stimulation. Although rotundal cell size is thus ontogenetically modi®ed in an activitydependent manner, a detailed comparison makes it likely that the mechanisms which govern developmental plasticity of visual pathways differ between birds and

The occupancy of the orthosteric ligand binding sites of P2X receptor (P2XR) channels causes the rapid opening of a small cation-permeable pore, followed by a gradual dilation that renders the pore permeable to large organic cations. Electrophysiologically, this phenomenon was shown using whole-cell current recording on P2X2R-, P2X2/X5R-, P2X4R- and P2X7R-expressing cells that were bathed in N-methyl-D-glucamine (NMDG+)-containing buffers in the presence and/or absence of small monovalent and divalent cations. The pore dilation of P2X4R and P2X7R caused a secondary current growth, whereas that of P2X2R showed a sustained kinetic coupling of dilation and desensitization, leading to receptor channel closure. The pore size of the P2X7R open and dilated states was estimated to be approximately 0.85 nm and greater than 1 nm, respectively. The P2XR pore dilation was also observed in intact cells by measurement of fluorescent dye uptake/release, application of polyethylene glycols of different sizes, and atomic force microscopy. However, pore dilation was not observed at the single channel level. Structural data describing the dilated state are not available, and the relevance of orthosteric and allosteric ligand interactions to pore dilation was not studied.

Prenatal inhibition of the kynurenine pathway leads to structural changes in the hippocampus of adult rat offspring

A developmental study of the structural integrity of white matter in autism

On behalf of:

doi:10.1111/j.1460-9568.2009.06701.x

Genetic mapping of Foxb1-cell lineage shows migration from caudal diencephalon to telencephalon and lateral hypothalamus

Retinoic acid receptor-a signalling antagonizes both intracellular and extracellular amyloid-b production and prevents neuronal cell death caused by amyloid-b

on nonhuman primates

SREB2/GPR85, a schizophrenia risk factor, negatively regulates hippocampal adult neurogenesis and neurogenesis-dependent learning and memory