Hippocampal NPY neurons project to the fascia dentata in organotypic cultures

The distribution of neuropeptide Y immunoreactive (NPY-ir) neurons in organotypic cultures of hippocampi from neonates was compared to that seen in adult rats. In addition to the known NPY-ir neurons in the hippocampus proper and in the hilus of the fascia dentata, isolated, large, multipolar, NPY-ir neurons were observed in the subiculum and in areas CA1 and CA3. Their axons projected into stratum radiatum of the hippocampus proper and into the molecular layers and hilus of the fascia dentata where they branched profusely. These NPY-ir neurons were regularly distributed throughout the septo temporal extent of the hippocampus and were present in both neonates and adult hippocampi. The hilar NPY-ir neurons have always been considered the source of the NPY-ir plexus in the outer molecular layer of the dentate gyrus. However, our results show that there is also a contribution from the NPY-ir neurons in the hippocampus proper. © 1996 Wiley-Liss, Inc.     

Regulatory volume increase in rat pancreatic β-cells

 This study investigated regulatory volume increase (RVI) in rat pancreatic β-cells. Volume changes in isolated β-cells were measured by a video-imaging method. Cell shrinkage was induced by exposure to solutions made hypertonic by the addition of 100 mM mannitol. In HEPES-buffered solutions, β-cells exhibited an RVI which was almost completely abolished by 10 μM bumetanide. These data indicate that Na⁺-2Cl^–-K⁺ cotransporters make a major contribution to RVI in β-cells. In HCO₃ ^–-buffered solutions, however, an RVI was observed in the presence of 10 μM bumetanide. This bumetanide-insensitive component of RVI was inhibited by 100 μM amiloride or 100 μM 4,4’-diisothiocyanatostilbene-2,2’-disulphonic acid (DIDS). These data suggest that, in addition to the Na⁺-2Cl^–-K⁺ cotransporter, functionally coupled Na⁺-H⁺ exchangers and Cl^–-HCO₃ ^– exchangers may also contribute to RVI in pancreatic β-cells. Received: 3 July 1997 / Received after revision and accepted: 1 September 1997     

Brain hydration during alcohol withdrawal in alcoholics measured by magnetic resonance imaging

Twenty-seven patients had a first Magnetic Resonance Imaging (MRI) scan 1-3 days after stopping drinking and a second approximately 2 weeks later with no change in whole brain T1 or T1 in selected brain areas. Six patients whose first scan was over 36 h after the last drink underwent an increase in whole brain T1 in the interval to the second scan. The later the first scan was performed the greater was the increase in T1. These results are compatible with a very early fall in brain water immediately on cessation of drinking (perhaps due to a rebound increase of vasopressin activity) with a return to 'baseline' after two weeks. A third scan after discharge from hospital in 23 individuals who had abstained from alcohol or drank very little did not reveal any further significant change in brain T1.