| 1. |
- Schubart, R, et al.
(författare)
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In-beam spectroscopy and shell model structure of the neutron deficient In-103 and CD-100,CD-102
- 1995
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Ingår i: Physica Scripta. - : ROYAL SWEDISH ACAD SCIENCES. - 0031-8949 .- 1402-4896. ; T56, s. 311-315
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Tidskriftsartikel (refereegranskat)abstract
- The ?-decay of the neutron deficient nuclei 103In and 100,102Cd has been studied following the reactions 58Ni + 50Cr and 58Ni + 46,48Ti at 250 MeV and 230 MeV bombarding energy of the 58Ni beam, respectively. Evaporation neutrons and charged particles were measured in coincidence with prompt and delayed ?-rays with the multidetector array OSIRIS. To investigate the decay of the I? = 8+ isomers of 100,102Cd a recoil catcher setup inside OSIRIS was used. Six new ?-ray transitions of 100Cd and four of 102Cd with intensities of 1-10% of the main ?-ray cascades were found. Two new states of 100Cd were established and firm spin-parity assignments were made to all states below the isomer. These new states were identified as the 4+ and the 6+ members of the proton ?g9/2?2 multiplet. The experimental states of 103In and of 100,102Cd are compared to shell model predictions in the ?(p1/2, g9/2) v(d5/2, g7/2, s1/2, d3/2, h11/2) configuration space.
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| 3. |
- Vlaskovska, Mila, et al.
(författare)
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Opioid effects on 45Ca2+ uptake and glutamate release in rat cerebral cortex in primary culture
- 1997
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Ingår i: Journal of Neurochemistry. - : Wiley. - 0022-3042 .- 1471-4159. ; 68:2, s. 517-524
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Tidskriftsartikel (refereegranskat)abstract
- Primary cultures of rat cortex, conveniently prepared from newborn animals, were used to study opioid effects on 45Ca2+ uptake and glutamate release. 45Ca2+ uptake, induced by treatment with glutamate or NMDA, was largely blocked by the NMDA antagonist MK-801. K+ depolarization-induced 45Ca2+ uptake was also reduced by MK-801, indicating that the effect was mediated by glutamate release. Direct analysis verified that glutamate, and aspartate, were indeed released. Opioid peptides of the prodynorphin system were also released and these, or other peptides, were functionally active, because naloxone treatment increased glutamate release, as well as the 45Ca2+ uptake induced by depolarization. Opioid agonists, selective for mu-, kappa-, and delta-receptors, inhibited the 45Ca2+ uptake induced by K+ depolarization. The combination of low concentrations of MK-801 and opioid agonists resulted in additive inhibition of K(+)-induced 45Ca2+ uptake. The results indicate that this system may be useful as an in vitro CNS model for studying modulation by opioids of glutamate release and Ca2+ uptake under acute, and perhaps also chronic, opiate treatment.
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