Phytohormone profiles and related gene expressions after endodormancy release in developing Pinus tabuliformis male strobili.

Development after endo-dormancy release ensures perennial plants, such as forest trees, proper response to environmental changes and enhances their adaptability. In northern hemisphere, megasporophore and microsporophore of conifers undergo dormancy to complete their development. Here combined with transcriptome data, we used high-performance liquid chromatography/electrospray ionization tandem mass spectrometry (ESI-HPLC-MS/MS) to quantitatively analyse the various hormones (Abscisic Acid (ABA), 3-Indoleacetic acid (IAA), Gibberellins (GAs), Cytokinin (CTK), Jasmonic acid (JA) and Salicylic acid (SA)) of Chinese pine (Pinus tabuliformis Carr.) male strobili after endo-dormancy release. More specifically, we analysed endogenous hormones and their related-genes and verified the important role of ABA in plants growth and development. We observed rapid decrease in ABA content after dormancy release, resulting in reducing the inhibitory effect on male strobili growth. Similarly, rapid drop in ABA/GA ratio was observed and was associated with the start of male strobili growth and development. Combined with transcriptome data, we found that HAB2-SnRK2.10 played a central role in the ABA pathway in the entire network of hormones regulating male strobili development. Due to external environment warming, the differentially expressed HAB2-SnRK gene led to ABA content rapid decline, thus initiating male strobili growth. We constructed a network of hormone-regulated development to understand the interactions between hormones after male strobili dormancy release of male strobili. This study provided essential foundations for studying megasporophore and microsporophore growth mechanism after endo-dormancy and offered new ideas for flower development in gymnosperms and angiosperms.

[Effects of enriched environment and impoverished environment on learning and memory ability of manganese-exposed mice].

OBJECTIVE: To investigate the effects of enriched environment and impoverished environment on the learning and memory ability of manganese-exposed mice and the mechanism. METHODS: Forty female Kunming mice were randomly and equally divided into 4 group: control group (CG), standard environment and manganese exposure group (SEG), enriched environment and manganese exposure group (EEG), and impoverished environment and manganese exposure group (IEG). The mouse model of manganese poisoning was established by intraperitoneal injection of manganese chloride. The learning and memory ability was tested by Morris water maze. The expression of cAMP response element-binding protein (CREB) in area CA1 of the hippocampus was measured by immunohistochemistry. RESULTS: In place navigation test, the SEG had a significantly longer escape latency than the CG (P < 0.05), and the EEG had a significantly shorter escape latency than the SEG (P < 0.05); there was no significant difference in escape latency between IEG and SEG (P > 0.05). In spatial probe test, the EEG had a significantly greater number of platform crossings than the SEG (P < 0.05), and the IEG had a significantly smaller number of platform crossings than the SEG (P < 0.05). The expression of CREB in area CA1 of the hippocampus was significantly lower in IEG and SEG than in CG (P < 0.05), and it was significantly higher in EEG than in SEG (P < 0.05). CONCLUSION: In the enriched environment, the learning and memory ability of manganese-exposed mice can be improved, which may be due to the increased expression of CREB in the hippocampus.

[Effect of Lycium barbarum polysaccharides on neurogenesis and learning & memory in manganese poisoning mice].

OBJECTIVE: To study the effect of Lycium barbarum polysaccharides (LBP) on neurogenesis and learning & memory of manganese poisoning mice. METHODS: Healthy adult Kunming mice were divided into 5 groups, the control group (A), the manganese poisoning (by manganese chloride peritoneal injection) group (B), the manganese poisoning and treated with gastric perfusion of high, medium, low dosage LBP groups (C, D and E). The spatial learning & memory capacity of mouse was determined by Morris water maze training test. The neurogenetic cells were labelled with bromodeoxyuridine (BrdU) and detected by immunohistochemistry. RESULTS: The average escape latency was significantly higher and the times of passing through platform lower in group B than those in group A (P<0.05). BrdU positive cells in groups C, D and E were significantly more than those in group B (P<0.05). CONCLUSION: LBP could enhance the learning & memory capability of the manganese poisoning mice by promoting neurogenesis in hippocampus.

[Effects of manganismus on proliferation of neural stem cells in mice's hippocampus].

OBJECTIVE: To explore the effects of manganese poisoning on the proliferation of neural stem cells (NSCs) in mice's hippocampus. METHODS: The mice (weight 8 approximately 10 g) were divided into control group(CG) low-dose group(LDG) middle-dose group(MDG) and high-dose group(HDG)by intraperitoneal injection of 0, 5, 20, 50 mg x kg(-1) x d(-1) of manganese chloride dissolved in physiological saline. The ability of learning and memory was detected by Morris Water Maze, and the proliferation of NSCs in subgranular zone (SGZ) in these mice's hippocampus was also detected by immunohistochemistry. RESULTS: 1) Compared with the CG, the ability of learning and memory in all manganism group decreased significantly (P < 0.01) and this phenomenon in HDG was most notable (P < 0.01). Meanwhile, the ability of memory was negatively correlated with the dose of manganese chloride (r(s) = -0.598, P < 0.01), but the difference of swimming speed in every group was of no statistic significance. (2) The numbers of NSCs in proliferation period in SGZ of all manganism groups was much lower than that of CG (P < 0.01) negatively correlated with the dose of manganese chloride (r(s) = -0.666, P < 0.01). (3) The reduction of NSCs had a positive correlation to the depression of learning and memory (r(s) = 0.734, P < 0.01). CONCLUSIONS: Manganismus can affect the ability of learning and memory, which is probably caused by the inhalation of manganese on NSCs in hippocampus.

Antinociceptive effects of galanin in the rat tuberomammillary nucleus and the plasticity of galanin receptor 1 during hyperalgesia.

Although the tuberomammillary nucleus (TM) is well defined in terms of anatomy and neurochemistry, little is known about its function in nociceptive modulation. There was an abundance of galanin-immunoreactive fibers in the TM, and galanin has been implicated in pain processing. The present study assessed the role of galanin in the modulation of nociception in the TM of rats. Intra-TM injection of galanin dose-dependently increased the hindpaw withdrawal latency of rats to a noxious thermal stimulus, indicating an antinociceptive role of galanin in the TM. The antinociceptive effect of galanin was blocked by a subsequent intra-TM injection of galantide, a putative galanin receptor antagonist, suggesting that the antinociceptive effect of galanin is mediated by galanin receptors. Moreover, there was abundant galanin receptor 1 (GalR1) in the TM, and the number of GalR1-positive neurons in the ipsilateral TM increased significantly after unilateral loose ligation of the sciatic nerve compared with the contralateral TM or the TM of intact rats. However, the number of GalR1-positive neurons was not significantly altered by carrageenan-induced inflammation, in either the ipsilateral or the contralateral TM. The results suggest that galanin and GalR1 in the TM may play important roles in pain regulation.