death after SCI are incompletely understood so that specific strategies for neuroprotection remain preliminary [2-4]. While many neuroprotective molecules have been reported to be experimentally effective for neuronal survival after SCI, very few have reached the clinical testing stage and none of them has provided efficacious treatment for SCI patients [5]. The reasons for such a clinical failure are complex and may include the diversity of protocols used to induce injury in animal models and the difficulty of detailed animal tissue analysis beyond a single time point so that a relatively narrow window of pathophysiology may be explored [6,7]. In clinical settings, the large majority of SCI cases are managed at late stages after the patient’s conditions have been stabilized following the primary lesion. Hence, damage repair rather than neuroprotection becomes a crucial goal
Early functional and morphological changes in locomotor networks induced by focal lesion in an in vitro spinal cord injury model
No full textEffects of 6(5H)phenanthridinone, an inhibitor of poly(ADP-ribose)polymerase-1 activity (PARP-1), on locomotor networks of the rat isolated spinal cord
No full text“Specific” oligonucleotides often recognise more than one gene: the limits of in situ hybridization applied to GABA receptors
No full textExtensive glial apoptosis develops early after hypoxic-dysmetabolic insult to the neonatal rat spinal cord in vitro
No full textEarly and delayed effects of kainate application on oscillatory networks of the rat spinal cord in vitro
No full textExcitotoxicity impairs synaptic transmission rather than neuronal survival or motoneuron function in the rat spinal cord in vitro: implications for acute spinal injury mechanisms
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