Design of an experimental setup for delivering intracortical microstimulation in vivo via Spiking Neural Network.

Electroceutical approaches for the treatment of neurological disorders, such as stroke, can take advantage of neuromorphic engineering, to develop devices able to achieve a seamless interaction with the neural system. This paper illustrates the development and test of a hardware-based Spiking Neural Network (SNN) to deliver neural-like stimulation patterns in an open-loop fashion. Neurons in the SNN have been designed by following the Hodgkin-Huxley formalism, with parameters taken from neuroscientific literature. We then built the set-up to deliver the SNN-driven stimulation in vivo. We used deeply anesthetized healthy rats to test the potential effect of the SNN-driven stimulation. We analyzed the neuronal firing activity pre- and post-stimulation in both the primary somatosensory and the rostral forelimb area. Our results showed that the SNN-based neurostimulation was able increase the spontaneous level of neuronal firing at both monitored locations, as found in the literature only for closed-loop stimulation. This study represents the first step towards translating the use of neuromorphic-based devices into clinical applications.Clinical Relevance- Stroke represents one of the leading causes of long-term disability and death worldwide. Intracortical microstimulation is an effective approach for restoring lost sensory motor integration by promoting plasticity among the affected brain areas. Stimulation delivered via neuromorphic-based open-loop systems (i.e. neuromorphic prostheses) can pave the way to novel electroceutical strategies for brain repair.

Seizure suppression by asynchronous non-periodic electrical stimulation of the amygdala is partially mediated by indirect desynchronization from nucleus accumbens.

Electrical stimulation (ES) of the nervous system is a promising alternative for the treatment of refractory epilepsy. Based on the understanding that seizures are the expression of neural hypersynchronism, our group developed and tested a non-standard form of low-energy temporally unstructured ES termed NPS (Non-periodic stimulation), with pseudo-randomized inter-pulse intervals. Previous investigation demonstrated that NPS applied to the amygdala has a robust anticonvulsant effect against both acute and chronic seizures, and suggested that its therapeutic effect is based on direct desynchronization of ictogenic neural circuits. Further mechanistic investigation using functional magnetic resonance imaging has shown that NPS also activates nucleus accumbens (NAc) in seizure-free rats, raising the hypothesis of an alternative therapeutic mechanism: NPS-enhanced indirect inhibition / desynchronization of ictogenic circuits by NAc. In order to investigate this idea, here we evaluated behavior and cortical electrographic activity from animals submitted to pentylenetetrazole (PTZ) induced seizures, treated with NPS and with or without bilateral electrolytic lesion of NAc. NPS-treated animals with bilateral lesion of NAc expressed unexpected straub tail in addition to other stereotypical convulsive behavior, displayed increased susceptibility to PTZ (lower drug threshold), and had a much longer electrographic seizure, with a greater number of spikes, firing at a higher rate. Moreover, analysis of spike morphology showed an increase in amplitude and slope in these animals, suggesting that ablation of NAc results in disinhibition and/or increase of neural synchronism within ictogenic circuits. NPS had no therapeutic effect whatsoever in lesioned animals, while it displayed a mild anticonvulsant effect in those with intact brains. Results corroborate the notion that NAc has a key role in controlling aberrant epileptiform activity in ictogenic circuits through indirect polysynaptic connections that may enroll the ventral pallidum and ventral tegmental area. They also point to the possibility that NPS may enhance this effect, putatively by benefiting from the structure's property of detecting saliences.