Predicting the connectivity of primate cortical networks from topological and spatial node properties

Abstract Background The organization of the connectivity between mammalian cortical areas has become a major subject of study, because of its important role in scaffolding the macroscopic aspects of animal behavior and intelligence. In this study we present a computational reconstruction approach to the problem of network organization, by considering the topological and spatial features of each area in the primate cerebral cortex as subsidy for the reconstruction of the global cortical network connectivity. Starting with all areas being disconnected, pairs of areas with similar sets of features are linked together, in an attempt to recover the original network structure. Results Inferring primate cortical connectivity from the properties of the nodes, remarkably good reconstructions of the global network organization could be obtained, with the topological features allowing slightly superior accuracy to the spatial ones. Analogous reconstruction attempts for the C. elegans neuronal network resulted in substantially poorer recovery, indicating that cortical area interconnections are relatively stronger related to the considered topological and spatial properties than neuronal projections in the nematode. Conclusion The close relationship between area-based features and global connectivity may hint on developmental rules and constraints for cortical networks. Particularly, differences between the predictions from topological and spatial properties, together with the poorer recovery resulting from spatial properties, indicate that the organization of cortical networks is not entirely determined by spatial constraints.

Comparison between the C5 or C6-Cz electrode assembly and C3 or C4-Cz assembly for transcranial electric motor activation of muscular response of the contralateral facial nerve

We used an assembly of electrodes C3 and C4-Cz in order to activate the motor cortical area of the corticobulbar tract to elucidate the motor-evoked potential of the contralateral mentalis muscle. We compared this setup to that of an assembly with electrodes C5 or C6-Cz using a train of electrical pulses and a single electrical pulse. This analysis was made in 23 consecutive patients who underwent several varied surgeries and were prospectively operated on at Santa Paula Hospital between January and June 2011. The results showed that the assembly with C5 or C6-Cz produced a multisynaptic motor-evoked potential in the contralateral mentalis muscle in 86.9 % of the patients, whereas 82.6 % of patients stimulated at points C3 or C4-Cz presented the same response. However, both assemblies showed similar behavior with the use of a single electrical pulse for peripheral contralateral nerve stimulation. We concluded that the C5 or C6-Cz assembly was similar to C3 or C4-Cz in obtaining a multisynaptic response in the contralateral mentalis muscle, although it required less intensive stimulation than the C3 or C4- Cz assembly.

Trabecular bone loss after administration of the second-generation antipsychotic risperidone is independent of weight gain

Second generation antipsychotics (SGAs) have been linked to metabolic and bone disorders in clinical studies, but the mechanisms of these side effects remain unclear. Additionally, no studies have examined whether SGAs cause bone loss in mice. Using in vivo and in vitro modeling we examined the effects of risperidone, the most commonly prescribed SGA, on bone in C57BL6/J (B6) mice. Mice were treated with risperidone orally by food supplementation at a dose of 1.25 mg/kg daily for 5 and 8 weeks, starting at 3.5 weeks of age. Risperidone reduced trabecular BV/TV, trabecular number and percent cortical area. Trabecular histomorphometry demonstrated increased resorption parameters, with no change in osteoblast number or function. Risperidone also altered adipose tissue distribution such that white adipose tissue mass was reduced and liver had significantly higher lipid infiltration. Next, in order to tightly control risperidone exposure, we administered risperidone by chronic subcutaneous infusion with osmotic minipumps (0.5 mg/kg daily for 4 weeks) in 7 week old female B6 mice. Similar trabecular and cortical bone differences were observed compared to the orally treated groups (reduced trabecular BV/TV, and connectivity density, and reduced percent cortical area) with no change in body mass, percent body fat, glucose tolerance or insulin sensitivity. Unlike in orally treated mice, risperidone infusion reduced bone formation parameters (serum P1NP, MAR and BFR/BV). Resorption parameters were elevated, but this increase did not reach statistical significance. To determine if risperidone could directly affect bone cells, primary bone marrow cells were cultured with osteoclast or osteoblast differentiation media. Risperidone was added to culture medium in clinically relevant doses of 0, 2.5 or 25 ng/ml. The number of osteoclasts was significantly increased by addition in vitro of risperidone while osteoblast differentiation was not altered. These studies indicate that risperidone treatment can have negative skeletal consequences by direct activation of osteoclast activity and by indirect non-cell autonomous mechanisms. Our findings further support the tenet that the negative side effects of SGAs on bone mass should be considered when weighing potential risks and benefits, especially in children and adolescents who have not yet reached peak bone mass. This article is part of a Special Issue entitled: Interactions Between Bone, Adipose Tissue and Metabolism. (C) 2011 Elsevier Inc. All rights reserved.

Mercury toxicity in Amazon gold miners: Visual dysfunction assessed by retinal and cortical electrophysiology

Amazonian gold mining activity results in human exposure to mercury vapor. We evaluated the visual system of two Amazonian gold miners (29 and 37 years old) by recording the transient pattern electroretinogram (tPERG) and transient pattern visual evoked potential (tPVEP). We compared these results with those obtained from a regional group of control subjects. For both tPERG and tPVEP, checkerboards with 0.5 or 2 cycles per degree (cpd) of spatial frequency were presented in a 16 degrees squared area, 100% Michelson contrast, 50cd/m(2) mean luminance, and 1 Hz square-wave pattern-reversal presentation. Two averaged waveforms (n = 240 sweeps, Is each) were monocularly obtained for each subject in each condition. Both eyes were monocularly tested only in gold miners. Normative data were calculated using a final pooled waveforin with 480 sweeps. The first gold miner, LCS, had normal tPERG responses. The second one, RNP, showed low tPERG (P50 component) amplitudes at 0.5cpd for both eyes, outside the normative data, and absence of response at 2 cpd for his right eye. Delayed tPVEP responses (P 100 component) were found at 2 cpd for LCS but the implicit times were inside the normative data. Subject RNP also showed delayed tPVEP responses (all components), but only the implicit time obtained with his right eye was outside the normative data at 2cpd. We conclude that mercury exposure levels found in the Amazon gold miners is high enough to damage the visual system and can be assessed by non-invasive electrophysiological techniques. (C) 2007 Elsevier Inc. All rights reserved.