BackgroundKiwifruit are classified as climacteric since exogenous ethylene (or its analogue propylene) induces rapid ripening accompanied by ethylene production under positive feedback regulation. However, most of the ripening–associated changes (Phase 1 ripening) in kiwifruit during storage and on–vine occur largely in the absence of any detectable ethylene. This ripening behavior is often attributed to basal levels of system I ethylene, although it is suggested to be modulated by low temperature.ResultsTo elucidate the mechanisms regulating Phase 1 ripening in kiwifruit, a comparative transcriptome analysis using fruit continuously exposed to propylene (at 20 °C), and during storage at 5 °C and 20 °C was conducted. Propylene exposure induced kiwifruit softening, reduction of titratable acidity (TA), increase in soluble solids content (SSC) and ethylene production within 5 days. During storage, softening and reduction of TA occurred faster in fruit at 5 °C compared to 20 °C although no endogenous ethylene production was detected. Transcriptome analysis revealed 3761 ripening–related differentially expressed genes (DEGs), of which 2742 were up–regulated by propylene while 1058 were up–regulated by low temperature. Propylene exclusively up–regulated 2112 DEGs including those associated with ethylene biosynthesis and ripening such as AcACS1, AcACO2, AcPL1, AcXET1, Acβ–GAL, AcAAT, AcERF6 and AcNAC7. Similarly, low temperature exclusively up–regulated 467 DEGS including AcACO3, AcPL2, AcPMEi, AcADH, Acβ–AMY2, AcGA2ox2, AcNAC5 and AcbZIP2 among others. A considerable number of DEGs such as AcPG, AcEXP1, AcXET2, Acβ–AMY1, AcGA2ox1, AcNAC6, AcMADS1 and AcbZIP1 were up–regulated by either propylene or low temperature. Frequent 1–MCP treatments failed to inhibit the accelerated ripening and up–regulation of associated DEGs by low temperature indicating that the changes were independent of ethylene. On–vine kiwifruit ripening proceeded in the absence of any detectable endogenous ethylene production, and coincided with increased expression of low temperature–responsive DEGs as well as the decrease in environmental temperature.ConclusionsThese results indicate that kiwifruit possess both ethylene−dependent and low temperature–modulated ripening mechanisms that are distinct and independent of each other. The current work provides a foundation for elaborating the control of these two ripening mechanisms in kiwifruit.Electronic supplementary materialThe online version of this article (10.1186/s12870-018-1264-y) contains supplementary material, which is available to authorized users.

l-3,4-Dihydroxyphenylalanine (l-DOPA) is the most effective therapeutic agent for Parkinson’s disease (PD). l-DOPA is traditionally believed to be an inert amino acid that exerts actions and effectiveness in PD through its conversion to dopamine. In contrast to this generally accepted idea, l-DOPA is proposed to be a neurotransmitter. Recently, GPR143 (OA1), the gene product of ocular albinism 1 was identified as a receptor candidate for l-DOPA. GPR143 is widely expressed in the central and peripheral nervous system. GPR143 immunoreactivity was colocalized with phosphorylated α-synuclein in Lewy bodies in PD brains. GPR143 may contribute to the therapeutic effectiveness of l-DOPA and might be related to pathogenesis of PD.

The responses of three kiwifruit cultivars, Actinidia chinensis 'Sanuki Gold', A. chinensis 'Rainbow Red', and A. deliciosa 'Hayward' to various storage temperatures (0, 5, 10, 15, and 20°C) for 8 weeks were investigated. The rate of fruit which initiated ethylene production due to rot development increased with increases in storage temperature. Early-maturing cultivars, 'Rainbow Red' and 'Sanuki Gold' fruit stored at 5, 10, and 15°C showed drastic softening and a decrease in titratable acidity (TA) to an edible level within 4 weeks without detectable ethylene production, whereas fruit stored at 0 and 20°C maintained high firmness and TA even after 8 weeks unless they were infected with rot. A late-maturing cultivar, 'Hayward' fruit stored at 5 and 10°C softened more rapidly than when stored at 0, 15, or 20°C. Treatment with 1-Methylcyclopropene (1-MCP) did not suppress the low temperature modulated fruit ripening in any cultivars, indicating its independence from ethylene. These results suggest that 'Sanuki Gold' and 'Rainbow Red' are more sensitive to low temperatures compared to 'Hayward' and the sensitivity is involved in the determination of storage life and how early the fruit matures on the vine.

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Current therapeutic strategies for epilepsy include anti-epileptic drugs and surgical treatments that are mainly focused on the suppression of existing seizures rather than the occurrence of the first spontaneous seizure. These symptomatic treatments help a certain proportion of patients, but these strategies are not intended to clarify the cellular and molecular mechanisms underlying the primary process of epilepsy development, i.e., epileptogenesis. Epileptogenic changes include reorganization of neural and glial circuits, resulting in the formation of an epileptogenic focus. To achieve the goal of developing “anti-epileptogenic” drugs, we need to clarify the step-by-step mechanisms underlying epileptogenesis for patients whose seizures are not controllable with existing “anti-epileptic” drugs. Epileptogenesis has been studied using animal models of neonatal seizures because such models are useful for studying the latent period before the occurrence of spontaneous seizures and the lowering of the seizure threshold. Further, neonatal seizure models are generally easy to handle and can be applied for in vitro studies because cells in the neonatal brain are suitable for culture. Here, we review two animal models of neonatal seizures for studying epileptogenesis and discuss their features, specifically focusing on hypoxia-ischemia (HI)-induced seizures and febrile seizures (FSs). Studying these models will contribute to identifying the potential therapeutic targets and biomarkers of epileptogenesis.

Hyperthermia-induced febrile seizures (FSs) are the most common seizures during childhood, and prolonged complex FSs can result in the development of epilepsy. Currently, GABA A receptor modulators such as benzodiazepines and barbiturates are used as medications for FSs with the aim of enhancing GABA-mediated inhibition of neuronal activity. However, it is still up for debate whether these enhancers of GABAergic neurotransmission could depolarize immature neurons with relatively higher levels of the intracellular Cl − in the developing brain during FSs. Here, we performed simultaneous video-local field potential monitoring to determine whether benzodiazepines and barbiturates affect the phenotypes of FSs in postnatal day (P)11 and P14 mice. We found that low-dose administration of diazepam decreased the incidence of clonic seizures at P11. We also found that high-dose administration of diazepam and pentobarbital exacerbated the behavioral and electrophysiological phenotypes of the induction phase of experimental FSs at P11 but not at P14. We further found that the deteriorated phenotypes at P11 were suppressed when Na + K + 2Cl − cotransporter isoform 1 (NKCC1), which mediates Cl − influx, was blocked by treatment with the diuretic bumetanide. Though our findings do not exclude the involvement of sedation effect of high-dose GABA A receptor modulators in worsening experimental FSs at P11, pharmacological enhancement of GABAergic signaling could aggravate seizure activity in the early phase of FSs.

'Rainbow Red' kiwifruit have been reported to gradually ripen during low temperature storage and on the vine in the absence of detectable ethylene. This study was conducted to compare the expression of ripeningrelated genes during storage at different temperatures and on the vine. Fruit at 5°C and 10°C ripened faster to eating quality within four weeks accompanied with increased expression of ripening-related genes: AcACO3, AcXET2, AcEXP1, AcPG, AcPMEi, AcSUS, AcβAMY1, AcβAMY2, AcGA2ox2, AcNAC3, AcNAC4, and AcMADS2. Fruit at 15°C required a longer period of eight weeks to attain eating quality in concurrence with delayed accumulation of the ripening-related genes. Fruit at 22°C ripened at the slowest rate and did not attain eating quality even after eight weeks, with very minimal accumulation of ripening-related genes. Onvine ripening occurred slowly at the early stages when the average field temperature was ~20°C, but the rate increased as the temperature dropped to ≤15°C accompanied by increased expression of ripening-related genes. These results indicate that both ripening on-vine and during low temperature storage are modulated by low temperature independent of ethylene.