During this period of flux studies there was

During this period of flux studies, there was also considerable interest in the regulation of the chloride conductances in apical membrane vesicles from human placenta. It has been suggested that apical membrane chloride conductances are inhibited by protein kinase A-dependent phosphorylation [14] and by unsaturated fatty acids such as arachidonic and linoleic Cy5.5 carboxylic acid (non-sulfonated) [19], [18], [21]. However, in order to identify which types of channels are specifically regulated in placental membranes and to determine their biophysical properties, it was necessary to develop new experiments involving electrophysiological and molecular biology methods that could contribute to identifying the channels that underlie these conductances. All of the studies referred to above were on microvillous membrane from hSTB; however, there is little information regarding conductances in the basal membrane. Illsley and Sellers, using a fluorescent technique, determined the relative permeabilities of cations and chloride in basal membrane vesicles. Their results showed that the permeability of Na+ is greater that the permeability of K+ and that chloride conductance is practically absent, since the permeability of Cl− relative to K+ is close to zero [15]. Later, in 1998, Powell et al. published their flux studies concerning the mechanism of chloride transport across the basal membrane. These authors suggested that, in addition to classical transporters like anion exchangers, there were chloride-conductive pathways, that were sensitive to both DIDS and DPC [22]. Additionally there were studies of the transplacental transfer of chloride. These experiments were performed in sheep, rat and human placentae perfused in vitro. DIDS markedly reduced materno-fetal clearance of chloride across rat placenta perfused in situ and the transplacental chloride transfer was bidirectional [20], [23]. In perfused human placental cotyledons the effect of DIDS and DPC on the materno-fetal clearance of Cl− was investigated. These data showed that approximately 16% of the total Cl− clearance was sensitive to both blockers [24]. A direct experimental system using electrophysiological methods, to identify the chloride conductances present in the hSTB membranes was necessary.
Characteristics of placental chloride channels Placental Cl− channels have been identified in both the plasma membranes and the intracellular organelles.
Possible roles of chloride channels in the placenta Membrane potential is a determinant component of the electrochemical gradient which is the driving force for materno-fetal solute transport across the syncytiotrophoblast. There is evidence that during gestation, the placental membrane potential value changes. A comparison of membrane potentials in villi from first trimester and human placenta at term were significantly different: −32 and −24mV, respectively. Some authors have suggested that the variation in membrane potential was a consequence of the changes in the relative contributions of potassium and chloride conductances present in the apical membrane [62], [63]. In that case, the chloride channels involved in membrane potential generation could change with placental development. A posteriori, a DIDS-sensitive anion conductance that contributes to the resting potential of the syncytiotrophoblast microvillous membrane was reported [2]. However, the nature of the apical anion channels responsible for the membrane potential has not been established but some candidates have been identified such as the Maxi-chloride channel.