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“A satisfactory management to ensure a full restoration of peripheral nerve after trauma is not yet available. Using an experimental protocol, in which crush injury was applied 1 cm above the bifurcation of the rat sciatic nerve for 20 s, we here demonstrate that the levels of neuroactive steroids, such as pregnenolone and progesterone I-BET-762 purchase (P) metabolites (i.e. dihydroprogesterone, DHP, and tetra hydro progesterone, THP) present in injured sciatic nerve were significantly decreased. On this basis, we have focused our attention on DHP and its direct precursor, P, analyzing whether these two neuroactive steroids may

have neuroprotective effects on biochemical, functional and morphological alterations occurring during crush-induced degeneration-regeneration. We demonstrate that DHP and/or P counteract biochemical alterations (i.e. myelin proteins and Na(+),K(+)-ATPase check details pump) and stimulate reelin gene expression. These two neuroactive steroids also counteract nociception impairment, and DHP treatment significantly decreases the up-regulation of myelinated fibers’ density occurring in crushed animals. Altogether, these observations suggest that DHP and P (i.e.

two neuroactive steroids interacting with progesterone receptor) may be considered protective agents in case of nerve crush injury. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Brain-derived neurotrophic factor (BDNF) has been implicated in mechanisms of synaptic plasticity such as long-term potentiation (LTP), but its role in associative learning remains largely unknown. In the present study, we investigated the function Galactokinase of BDNF and its receptor tropornyosin-related kinase B (TrkB) in an in vitro model of classical conditioning using pond turtles, Pseudemys scripta elegans. Conditioning resulted in a significant increase in BDNF and phospho (p)-Trk expression. Bath application of antibodies directed against TrkB, but not TrkA or TrkC, abolished

acquisition of conditioning, as did a receptor tyrosine kinase inhibitor K252a and an inhibitor of nitric oxide synthase 7-nitroindazole. Significantly, injections of BDNF Ab into the nerve roots of presynaptic axonal projections or postsynaptic motor neurons prevented acquisition of conditioning, suggesting that BDNF is required on both sides of the synapse for modification to occur. The presynaptic proteins synaptophysin and synapsin I were increased upon conditioning or BDNF application. Furthermore, BDNF application alone mimicked conditioning-induced synaptic insertion of GluR1 and GluR4 AMPAR subunits into synapses, which was inhibited by co-application of BDNF and K252a. Data also show that extracellular signal-regulated kinase (ERK) was activated in BDNF-treated preparations. We conclude that coordinate pre- and postsynaptic actions of BDNF are required for acquisition of in vitro classical conditioning. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.