Localization of odors can be learned

Chemicals selectively stimulating the olfactory nerve typically cannot be localized in a lateralization task. Purpose of this study was to investigate whether the ability of subjects to localize an olfactory stimulus delivered passively to 1 of the 2 nostrils would improve under training. Fifty-two young, normosmic women divided in 2 groups participated. One group performed olfactory lateralization training, whereas the other group performed cognitive tasks. Results showed that only subjects performing lateralization training significantly improved in their ability to lateralize olfactory stimuli compared with subjects who did not undergo such training.

The effect of alternative neuronal differentiation pathways on PC12 cell adhesion and neurite alignment to nanogratings

During development and regeneration of the mammalian nervous system, directional signals guide differentiating neurons toward their targets. Soluble neurotrophic molecules encode for preferential direction over long distances while the local topography is read by cells in a process requiring the establishment of focal adhesions. The mutual interaction between overlapping molecular and topographical signals introduces an additional level of control to this picture. The role of the substrate topography was demonstrated exploiting nanotechnologies to generate biomimetic scaffolds that control both the polarity of differentiating neurons and the alignment of their neurites. Here PC12 cells contacting nanogratings made of copolymer 2-norbornene ethylene (COC), were alternatively stimulated with Nerve Growth Factor, Forskolin, and 8-(4-chloro-phenylthio)-2'-O-methyladenosine-3',5'-cyclic (8CPT-2Me-cAMP) or with a combination of them. Topographical guidance was differently modulated by the alternative stimulation protocols tested. Forskolin stimulation reduced the efficiency of neurite alignment to the nanogratings. This effect was linked to the inhibition of focal adhesion maturation. Modulation of neurite alignment and focal adhesion maturation upon Forskolin stimulation depended on the activation of the MEK/ERK signaling but were PkA independent. Altogether, our results demonstrate that topographical guidance in PC12 cells is modulated by the activation of alternative neuronal differentiation pathways.

Olfactory bulb interneurons releasing NO exhibit the Reelin receptor ApoEr2 and part of those targeted by NO express Reelin

Nitric oxide (NO) and Reelin both modulate neuronal plasticity in developing and mature synaptic networks. We recently showed a loss of neuronal nitric oxide synthase (nNOS) protein in the olfactory bulb of reeler mutants and advanced the hypothesis that the Reelin and NO signalling pathways may influence each other. We now studied the distribution of NO sensitive guanylyl cyclase (NOsGC), Reelin and its receptor Apolipoprotein E2 (ApoEr2) in the olfactory bulb by multiple fluorescence labelling and tested whether nNOS and ApoEr2 colocalize in this area. We also essayed the protein content of NOsGC in the reeler olfactory bulb and tested whether there are any changes in nNOS and NOsGC protein in other reeler brain areas. Olfactory bulb interneurons expressing ApoEr2 and nNOS are only few in the glomerular layer but represent the large majority of granule cell layer interneurons. Conversely, NOsGC interneurons are rare in the granule cell layer and abundant as periglomerular cells. Reelin containing periglomerular cells almost entirely belong to the NOsGC subset. These data further support the hypothesis of a reciprocal signalling between Reelin/NOsGC and ApoEr2/nNOS expressing neurons to affect olfactory bulb activity. We also show that a significant rise in NOsGC content accompanies the decrease of nNOS protein in the reeler olfactory bulb. The same reciprocal changes present in the cortex/striatum and the hippocampus of reeler mice. Thus, the influence that the deficit of extracellular Reelin seems to exert on nNOS and its receptor is not limited to the olfactory bulb but is a general feature of the reeler brain.

Enhancing rehabilitation of motor deficits with peripheral nerve stimulation

A number of different neurorehabilitation strategies include manipulation of the somatosensory system, e.g. in the form of training by passive movement. Recently, peripheral electrical nerve stimulation has been proposed as a simple, painless method of enhancing rehabilitation of motor deficits. Several physiological studies both in animals and in humans indicate that a prolonged period of patterned peripheral electrical stimulation induces short-term plasticity at multiple levels of the motor system. Small-scale studies in humans indicate that these plastic changes are linked with improvement in motor function, particularly in patients with chronic motor deficits after stroke. Somatosensory-mediated disinhibition of motor pathways is a possible underlying mechanism and might explain why peripheral electrical stimulation is more effective when combined with active training. Further large-scale studies are needed to identify the optimal stimulation protocol and the patient groups that stand to benefit the most from this technique.