Pituicyte stellation is prevented by RhoA-or Cdc42-dependent actin polymerization.

Our aim was to shed light on different steps leading from metabotropic receptor activation to changes in cell shape, such as those that characterize the morphological plasticity of neurohypophysial astrocytes (pituicytes). Using explant cultures of adult rat pituicytes, we have previously established that adenosine A1 receptor activation induces stellation via inhibition of RhoA monomeric GTPase and subsequent disruption of actin stress fibers. Here, we rule out RhoA phosphorylation as a mechanism for that inhibition.

A(2b) receptor mediates adenosine inhibition of taurine efflux from pituicytes.

Background Information: Recent work suggests that part of the control of vasopressin output is mediated by taurine released from pituicytes, the astroglial cells of the neurohypophysis. Taurine release, in turn, is stimulated by hypotonic conditions and by vasopressin itself. As adenosine is generated from ATP co-released with vasopressin, it appeared important to study its effects on taurine efflux from pituicytes.

Suppression of potassium channels elicits calcium-dependent plateau potentials in suprachiasmatic neurons of the rat.

By using whole-cell recordings in acute and organotypic hypothalamic slices, we found that following K+ channel blockade, sustained plateau potentials can be elicited by current injection in suprachiasmatic neurons. In an attempt to determine the ionic basis of these potentials, ion-substitution experiments were carried out. It appeared that to generate plateau potentials, calcium influx was required.

Myodulin is a novel potential angiogenic factor in skeletal muscle.

We examined the expression and function of a gene we previously cloned from its downregulation in a muscle atrophy model. The encoded protein was named myodulin because of sequence homologies with the cartilage-specific chondromodulin-I (ChM-I) protein, its restricted expression in skeletal muscle tissue, and its modulating properties on vascular endothelial cells described here. We investigated the expression of myodulin in muscle fibers and cultured muscle cells.