Magnetic properties induced by the Yb-valence inhomogeneity in the layered Kondo-lattice compound Yb4RuGe8.

We have successfully grown single crystals of a novel ytterbium-based layered compoundYb4RuGe8and studied its structural, magnetic, thermal, and transport properties. The magnetic susceptibility has a broad peak caused by the Kondo effect at approximately40 Kand is enhanced below15 Kowing to the development of additional magnetic correlations. An analysis with the grand-Kadowaki-Woods relation reveals that the low-temperature state except for the effect of the additional magnetic correlations is a heavy-mass Fermi liquid.

Increase of kainate receptor mRNA in the hippocampal CA3 of amygdala-kindled rats detected by in situ hybridization.

To investigate whether lasting changes in excitatory amino acid (EAA) receptor subtypes occurred at their mRNA levels as a result of kindling, we carried out in situ hybridization of rat brain sections using synthetic oligonucleotide probes, which were complementary to cloned EAA receptor subunits, namely NMDAR1 for N-methyl-D-aspartate (NMDA), GluR-2 for alpha-amino-3-hydroxy-5-methylisoxazole 4-propionic acid (AMPA), KA-1 for kainate (KA) and mGluR1 for metabotropic EAA receptors. Rats in which left-amygdala-kindling had been established were decapitated 28 days after the last kindled seizure along with the matched controls, which had been subjected to electrode implantation but not to kindling, and the brain sections were hybridized with the probes. The amount of KA receptor mRNA detected with the KA-1 probe increased (25%) on both the left and right sides of the hippocampal CA3 region in the kindled rats, but in no other brain areas (hippocampal CA1, dentate gyrus, amygdala nuclei and pyriform cortex). There was no significant modification of NMDAR1, GluR-2 or mGluR1 receptor mRNAs in any brain area examined. The increase of KA receptor mRNA in the CA3 of amygdala-kindled rats may indicate that the excitability of the neural circuits mediated by KA receptors increased in the hippocampus as a consequence of kindling.

Characterization of a cloned rat serotonin 5-HT1A receptor expressed in the HeLa cell line.

We have previously isolated the rat serotonin (5-HT)1A receptor gene (G21Y2) and now report the expression and characterization of this receptor. The BamHI/Xbal fragment of this gene was cloned into Rc/RSV and stably transfected into HeLa cells by the calcium phosphate method. For determination of specific 5-HT1A receptor binding, [3H]8OH-DPAT was used as the radioligand and incubated with HeLa cell membranes. The cells expressed specific and saturable binding of [3H]8OH-DPAT with a Kd value of 0.3 nM and a Bmax value of 2 pmol/mg protein. GTP (50 microM) added to the incubation mixture increased the Kd value to 3 nM indicating that the expressed receptor is coupled to a G protein. The specific binding was inhibited by selective 5-HT1A partial agonists, such as buspirone, ipsapirone, gepirone, tandospirone, zalospirone and SUN8399 with Ki values of 1-30nM, whereas other neurotropic drugs except for spiperone (Ki = 46 nM) and nemonapride (Ki = 2.3 nM) were effective only at concentrations of more than 100 microM. The potencies of these compounds to inhibit [3H]8OH-DPAT from its specific binding sites were similar to their affinities determined in rat hippocampus binding studies. These data suggest that the expressed receptor is a 5-HT1A-type similar to 5-HT1A receptors in the rat hippocampus.

Changes in dopamine D2 and GluR-1 glutamate receptor mRNAs in the rat brain after treatment with phencyclidine.

In situ hybridization of slide-mounted brain sections from rats subjected to acute and chronic phencyclidine treatment was carried out using synthetic oligonucleotides complementary to dopamine D2-receptor and non-N-methyl-D-aspartate (NMDA) glutamate-receptor-subunit (GluR-1) mRNAs. There was no significant difference in either the D2-receptor or the GluR-1 mRNA levels in any brain region of the acute phencyclidine (10 mg/kg)-treated and control groups. However, chronic administration of phencyclidine (10 mg/kg/day, 14 days) significantly decreased the dopamine D2-receptor mRNA level in the caudate-putamen (by 27%, P < 0.01) and significantly increased the GluR-1 mRNA level in the prefrontal cortex (by 29%, P < 0.001). These results suggest that the chronic pharmaco-behavioral effects of phencyclidine may involve expression of both dopamine- and non-NMDA glutamate-receptor mRNAs.

Effect of chronic ipsapirone treatment on the density of 5-HT1A receptors and 5-HT1A receptor mRNA in discrete regions of the rat brain.

There is increasing evidence that the 5-hydroxytryptamine (HT)1A partial agonist ipsapirone is an effective anxiolytic/antidepressant agent, although its mechanism of action is not clear. In this study, we investigated the effects of chronic ipsapirone treatment (5 or 10 mg/kg; twice daily, 3 weeks) on 5-HT1A receptor density 8-hydroxy-2-(di-n-propyl amino) tetralin (8O H-DPAT) binding and the level of its mRNA (in situ hybridization) in various regions of the rat (male Wistar 250 g) brain. Receptor density was reduced in the frontal cortex, but did not change significantly in the hippocampus and dorsal raphe nucleus. The level of receptor mRNA was unchanged in each of these brain regions. The present results suggest that the clinical anxiolytic effects of ipsapirone may be mediated partly by postsynaptic action on serotonergic transmission in the frontal cortex, but not in the hippocampus or dorsal raphe nuclei.