Three-tier regulation of cell number plasticity by neurotrophins and Tolls in .

Cell number plasticity is coupled to circuitry in the nervous system, adjusting cell mass to functional requirements. In mammals, this is achieved by neurotrophin (NT) ligands, which promote cell survival via their Trk and p75 receptors and cell death via p75 and Sortilin. NTs (DNTs) bind Toll receptors instead to promote neuronal survival, but whether they can also regulate cell death is unknown.

A missense mutation in PIK3R5 gene in a family with ataxia and oculomotor apraxia.

Autosomal recessive ataxias are heterogeneous group of disorders characterized by cerebellar atrophy and peripheral sensorimotor neuropathy. Molecular characterization of this group of disorders identified a number of genes contributing to these overlapping phenotypes. Ataxia with oculomotor apraxia type 2 (AOA2) is an autosomal recessive form of ataxia caused by mutations in the SETX gene.

Trophic neuron-glia interactions and cell number adjustments in the fruit fly.

Trophic interactions between neurons and enwrapping glia, and between neurons and target cells, provide plasticity to the mammalian nervous system. Here, we review evidence that analogous cell interactions operate in the development of the nervous system of the fruit-fly Drosophila. Homologues of the canonical mammalian trophic factors also maintain neuronal and glial survival in Drosophila, adjusting cell populations to enable appropriate function, and revealing commonalities in nervous system development across the animals.

Effect of agomelatine and its interaction with the daily corticosterone rhythm on progenitor cell proliferation in the dentate gyrus of the adult rat.

Agomelatine, a novel melatonin analogue and anti-depressant that acts as an agonist on melatonin receptors 1 and 2 and as an antagonist at the 5HT2C receptor, was tested for its effects on cell proliferation in the dentate gyrus of the adult rat hippocampus under intact and flattened corticosterone rhythm conditions. Agomelatine stimulated mitosis rates in the intact male rat. Flattening the daily corticosterone rhythm by inserting a subcutaneous pellet of this steroid prevented the action of agomelatine.

A pressure overload model to track the molecular biology of heart failure.

Objectives: Pressure overload plays an important role in left ventricular remodelling and the development of heart failure. The underlying molecular mechanisms behind these processes are poorly understood at the myocyte level. To investigate this, we developed an ovine model of pressure overload-induced heart failure, in which serial left ventricular biopsies were obtained.

Sustained orexigenic effect of Agouti related protein may be not mediated by the melanocortin 4 receptor.

Intracerebroventricular (ICV) injection of Agouti related protein (AgRP), an endogenous melanocortin 3 and 4 receptor (MC3/4-R) antagonist, produces a prolonged increase in food intake. To clarify the roles of the MC3-R and MC4-R in AgRP-induced hyperphagia, the feeding effect of AgRP (83-132) was compared with that of the selective MC4-R antagonist, JKC-363 (cyclic [Mpr11, D-Nal14, Cys18, Asp22-NH2]-beta-MSH11-22). Single ICV administration of AgRP (83-132) increased food intake for 48 h whilst ICV JKC-363 increased food intake for 8h.