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Burst firing has been reported as a pathological activity of subthalamic nucleus (STN) neurons in

This paper describes a Deep Brain Stimulation device, portable, for chronic experiments on rodents in the context of Parkinson's disease. Our goal is to equip the animal with a device that mimics the human therapeutic conditions. It implies to respect a set of properties such as bilateral current-mode and charge-balanced stimulation, as well as programmability, low power consumption and re-usability to finally reach a suitable weight for long-term experiments. After the analysis of the solutions found in the literature, the full design of the device is explained. First, the stimulation front-end circuit driven by a processor unit, then the choice of supply sources which is a critical point for the weight and life-time of our system. Our low cost system has been realized using commercial discrete components and the overall power consumption was minimized. We achieved 6 days of maximal current stimulation with the chosen battery for a weight of 13.8 g . Finally, the device was carried out in vivo on rats during a 3 weeks experiment as the used implantation technique allows battery changing. This experiment also permits to emphasize the mechanical aspects including the packaging and electrodes holding.

There is increasing evidence to suggest that the neuronal response to hypoxia is regulated through their interactions with astrocytes. However, the hypoxia-induced molecular mechanisms within astrocytes which influence neuronal death have yet to be characterized. In this study, we investigated the roles of the nuclear receptor ROR␣ (retinoid-related orphan receptor-␣) respectively in neurons and astrocytes during hypoxia using cultures and cocultures of neurons and astrocytes obtained from ROR␣-deficient mice. We found that loss of ROR␣ function in neuronal cultures increases neuronal death after hypoxia, suggesting a cell-autonomous neuroprotective effect of ROR␣. Moreover, wild-type neurons cocultured with ROR␣-deficient astrocytes are characterized by a higher death rate after hypoxia than neurons cocultured with wild-type astrocytes, suggesting that ROR␣ also has a non-cell-autonomous action. By using cocultures of neurons and astrocytes of different genotypes, we showed that this neuroprotective effect of ROR␣ in astrocytes is additive to its effect in neurons, and is mediated in part by cell-to-cell interactions between neurons and astrocytes. We also found that ROR␣ is upregulated by hypoxia in both neurons and astrocytes. Furthermore, our data showed that ROR␣ does not alter oxidative mechanisms during hypoxia but regulates hypoxic inducible factor 1␣ (HIF-1␣) expression, a major regulator of hypoxia sensing, in a cell-specific manner. Indeed, the neuroprotective function of ROR␣ in astrocytes correlates with a downregulation of HIF-1␣ selectively in these cells. Altogether, our results show that ROR␣ is a key molecular player in hypoxia, protecting neurons through its dual action in neurons and astrocytes.

These results provide evidence for alteration of nociceptive integration in the spinal dorsal horn neurons in 6-OHDA rats that can reflect changes in pain behavior. © 2018 International Parkinson and Movement Disorder Society.

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The design of neuro-stimulators must include a realistic model of electrode-tissue interface. Complex electrochemical phenomena associated to high levels of stimulation current give fractional and non linear behavior to this interface that simple linearized models fail to fit. This paper describes both a measurement protocol based on biphasic current-controlled solicitations and a modeling procedure relying on an original approach of multi-model, taking into account the non-linear and fractional effects. This model fits correctly the measurement results with current levels varying from 50µA to 1mA. Furthermore the whole characterization protocol can be safely transposed to in vivo measurements.