Microelectrode arrays in combination with in vitro models of spinal cord injury as tools to investigate pathological changes in network activity: facts and promises

Abstract

Microelectrode 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 neighboring circuits. A novel challenge will be to apply this technology to unveil the mechanisms underlying pathological processes evoked by spinal cord injury (SCI). 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 SCI by evoking excitotoxic (or even hypoxic/dysmetabolic) damage to spinal networks and assessing the 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.

Application of the sodium hyaluronate-CNTF scaffolds in repairing adult rat spinal cord injury and facilitating neural network formation

“…The device had an array of 64 planar microelectrodes, each 50 µm×50 µm, arranged in an 8×8 pattern (interelectrode distance, 150 µm). Preparation of acute spinal cord slices including the lesioned area 8 weeks after operation as well as the electrophysiological recordings protocol were almost the same as described previously (Yang et al, 2015;Oka et al, 1999;Mladinic et al, 2013) with slight modifications; i.e., the spinal cord tissue including the lesion area was sliced longitudinally.…”

The Differential Intracellular Expression of the Novel Marker ATF-3 Characterizes the Quiescent or Activated State of Endogenous Spinal Stem Cells: A Tool to Study up Neurorepair?

“…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.…”