Light disrupts social memory via a retina-to-supraoptic nucleus circuit.

The formation of social memory between individuals of the opposite sex is crucial for expanding mating options or establishing monogamous pair bonding. A specialized neuronal circuit that regulates social memory could enhance an individual's mating opportunities and provide a parallel pathway for computing social behaviors. While the influence of light exposure on various forms of memory, such as fear and object memory, has been studied, its modulation of social recognition memory remains unclear. Here, we demonstrate that acute exposure to light impairs social recognition memory (SRM) in mice. Unlike sound and touch stimuli, light inhibits oxytocin neurons in the supraoptic nucleus (SON) via M1 SON-projecting intrinsically photosensitive retinal ganglion cells (ipRGCs) and GABAergic neurons in the perinuclear zone of the SON (pSON). We further show that optogenetic activation of SON oxytocin neurons using channelrhodopsin is sufficient to enhance SRM performance, even under light conditions. Our findings unveil a dedicated neuronal circuit through which luminance affects SRM, utilizing a non-image-forming visual pathway, distinct from the canonical modulatory role of the oxytocin system.

Towards precision sleep medicine: Self-attention GAN as an innovative data augmentation technique for developing personalized automatic sleep scoring classification.

It is very important to have good quality sleep, which can affect aspects such as memory consolidation, emotional regulation, learning, physical development, and quality of life. Diagnosing human sleep quality and problems quickly and accurately is an important issue for human well-being. Therefore, many automatic sleep scoring methods have been proposed. However, the methods have been developed using sleep data from different individuals or groups. The accuracies of these proposed methods might decrease, due to existing individual differences. In this study, the self-attention generative adversarial network (SAGAN) was applied as an advanced data augmentation technique to propose an improved personalized automatic sleep scoring classification. First, the spectrograms were converted from electroencephalography (EEG). Then, SAGAN was used to generate synthesized spectrograms for each subject. Finally, the real and synthesized spectrograms of each subject were utilized to train a personalized classifier. The averaged accuracy and standard deviation of the proposed method are 95.74% and 3.78%, respectively. Compared to the classifier trained with all subjects' training data, the average accuracy increased by 8.08%. The results proved that the generated spectrograms significantly improved the performance of the personalized automatic sleep scoring classification. The contributions of the proposed method were that made the medical staff and subjects save massive medical resources and time for manual recording and scoring.

Mapping Central Projection of Oxytocin Neurons in Unmated Mice Using Cre and Alkaline Phosphatase Reporter.

Oxytocin, a neuropeptide and peptide hormone, is produced by neurons in the hypothalamus and released by the posterior pituitary to control breastfeeding and labor. Recent studies have revealed that oxytocin in the central nervous system is also involved in modulating social interaction. To understand the potential role and innervation pattern of oxytocin neurons before sexual interaction, here we used transgenic mice which have the Cre recombinase under the control of an endogenous oxytocin promoter and Cre-dependent human placental alkaline phosphatase (AP) reporter to label the oxytocin neurons in the naive mouse brain. Since AP is located on the membrane of oxytocin neurons, AP histochemistry staining enabled us to observe the fine axonal terminals and the innervation pattern of oxytocin neurons in the thick serial coronal brain slices. Here we show that the number of AP-labeled cells varies with staining reaction time and ranges from 30% of the oxytocin immune-positive cell count to slightly higher than the oxytocin immune-positive cell count. Using AP staining with extended reaction time, which may not label all oxytocin neurons, we confirmed many innervation targets of oxytocin neurons from the anterior olfactory nucleus, some cortex regions, the limbic system, the hypothalamus, and the hindbrain, while the cell bodies were exclusively located in the hypothalamus and the bed nucleus of the stria terminalis. Finally, we observe some individual variance at the olfactory area, isocortex, striatum, paraventricular nucleus of thalamus, locus coeruleus, and Barrington's nucleus.

Degeneration of ipRGCs in Mouse Models of Huntington's Disease Disrupts Non-Image-Forming Behaviors Before Motor Impairment.

Intrinsically photosensitive retinal ganglion cells (ipRGCs), which express the photopigment melanopsin, are photosensitive neurons in the retina and are essential for non-image-forming functions, circadian photoentrainment, and pupillary light reflexes. Five subtypes of ipRGCs (M1-M5) have been identified in mice. Although ipRGCs are spared in several forms of inherited blindness, they are affected in Alzheimer's disease and aging, which are associated with impaired circadian rhythms. Huntington's disease (HD) is an autosomal neurodegenerative disease caused by the expansion of a CAG repeat in the huntingtin gene. In addition to motor function impairment, HD mice also show impaired circadian rhythms and loss of ipRGC. Here, we found that, in HD mouse models (R6/2 and N171-82Q male mice), the expression of melanopsin was reduced before the onset of motor deficits. The expression of retinal T-box brain 2, a transcription factor essential for ipRGCs, was associated with the survival of ipRGCs. The number of M1 ipRGCs in R6/2 male mice was reduced due to apoptosis, whereas non-M1 ipRGCs were relatively resilient to HD progression. Most importantly, the reduced innervations of M1 ipRGCs, which was assessed by X-gal staining in R6/2-OPN4Lacz/+ male mice, contributed to the diminished light-induced c-fos and vasoactive intestinal peptide in the suprachiasmatic nuclei (SCN), which may explain the impaired circadian photoentrainment in HD mice. Collectively, our results show that M1 ipRGCs were susceptible to the toxicity caused by mutant Huntingtin. The resultant impairment of M1 ipRGCs contributed to the early degeneration of the ipRGC-SCN pathway and disrupted circadian regulation during HD progression.SIGNIFICANCE STATEMENT Circadian disruption is a common nonmotor symptom of Huntington's disease (HD). In addition to the molecular defects in the suprachiasmatic nuclei (SCN), the cause of circadian disruption in HD remains to be further explored. We hypothesized that ipRGCs, by integrating light input to the SCN, participate in the circadian regulation in HD mice. We report early reductions in melanopsin in two mouse models of HD, R6/2, and N171-82Q. Suppression of retinal T-box brain 2, a transcription factor essential for ipRGCs, by mutant Huntingtin might mediate the reduced number of ipRGCs. Importantly, M1 ipRGCs showed higher susceptibility than non-M1 ipRGCs in R6/2 mice. The resultant impairment of M1 ipRGCs contributed to the early degeneration of the ipRGC-SCN pathway and the circadian abnormality during HD progression.

Revisiting La0.5Sr1.5MnO4 lattice distortion and charge ordering with multi-beam resonant diffraction.

Sinusoidal wave type distortions of La0.5Sr1.5MnO4 in the low-temperature orthorhombic phase were observed using multi-beam resonant X-ray diffraction (MRXD) with (7/4 7/4 0) fractional primary diffraction. Two four-beam diffractions with opposite asymmetry were measured at 6.5545 keV and compared with the curves simulated by the dynamical X-ray diffraction theory. This approach provides the possibility of resolving the distortion modes which are perpendicular to the momentum transfer by a single azimuthal scan. The paper also demonstrates the sensitivity of MRXD profiles versus incident X-ray energy in the vicinity of the Mn K edge to the charge disproportion between the two manganese sites, reconfirming the small charge disproportion feature.

Temperature- and energy-dependent phase shifts of resonant multiple-beam X-ray diffraction in germanium crystals.

This paper reports temperature- and energy-dependent phase shifts of resonant multiple-beam X-ray diffraction in germanium crystals, involving forbidden (002) and weak (222) reflections. Phase determination based on multiple-beam diffraction is employed to estimate phase shifts from (002)-based {(002)(375)(373̅)} four-beam cases and (222)-based { (222)(5̅33̅)} three-beam cases in the vicinity of the Ge K edge for temperatures from 20 K up to 300 K. The forbidden/weak reflections enhance the sensitivity of measuring phases at resonance. At room temperature, the resonance triplet phases reach a maximum of 8° for the four-beam cases and -19° for the three-beam cases. It is found that the peak intensities and triplet phases obtained from the (002) four-beam diffraction are related to thermal motion induced anisotropy and anomalous dispersion, while the (222) three-beam diffraction depends on the aspherical covalent electron distribution and anomalous dispersion. However, the electron-phonon interaction usually affects the forbidden reflections with increasing temperatures and seems to have less effect on the resonance triplet phase shifts measured from the (002) four-beam diffraction. The resonance triplet phase shifts of the (222) three-beam diffraction versus temperature are also small.