Transplantation of olfactory ensheathing cells (OECs) into photochemically damaged rat spinal cord diminished astrocyte reactivity and parenchyma cavitation. The photochemical lesion performed at T12--L1 resulted in severe damage to the spinal cord, so that during the first 15 days postoperation all rats dragged their hindlimbs and did not respond to pinprick. The maximal area and volume of the cystic cavities were lower in transplanted than in non-transplanted rats, not significantly at the T12--L1 lesion site, but significantly at T9--T10 and L4--L6 cord levels. The density of astrocytes in the grey matter was similar at T12--L1 and L4--L6 in non-transplanted and trans- planted rats, but lower in the latter at T9--T10 level. However, in non-transplanted rats all astrocytes showed a hypertrophied appearance, with long and robust processes heavily GFAP-positive, and overexpression of proteoglycan inhibitor of neuritogenesis, whereas in transplanted rats only a few astrocytes showed hypertrophy and the majority had short, thin processes. These results indicate that OECs transplanted into damaged adult rat spinal cord exert a neuroprotective role by reducing astrocytic gliosis and cystic cavitation.

Damaged axons do not regenerate after axotomy in the adult mammalian central nervous system (CNS). This may be due to local inhibitory factors at the site of injury, such as overexpression of chondroitin sulfate (CS) proteoglycans (CSPG), and the presence of myelin-associated inhibitors (MAI). To overcome CSPG- or myelin-induced inhibition, strategies based on extrinsic and intrinsic treatments have been developed. For example, NEP1-40 is a synthetic peptide that promotes axonal regeneration by blocking Nogo-66/NgR interaction and chondroitinase ABC (ChABC), which degrades CS, thereby also promoting axon regrowth. Here, we examined whether the combination of these complementary strategies facilitates regeneration of the lesioned entorhino-hippocampal pathway (EHP) in slice cultures. In this model, overexpressed CSPG and MAI impaired axon regrowth, which mimics regeneration failure in vivo. Both CS cleavage with ChABC and NEP1-40 strongly facilitated the regrowth of entorhinal axons after axotomy, permitting the re-establishment of synaptic contacts with target cells. However, the combined treatment did not improve the regeneration induced by ChABC alone, and the delayed treatment of ChABC, but not NEP1-40, had a less pronounced effect on axonal regrowth compared with acute treatment. These results provide insight into the development of new assays and strategies to enhance axon regeneration in injured cortical connections.

No abstract

ResumenAlgunos aspectos de la fisiopatología del sistema nervioso periférico pueden ser ampliamente estudiados en un modelo celular in vitro, enriquecido en células de Schwann. La célula de Schwann como glía del sistema nervioso periférico produce la mielina responsable de la transmisión saltatoria del impulso, influye en la actividad neuronal y da soporte y protección axonal. A su vez es blanco de procesos que alteran la normalidad del sistema nervioso periférico como neuropatías congénitas y10 desmielinizantes, lesiones nerviosas, respuesta a patógenos neurotrópicos, etc., eventos más frecuentes y discapacitantes en individuos adultos. De ahí la importancia de obtener células a partir de animales adultos. Sin embargo, estas células son mitóticamente "lentas" y su obtención en cultivo requiere de condiciones específicas que estimulen su proliferación y actividad. Describimos a continuación, un modelo in vitro mediante el cual se obtienen cultivos enriquecidos en células de Schwann de ratón adulto, las cuales conservan características de las células in vivo, lo cual permite estudiar diversos fenómenos específicos del sistema nervioso periférico.Schwann cell cultures: a model of the nervous system microenvironment Some of the peripheral nervous system (PNS) physiopathological aspects can be studied in an in vitro cellular model of Schwann Cells (SC). SC as PNS glia produces myelin. Myelination increases the rate of impulse conduction. SCs influence neuronal activity and axonal support and protection. Also, they are the target of the process which alters the PNS, such as congenital andlor demyelinating neuropathies, nervous lesions, response to neurotrophic pathogens, etc., being the events most frequently found in adults. It is then important to obtain cells from adult animals. However, these cells are mytotically "slow" and growing them in culture needs specific conditions which stimulate proliferation and activity. An in vitro model to obtain highly enriched adult mouse SC cultures which have some of the in vivo SC cell cultures' features, is described. This method can be used to study several aspects of the nervous system biology.