Publisher Correction: Cortical-like mini-columns of neuronal cells on zinc oxide nanowire surfaces.

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Cortical-like mini-columns of neuronal cells on zinc oxide nanowire surfaces.

A long-standing goal of neuroscience is a theory that explains the formation of the minicolumns in the cerebral cortex. Minicolumns are the elementary computational units of the mature neocortex. Here, we use zinc oxide nanowires with controlled topography as substrates for neural-cell growth. We observe that neuronal cells form networks where the networks characteristics exhibit a high sensitivity to the topography of the nanowires. For certain values of nanowires density and fractal dimension, neuronal networks express small world attributes, with enhanced information flows. We observe that neurons in these networks congregate in superclusters of approximately 200 neurons. We demonstrate that this number is not coincidental: the maximum number of cells in a supercluster is limited by the competition between the binding energy between cells, adhesion to the substrate, and the kinetic energy of the system. Since cortical minicolumns have similar size, similar anatomical and topological characteristics of neuronal superclusters on nanowires surfaces, we conjecture that the formation of cortical minicolumns is likewise guided by the interplay between energy minimization, information optimization and topology. For the first time, we provide a clear account of the mechanisms of formation of the minicolumns in the brain.

The effect of connectivity on information in neural networks.

We present a mathematical model that quantifies the amount of information exchanged in bi-dimensional networks of nerve cells as a function of network connectivity Q. Upon varying Q over a significant range, we found that, from a certain cell density onwards, 90% of the maximal information transferred I(Q) in a random neuronal network is already reached with just 40% of the total possible connections Q among the cells. As a consequence, the system would not benefit from additional connections in terms of the amount of I(Q), in agreement with the tendency of brains to minimize Q because of its energetic costs. The model may reveal the circuits responsible for neurodegenerative disorders in that neurodegeneration can be regarded as a connective failure affecting information.

Nano-topography Enhances Communication in Neural Cells Networks.

Neural cells are the smallest building blocks of the central and peripheral nervous systems. Information in neural networks and cell-substrate interactions have been heretofore studied separately. Understanding whether surface nano-topography can direct nerve cells assembly into computational efficient networks may provide new tools and criteria for tissue engineering and regenerative medicine. In this work, we used information theory approaches and functional multi calcium imaging (fMCI) techniques to examine how information flows in neural networks cultured on surfaces with controlled topography. We found that substrate roughness S a affects networks topology. In the low nano-meter range, S a = 0-30 nm, information increases with S a . Moreover, we found that energy density of a network of cells correlates to the topology of that network. This reinforces the view that information, energy and surface nano-topography are tightly inter-connected and should not be neglected when studying cell-cell interaction in neural tissue repair and regeneration.

Requirement of ERK activation for visual cortical plasticity.

Experience-dependent plasticity in the developing visual cortex depends on electrical activity and molecular signals involved in stabilization or removal of inputs. Extracellular signal-regulated kinase 1,2 (also called p42/44 mitogen-activated protein kinase) activation in the cortex is regulated by both factors. We show that two different inhibitors of the ERK pathway suppress the induction of two forms of long-term potentiation (LTP) in rat cortical slices and that their intracortical administration to monocularly deprived rats prevents the shift in ocular dominance towards the nondeprived eye. These results demonstrate that the ERK pathway is necessary for experience-dependent plasticity and for LTP of synaptic transmission in the developing visual cortex.

Release of dopamine from human neocortex nerve terminals evoked by different stimuli involving extra- and intraterminal calcium.

The release of [(3)H]-dopamine ([(3)H]-DA) from human neocortex nerve terminals was studied in synaptosomes prepared from brain specimens removed in neurosurgery and exposed during superfusion to different releasing stimuli. Treatment with 15 mM KCl, 100 microM 4-aminopyridine, 1 microM ionomycin or 30 mM caffeine elicited almost identical overflows of tritium. Removal of external Ca(2+) ions abolished the overflow evoked by K(+) or ionomycin and largely prevented that caused by 4-aminopyridine; the overflow evoked by caffeine was completely independent of external Ca(2+). Exposure of synaptosomes to 25 microM of the broad spectrum calcium channel blocker CdCl(2) strongly inhibited the 4-aminopyridine-induced tritium overflow while that evoked by ionomycin remained unaffected. The Ca(2+) chelator, 1,2-bis-(2-aminophenoxy)ethane-N,N,N',N' tetraacetic acid (BAPTA), reduced significantly the K(+)- and the caffeine-induced tritium overflow. The effect of caffeine was attenuated by exposure to the ryanodine receptor blocker dantrolene or when the membrane-impermeant inositol trisphosphate receptor antagonist, heparin, was entrapped into synaptosomes; the combined treatment with dantrolene and heparin abolished the release elicited by caffeine. Tetanus toxin, entrapped into human neocortex synaptosomes to avoid prolonged incubation, inhibited in a concentration-dependent manner the K(+)- or the 4-aminopyridine-evoked tritium overflow; in contrast, the release stimulated by ionomycin and by caffeine were both totally insensitive to the same concentrations of tetanus toxin. Western blot analysis showed about 50% reduction of the content of the vesicular protein, synaptobrevin, in synaptosomes poisoned with tetanus toxin. In conclusion, the release of dopamine from human neocortex nerve terminals can be triggered by Ca(2+) ions originating from various sources. It seems that stimuli not leading to activation of voltage-sensitive Ca(2+) channels elicit Ca(2+)-dependent, probably exocytotic, release that is insensitive to tetanus toxin.