This study focuses on nickel oxide nanoparticles as efficient nanocatalysts in the synthesis of oxindoles as an important class of potentially bioactive compounds.

Memory deficits are a debilitating symptom of epilepsy, but little is known about mechanisms underlying cognitive deficits. Here, we describe a Na+ channel-dependent mechanism underlying altered hippocampal dendritic integration, degraded place coding, and deficits in spatial memory. Two-photon glutamate uncaging experiments revealed a marked increase in the fraction of hippocampal 1st order CA1 pyramidal cell dendrites capable of generating dendritic spikes in the kainate model of chronic epilepsy. Moreover, in epileptic mice dendritic spikes were generated with lower input synchrony inputs, and with a lower threshold. The Nav1.3/1.1 selective Na+ channel blocker ICA-121431 reversed dendritic hyperexcitability in epileptic mice, while the Nav1.2/1.6 preferring anticonvulsant S-Lic did not. We used in-vivo two-photon imaging to determine if aberrant dendritic excitability is associated with altered place-related firing of CA1 neurons. We show that ICA-121431 improves degraded hippocampal spatial representations in epileptic mice. Finally, behavioural experiments show that reversing aberrant dendritic excitability with ICA-121431 reverses hippocampal memory deficits. Thus, a dendritic channelopathy may underlie cognitive deficits in epilepsy and targeting it pharmacologically may constitute a new avenue to enhance cognition.

No abstract

Spirooxindoles. -The reaction between malonitrile, isatins, and 1,3-dicarbonyl compounds including 1,3-cyclohexadione, dimedone, and 4-hydroxycoumarine provides indoline derivatives in high yields. The catalyst is reused in five consecutive cycles with only slight loss of its activity. -(NASSERI*, M. A.; KAMALI, F.; ZAKERINASAB, B.; RSC Adv. 5 (2015) 34, 26517-26520, http://dx.