Seedling establishment: The neglected trait in the seed longevity field.

Seed longevity is a central actor in plant germplasm resource conservation, species reproduction, geographical distribution, crop yield and quality and food processing and safety. Seed longevity and vigor decrease gradually during storage, which directly influences seed germination and post-germination seedling establishment. It is noted that seedling establishment is a key shift from heterotropism to autotropism and is fueled by the energy reserved in the seeds per se. Numerous studies have demonstrated that expedited catabolism of triacylglycerols, fatty acid and sugars during seed storage is closely related to seed longevity. Storage of farm-saved seeds of elite cultivars for use in subsequent years is a common practice and it is recognized that aged seed (especially those stored under less-than-ideal conditions) can lead to poor seed germination, but the significance of poor seedling establishment as a separate factor capable of influencing crop yield has been overlooked. This review article summarizes the relationship between seed germination and seedling establishment and the effect of different seed reserves on seed longevity. Based on this, we emphasize the importance of simultaneous scoring of seedling establishment and germination percentage from aged seeds and discuss the reasons.

Oral Delivered Dexmedetomidine Promotes and Consolidates Non-rapid Eye Movement Sleep via Sleep-Wake Regulation Systems in Mice.

Dexmedetomidine, a highly selective α2-adrenergic agonist, is widely used in clinical anesthesia and ICU sedation. Recent studies have found that dexmedetomidine-induced sedation resembles the recovery sleep that follows sleep deprivation, but whether orally delivered dexmedetomidine can be a candidate for the treatment of insomnia remains unclear. In this study, we estimated the sedative effects of orally delivered dexmedetomidine by spontaneous locomotor activity (LMA), and then evaluated the hypnotic effects of dexmedetomidine on sleep-wake profiles during the dark and light phase using electroencephalography/electromyogram (EEG/EMG), respectively. Using c-Fos staining, we explored the effects of dexmedetomidine on the cerebral cortex and the sub-cortical sleep-wake regulation systems. The results showed that orally delivered dexmedetomidine at 2 h into the dark cycle reduced LMA and wakefulness in a dose-dependent manner, which was consistent with the increase in non-rapid eye movement sleep (NREM sleep). However, dexmedetomidine also induced a rebound in LMA, wake and rapid eye movement sleep (REM sleep) in the later stage. In addition, orally delivered dexmedetomidine 100 µg/kg at 2 h into the light cycle shortened the latency to NREM sleep and increased the duration of NREM sleep for 6 h, while decreased REM sleep for 6 h. Sleep architecture analysis showed that dexmedetomidine stabilized the sleep structure during the light phase by decreasing sleep-wake transition and increasing long-term NREM sleep (durations of 1024-2024 s and >2024 s) while reducing short-term wakefulness (duration of 4-16 s). Unlike the classic hypnotic diazepam, dexmedetomidine also increased the delta power in the EEG spectra of NREM sleep, especially at the frequency of 1.75-3.25 Hz, while ranges of 0.5-1.0 Hz were decreased. Immunohistochemical analysis showed that orally delivered dexmedetomidine 100 µg/kg at 2 h into the dark cycle decreased c-Fos expression in the cerebral cortex and sub-cortical arousal systems, while it increased c-Fos expression in the neurons of the ventrolateral preoptic nucleus. These results indicate that orally delivered dexmedetomidine can induce sedative and hypnotic effects by exciting the sleep-promoting nucleus and inhibiting the wake-promoting areas.