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The f-electron compound CeAuSb2, which crystallizes in the ZrCuSi2-type tetragonal structure, orders antiferromagnetically between 5 and 6.8 K, where the antiferromagnetic transition temperature TN depends on the occupancy of the Au site. Here we report the electrical resistivity and heat capacity of a high-quality crystal CeAuSb2 with TN of 6.8 K, the highest for this compound. The magnetic transition temperature is initially suppressed with pressure, but is intercepted by a new magnetic state above 2.1 GPa. The new phase shows a dome shape with pressure and coexists with another phase at pressures higher than 4.7 GPa. The electrical resistivity shows a T 2 Fermi liquids behavior in the complex magnetic state, and the residual resistivity and the T 2 resistivity coefficient increases with pressure, suggesting the possibility of a magnetic quantum critical point at a higher pressure.

The non-competitive NMDA receptor antagonist memantine, currently prescribed for the treatment of Alzheimer's disease, is assumed to prevent the excitotoxicity implicated in neurodegenerative processes. Here, we investigated the actions of memantine on hippocampal function and signalling. In behavioural experiments using the water maze, we observed that memantine (at 2 mg/kg) reversed scopolamine-induced learning deficits in mice. When acutely applied to mouse hippocampal slices, memantine caused a significant upward shift in the population spike input-output relationship at 10 and 100 µM, and a corresponding downward shift in latency, indicative of overall enhanced synaptic transmission. This action was blocked by the muscarinic antagonist scopolamine (10 µM) but not by the NMDA antagonist MK-801 (10 µM) or the GABA antagonist bicuculline (20 µM). Further, memantine occluded potentiation induced by 50 nM carbachol (CCh), while enhancing inhibitory actions of CCh at 1 µM, suggesting additive actions. As anticipated for an NMDA antagonist, 100 µM (but not 10 µM) memantine also inhibited tetanus-induced long-term potentiation (LTP), and NMDA-induced Ca 2+ signals were blocked in cultured hippocampal neurones at 10 µM (by 88%). Overall, our data suggest actions of memantine beyond NMDA receptor antagonism, including stimulating effects on cholinergic signalling via muscarinic receptors. These interactions with the cholinergic system are likely to contribute to memantine's therapeutic potential.