Galantamine, an inhibitor of acetylcholinesterase, promotes hippocampal neurogenesis, but the exact mechanism for this is not known. In the present study, we examined the mechanisms underlying the effects of acute galantamine on neurogenesis in the mouse hippocampus. Galantamine (3 mg/kg) increased the number of 5-bromo-2'-deoxyuridine (BrdU)-positive cells in the subgranular zone of the dentate gyrus. This effect was blocked by the muscarinic receptor antagonist scopolamine and the preferential M1 muscarinic receptor antagonist telenzepine, but not by the nicotinic receptor antagonists mecamylamine and methyllycaconitine. Galantamine did not alter the ratio of neuronal nuclei (NeuN)- or glial fibrillary acidic protein (GFAP)-positive cells to BrdU-labeled cells in the subgranular zone and granule cell layer. Galantamine (1, 3 mg/kg) promoted the survival of 2-wk-old newly divided cells in mice in the granule cell layer of the dentate gyrus, whereas it did not affect the survival of newly divided cells at 1 and 4 wk. Galantamine-induced increases in cell survival were blocked by the α7 nicotinic receptor antagonist methyllycaconitine, but not by scopolamine. Bilateral injection of recombinant IGF2 into the dentate gyrus of the hippocampus mimicked the effects of galantamine. The effects of galantamine were blocked by direct injection of the IGF1 receptor antagonist JB1. These findings suggest that galantamine promotes neurogenesis via activation of the M1 muscarinic and α7 nicotinic acetylcholine receptors. The present study also suggests that IGF2 is involved in the effects of galantamine on the survival of 2-wk-old immature cells in the granule cell layer.

Summary Background Curcuma longa has been reported to have anti‐inflammatory effects. Skin inflammation impairs skin functions. Objectives Our aim was to investigate the effect of a hot water extract of C longa (WEC) on skin conditions in cell studies using keratinocytes and in clinical trials. Methods We measured proinflammatory cytokine levels in ultraviolet B‐irradiated keratinocytes in the presence or absence of WEC. The effects of WEC on hyaluronan production in keratinocytes were also determined. In a randomized, double‐blind, placebo‐controlled trial, 47 healthy participants were assigned to 8‐week intervention groups with daily intakes of WEC with or without curcumin or a placebo. The water content and transepidermal water loss in the face and minimal erythema dose on the back after ultraviolet B irradiation were evaluated every 4 weeks. Results Hot water extract of C longa significantly inhibited increases in ultraviolet B‐induced tumor necrosis factor α and interleukin 1β at the mRNA and protein levels. WEC also significantly increased hyaluronan production from nonstimulated keratinocytes. In the randomized, double‐blind, placebo‐controlled trial, increases from baseline in the water content of the face were significantly greater at weeks 4 and 8 in the WEC group, but not in the WEC + curcumin group, than in the placebo group. There were no significant differences in transepidermal water loss and minimal erythema dose among the groups. Conclusions The cell studies confirmed that WEC has anti‐inflammatory effects and augments hyaluronan production in the skin. The results of clinical trials suggest that WEC may be useful for moisturizing facial skin. Trial registration UMIN Clinical Trials Registry 000028510. Retrospectively registered.

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These findings suggest that isolation rearing causes hypoalgesia in mouse models of acute pain and imply that the spinal 5-HT1A receptor activation probably through descending serotonergic inhibitory pathway is involved in isolation rearing-induced hypoalgesia.