title: Chronic electrical stimulation of transected peripheral nerves preserves anatomy and function in the primary somatosensory cortex.
abstract: The structure and function of the central nervous system strongly depend on the organization and efficacy of the incoming sensory input. A disruption of somesthetic input severely alters the metabolic activity, electrophysiological properties and even gross anatomical features of the primary somatosensory cortex. Here we examined, in the rat somatosensory cortex, the neuroprotective and therapeutic effects of artificial sensory stimulation after irreversible unilateral transection of a peripheral sensory nerve (the infraorbital branch of the trigeminal nerve). The proximal stump of the nerve was inserted into a silicon tube with stimulating electrodes, through which continuous electrical stimulation was applied for 12 h/day (square pulses of 100 μs, 3.0 V, at 20 Hz) for 4 weeks. Deafferented animals showed significant decreases in cortical evoked potentials, cytochrome oxidase staining intensity (layers II-IV), cortical volume (layer IV) and number of parvalbumin-expressing (layers II-IV) and calbindin-D28k-expressing (layers II/III) interneurons. These deafferentation-dependent effects were largely absent in the nerve-stimulated animals. Together, these results provide evidence that chronic electrical stimulation has a neuroprotective and preservative effect on the sensory cortex, and raise the possibility that, by controlling the physical parameters of an artificial sensory input to a sectioned peripheral nerve, chronically deafferented brain regions could be maintained at near-'normal' conditions. Our findings could be important for the design of sensory neuroprostheses and for therapeutic purposes in brain lesions or neural degenerative processes.
authors.affiliation: Neurocomputing and Neurorobotics Research Group, Universidad Complutense de Madrid, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos, Madrid, Spain.
authors.forename: Celia
authors.initials: C
authors.lastname: Herrera-Rincon
authors.forename: Carlos
authors.initials: C
authors.lastname: Torets
authors.forename: Abel
authors.initials: A
authors.lastname: Sanchez-Jimenez
authors.forename: Carlos
authors.initials: C
authors.lastname: Avendaño
authors.forename: Fivos
authors.initials: F
authors.lastname: Panetsos
mesh_terms: D000818:Animals; D064092:Calbindin 1; D064026:Calbindins; D003714:Denervation; D004558:Electric Stimulation; D003576:Electron Transport Complex IV / Q000032:analysis; D005071:Evoked Potentials; D005260:Female; D007395:Interneurons / Q000473:pathology / Q000502:physiology; D010320:Parvalbumins / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D064030:S100 Calcium Binding Protein G / Q000032:analysis; D013003:Somatosensory Cortex / Q000737:chemistry / Q000473:pathology / Q000503:physiopathology*; D014276:Trigeminal Nerve / Q000503:physiopathology* / Q000601:surgery
chemical_list: C576500:Calb1 protein, rat; D064092:Calbindin 1; D064026:Calbindins; D010320:Parvalbumins; D064030:S100 Calcium Binding Protein G; D003576:Electron Transport Complex IV