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Effects of mercury and lead on rubidium uptake and efflux in cultured rat astrocytes.

Astrocytes readily sequester lead and mercury (8, 10, 19, 22). Accordingly, studies were undertaken to assess the effects of lead and mercury on homeostatic functions in neonatal rat brain primary astrocyte cultures. Both inorganic and organic mercury, but not lead, significantly inhibited the initial rate (5 min) of uptake of 86RbCl, used as a tracer for K+, at concentrations of 10-100 microM. Mercury and to a lesser extent lead also stimulated the efflux of intracellular 86Rb+ at 10-500 microM. These observations suggest that the astrocyte plasma membrane may be an important target for lead and mercury, and that relatively low concentrations of these heavy metals should inhibit the ability of astrocytes to maintain a transmembrane K+ gradient.

Animals↗

Effects of lithium and rubidium on immune responses of rats.

Rats were treated with LiCl or RbCl in drinking water for 65 days. Spleen cells from both treated groups exhibited significantly greater proliferative responses to lipopolysaccharide (LPS) than those from untreated controls. Responses to concanavalin A (Con A) were not affected. Cytotoxic activities of natural killer (NK) cells from both treated groups were significantly less than those from untreated controls. In vitro, Li augmented responses of spleen cells to LPS, but the same doses of Rb suppressed the responses. Effects on responses to Con A were variable. Both Li and Rb alone had a small mitogenic effect on spleen cells.

Animals↗

Essentials of a rubidium-82 generator for nuclear medicine.

The use of generator-produced 82Rb for positron emission tomography studies in clinical nuclear medicine requires a number of factors to be considered. These include 82Sr availability, methods of recharging the generator with fresh 82Sr, adequate elution yield of 82Rb, low breakthrough of 82-85Sr, simple and reliable operation of the generator, and delivery of a sterile and pyrogen free eluate of 82Rb.

Electrons↗

Production and separation of no-carrier-added radioactive tracers of yttrium, strontium and rubidium from heavy-ion irradiated germanium target: applicability to the standardization of a separation technique for production of positron-emitting radionuclide 86Y.

Among various positron-emitting radionuclides, certain radioisotopes of Y, Sr and Rb have important applications in diagnostic and therapeutic nuclear medicine. In the present work, an attempt has been made to produce some of those radioisotopes by irradiating a natural Ge-target material with heavy-ion oxygen ((16)O(+6)) projectiles. An effective radiochemical separation scheme was developed to isolate Y, Sr and Rb radiotracers from the irradiated Ge-matrix in no-carrier-added form with a view to applying those radiotracers for standardization of a technique for the radiochemical separation of Y from natural Sr target. The standardized separation technique could be utilized for the production of the positron-emitting (86)Y from an enriched (86)Sr target irradiated at a medical cyclotron.

Electrons↗

Axonal transport of rubidium and thallium in the olfactory nerve of mice.

Following intranasal administration of radioactive (86)Rb(+) and (201)Tl(+) in mice, we observed this direct transport via the olfactory nerve pathway. The (86)RbCl and (201)TlCl solutions were administered to two groups of mice, the unilateral intranasal and intravenous administration groups. After sacrifice, their heads were divided into the right and left side, which were then subdivided into seven parts; the nasal mucosa and brain regions were separated. Following the unilateral intranasal administration, uptake after 6 h by the olfactory bulb was significantly higher on the ipsilateral side ((86)Rb, 0.7 %dose; (201)Tl, 0.5 %dose) than on the contralateral side ((86)Rb, 0.08 %dose; (201)Tl, 0.15 %dose). Moreover, the (86)Rb and (201)Tl that accumulated in the olfactory bulb were gradually transported to other brain regions of the olfactory tract, the telencephalon and the diencephalon on the side corresponding to the nostril used for administration. Significant differences were observed between the right and left side of the brain regions 6 and 12 h after administration. Further, (201)Tl autoradiography clearly showed striped patterns of dense accumulation, localized in the region around the glomerular layer and granule cell layer of the olfactory bulb and around the olfactory cortex. These results provide clear evidence of axonal transport via the olfactory nerve pathway, from nasal cavity to the olfactory bulb, as well as to the olfactory cortex through the synaptic junctions. The olfactory transport of the (86)Rb(+) and (201)Tl(+) is thought to represent the behavior of K(+) in the olfactory system.

Animals↗

Gamma-hydroxybutyrate receptor function determined by stimulation of rubidium and calcium movements from NCB-20 neurons.

Gamma-Hydroxybutyrate is derived from GABA in brain and plays specific functional roles in the CNS. It is thought to exert a tonic inhibitory control on dopamine and GABA release in certain brain areas, through specific gamma-hydroxybutyrate receptors. Apart from modifying certain calcium currents, the specific transduction mechanism induced by stimulation of gamma-hydroxybutyrate receptors remains largely unknown. We investigated the possible contribution of K(+) channels to the hyperpolarization phenomena generally induced by gamma-hydroxybutyrate in brain, by monitoring (86)Rb(+) movements in a neuronal cell line (NCB-20 cells), which expresses gamma-hydroxybutyrate receptors. Physiological concentrations of gamma-hydroxybutyrate (5-25 microM) induce a slow efflux of (86)Rb(+), which peaks at 5-15 min and returns to baseline levels 20 min later after constant stimulation. This effect can be reproduced by the gamma-hydroxybutyrate receptor agonist NCS-356 and blocked by the gamma-hydroxybutyrate receptor antagonist 6,7,8,9-tetrahydro-5-[H]-benzocycloheptene-5-ol-4-ylidene. The GABA(B) receptor antagonist CGP 55845 has no effect on gamma-hydroxybutyrate-induced (86)Rb(+) efflux. The pharmacology of this gamma-hydroxybutyrate-dependent efflux of (86)Rb(+) is in favor of the involvement of tetraethylammonium and charybdotoxin insensitive, apamin sensitive Ca(2+) activated K(+) channels, identifying them as small conductance calcium activated channels. We demonstrated a gamma-hydroxybutyrate dose-dependent entry of calcium ions into NCB-20 neuroblastoma cells at resting potential. Electrophysiological data showed that this Ca(2+) entry corresponded mainly to a left-hand shift of the current/voltage relation of the T-type calcium channel. This process must at least partially trigger small conductance calcium activated channel activation leading to gamma-hydroxybutyrate-induced hyperpolarization.

Animals↗