Oxidation of germa- and stanna-closo-dodecaborate.

The oxidation of closo-heteroborates [GeB11H11](2-) and [SnB11H11](2-) is presented. Upon oxidation germa-closo-dodecaborate yields a symmetrical dimer exhibiting a Ge-Ge bond between two clusters. This dimer shows sulphur insertion into the Ge-Ge bond at room temperature. In contrast, oxidation of the homologous tin cluster results in an unsymmetrical dimer bearing an Sn-B bond between two clusters. The Sn-B dimer is also the product of the hydride abstraction reaction. In the presence of the donor ligand 2,2'-bipyridine, the oxidation of closo-cluster [SnB11H11](2-) leads to the Sn(IV)-half sandwich coordination compound [bipy-SnB11H11] which dissolves in DMSO to give the Sn(IV)-adduct [bipy(DMSO)-SnB11H11].

Motor skill learning depends on protein synthesis in the dorsal striatum after training.

Functional imaging studies in humans and electrophysiological data in animals suggest that corticostriatal circuits undergo plastic modifications during motor skill learning. In motor cortex and hippocampus circuit plasticity can be prevented by protein synthesis inhibition (PSI) which can interfere with certain forms learning. Here, the hypothesis was tested that inducing PSI in the dorsal striatum by bilateral intrastriatal injection of anisomycin (ANI) in rats interferes with learning a precision forelimb reaching task. Injecting ANI shortly after training on days 1 and 2 during 4 days of daily practice (n = 14) led to a significant impairment of motor skill learning as compared with vehicle-injected controls (n = 15, P = 0.033). ANI did not affect the animals' motivation as measured by intertrial latencies. Also, ANI did not affect reaching performance once learning was completed and performance reached a plateau. These findings demonstrate that PSI in the dorsal striatum after training impairs the acquisition of a novel motor skill. The results support the notion that plasticity in basal ganglia circuits, mediated by protein synthesis, contributes to motor skill learning.

Redox dysregulation, neurodevelopment, and schizophrenia.

In schizophrenia, a developmental redox dysregulation constitutes one 'hub' on which converge genetic impairments of glutathione synthesis and environmental vulnerability factors generating oxidative stress. Their timing at critical periods of neurodevelopment could play a decisive role in inducing impairment of neural connectivity and synchronization as observed in schizophrenia. In experimental models, such redox dysregulation induces anomalies strikingly similar to those observed in patients. This is mediated by hypoactive NMDA receptors, impairment of fast-spiking parvalbumin GABA interneurons and deficit in myelination. A treatment restoring the redox balance without side effects yields improvements of negative symptoms in chronic patients. Novel interventions based on these mechanisms if applied in early phases of the disease hold great therapeutic promise.