Optical information hiding for different surface images.

Optical hiding often requires the selection of specific artificial optical components as carriers, which results in poor versatility of the carriers and high costs for the hiding system. To conceal secret information on different surfaces such as metal, wood, and paper, we propose an optical information hiding method. In this method, we use images of surfaces, whose grayscale histograms have the characteristic of symmetric distribution. Based on this characteristic, we first scramble the surface image, and then adjust part of the gray value of the surface image to the complementary value to embed the secret information into a scrambled surface image to generate a key image. In the extraction process, a projector is used to reproduce the scrambled surface image and the key image, which are then incoherently superimposed to extract the secret information using the human visual system. The extraction process does not require complex optical knowledge and is simple and feasible. Simulation experiments and optical experiments indicate that this method is applicable in practice and possesses good security and imperceptibility. Furthermore, we prove the reliability of this method by embedding secret information in different surface images, demonstrating the potential application of more surface images in the field of optical information hiding. Finally, we discuss the applicability of surface information images and analyze the imperceptibility of key images.

Role of TRP Channels in Metabolism-Related Diseases.

Metabolic syndrome (MetS), with its high prevalence and significant impact on cardiovascular disease, poses a substantial threat to human health. The early identification of pathological abnormalities related to MetS and prevention of the risk of associated diseases is of paramount importance. Transient Receptor Potential (TRP) channels, a type of nonselective cation channel, are expressed in a variety of tissues and have been implicated in the onset and progression of numerous metabolism-related diseases. This study aims to review and discuss the expression and function of TRP channels in metabolism-related tissues and blood vessels, and to elucidate the interactions and mechanisms between TRP channels and metabolism-related diseases. A comprehensive literature search was conducted using keywords such as TRP channels, metabolic syndrome, pancreas, liver, oxidative stress, diabetes, hypertension, and atherosclerosis across various academic databases including PubMed, Google Scholar, Elsevier, Web of Science, and CNKI. Our review of the current research suggests that TRP channels may be involved in the development of metabolism-related diseases by regulating insulin secretion and release, lipid metabolism, vascular functional activity, oxidative stress, and inflammatory response. TRP channels, as nonselective cation channels, play pivotal roles in sensing various intra- and extracellular stimuli and regulating ion homeostasis by osmosis. They present potential new targets for the diagnosis or treatment of metabolism-related diseases.

Risk factors of non-sentinel lymph node metastasis in breast cancer with 1-2 sentinel lymph node macrometastases underwent total mastectomy: a case-control study.

BACKGROUND: The randomized trials which include ACOSOG Z0011 and IBCSG 23-01 had found that the survival rates were not different in patients with cT1/2N0 and 1-2 sentinel lymph node (SLN)-positive, macro/micrometastases who underwent breast-conserving therapy, and micrometastases who underwent total mastectomy (TM), when axillary lymph node dissection (ALND) was omitted. However, for patients with cT1/2N0 and 1-2 SLN macrometastases who underwent TM; there was still insufficient evidence from clinical studies to support whether ALND can be exempted. This study aimed to investigate the risk factors of non-sentinel lymph node (nSLN) metastasis in breast cancer patients with 1-2 SLN macrometastases undergoing TM. METHODS: The clinicopathological data of 1491 breast cancer patients who underwent TM and SLNB from January 2017 to February 2022 were retrospectively analyzed. Univariate and multivariate analyses were performed to analyze the risk factors for nSLN metastasis. RESULTS: A total of 273 patients with 1-2 SLN macrometastases who underwent TM were enrolled. Postoperative pathological data showed that 35.2% patients had nSLN metastasis. The results of multivariate analysis indicated that tumor size (TS) (P = 0.002; OR: 1.051; 95% CI: 1.019-1.084) and ratio of SLN macrometastases (P = 0.0001; OR: 12.597: 95% CI: 4.302-36.890) were the independent risk factors for nSLN metastasis in breast cancer patients with 1-2 SLN macrometastases that underwent TM. The ROC curve analysis suggested that when TS ≤22 mm and ratio of SLN macrometastases ≤0.33, the incidence of nSLN metastasis could be reduced to 17.1%. CONCLUSIONS: The breast cancer patients with cT1/2N0 stage, undergoing TM and 1-2 SLN macrometastases, when the TS ≤22 mm and macrometastatic SLN does not exceed 1/3 of the total number of detected SLN, the incidence of nSLN metastasis is significantly reduced, but whether ALND can be exempted needs further exploration.

Impaired learning and memory generated by hyperthyroidism is rescued by restoration of AMPA and NMDA receptors function.

Hyperthyroidism has been identified as a risk factor for cognitive disorders. The hippocampus is a key brain region associated with cognitive function, among which excitatory synapse transmission plays an important role in the process of learning and memory. However, the mechanism by which hyperthyroidism leads to cognitive dysfunction through a synaptic mechanism remains unknown. We investigated the synaptic mechanisms in the effects of hyperthyroidism in an animal model that involved repeated injection of triiodothyronine (T3). These mice displayed impaired learning and memory in the Novel object recognition test, Y-maze test, and Morris Water Maze test, as well as elevated anxiety in the elevated plus maze. Mature dendritic spines in the hippocampal CA1 region of hyperthyroid mice were significantly decreased, accompanied by decreased level of AMPA- and NMDA-type glutamate receptors in the hippocampus. In primary cultured hippocampal neurons, levels of AMPA- and NMDA-type glutamate receptors also decreased and whole-cell patch-clamp recording revealed that excitatory synaptic function was obviously attenuated after T3 treatment. Notably, pharmacological activation of AMPAR or NMDAR by intraperitoneal injection of CX546, an AMPAR agonist, or NMDA, an NMDAR agonist can restore excitatory synaptic function and corrected impaired learning and memory deficit in hyperthyroid mice. Together, our findings uncovered a previously unrecognized AMPAR and NMDAR-dependent mechanism involved in regulating hippocampal excitatory synaptic transmission and learning and memory disorders in hyperthyroidism.

A novel model of home-based, patient-tailored and mobile application-guided cardiac telerehabilitation in patients with atrial fibrillation: A randomised controlled trial.

OBJECTIVE: To assess the effectiveness of tele-monitored cardiac rehabilitation in patients who have undergone ablation for atrial fibrillation. DESIGN: Single-centre, prospective, assessment-blinded, randomised controlled trial. SETTING: Domiciliary rehabilitation with support from a tertiary care hospital. SUBJECTS: One hundred patients who underwent ablation for atrial fibrillation were recruited. INTERVENTIONS: Participants were randomly allocated to a 12-week standard rehabilitation treatment (control group) or a comprehensive, domiciliary, mobile application-guided and tele-monitored cardiac rehabilitation program (intervention group) in a 1:1 fashion. MAIN OUTCOME MEASURES: The primary endpoint was the improvement in VO2peak. The secondary outcomes included adherence, physical activity, beliefs related to cardiovascular disease and exercise self-efficacy. RESULTS: Ninety-seven patients completed follow-up. The mean VO2peak increased significantly in both the intervention group (n = 49) (baseline vs 12 weeks: 19.1 ± 4.7 vs 27.3 ± 5.6 ml/(min kg), P < 0.01) and the control group (n = 48) (baseline vs 12 weeks: 18.7 ± 4.9 vs 22.9 ± 6.3 ml/(min kg), P < 0.01). The results of the between-group analysis of aerobic capacity were significantly in favour of the intervention group. During the 12-week program, patients in the intervention group exhibited better adherence than those in the control group. Moreover, self-reported physical activity improved more in the intervention group than in the control group, as did the beliefs related to cardiovascular disease and exercise self-efficacy (all P < 0.01). CONCLUSIONS: Our domiciliary, mobile application-guided and tele-monitored cardiac rehabilitation program could lead to a more significant improvements in physical fitness, adherence and health beliefs than standard cardiac rehabilitation in patients who have undergone ablation for atrial fibrillation.

Structural Investigation of the Interaction Mechanism between Chlorogenic Acid and AMPA Receptor via In Silico Approaches.

Chlorogenic acid (CGA), an important metabolite in natural plant medicines such as honeysuckle and eucommia, has been shown to have potent antinociceptive effects. Nevertheless, the mechanism by which CGA relieves chronic pain remains unclear. α-amino-3-hydroxy-5-methyl-4-isooxazolpropionic acid receptor (AMPAR) is a major ionotropic glutamate receptor that mediates rapid excitatory synaptic transmission and its glutamate ionotropic receptor AMPA type subunit 1 (GluA1) plays a key role in nociceptive transmission. In this study, we used Western blot, surface plasmon resonance (SPR) assay, and the molecular simulation technologies to investigate the mechanism of interaction between CGA and AMPAR to relieve chronic pain. Our results indicate that the protein expression level of GluA1 showed a dependent decrease as the concentration of CGA increased (0, 50, 100, and 200 µM). The SPR assay demonstrates that CGA can directly bind to GluA1 (KD = 496 µM). Furthermore, CGA forms a stable binding interaction with GluA1, which is validated by molecular dynamics (MD) simulation. The binding free energy between CGA and GluA1 is -39.803 ± 14.772 kJ/mol, where van der Waals interaction and electrostatic interaction are the major contributors to the GluA1-CGA binding, and the key residues are identified (Val-32, Glu-33, Ala-36, Glu-37, Leu-48), which play a crucial role in the binding interaction. This study first reveals the structural basis of the stable interaction between CGA and GluA1 to form a binding complex for the relief of chronic pain. The research provides the structural basis to understand the treatment of chronic pain and is valuable to the design of novel drug molecules in the future.

CRMP4 and CRMP2 Interact to Coordinate Cytoskeleton Dynamics, Regulating Growth Cone Development and Axon Elongation.

Cytoskeleton dynamics are critical phenomena that underpin many fundamental cellular processes. Collapsin response mediator proteins (CRMPs) are highly expressed in the developing nervous system, mediating growth cone guidance, neuronal polarity, and axonal elongation. However, whether and how CRMPs associate with microtubules and actin coordinated cytoskeletal dynamics remain unknown. In this study, we demonstrated that CRMP2 and CRMP4 interacted with tubulin and actin in vitro and colocalized with the cytoskeleton in the transition-zone in developing growth cones. CRMP2 and CRMP4 also interacted with one another coordinately to promote growth cone development and axonal elongation. Genetic silencing of CRMP2 enhanced, whereas overexpression of CRMP2 suppressed, the inhibitory effects of CRMP4 knockdown on axonal development. In addition, knockdown of CRMP2 or overexpression of truncated CRMP2 reversed the promoting effect of CRMP4. With the overexpression of truncated CRMP2 or CRMP4 lacking the cytoskeleton interaction domain, the promoting effect of CRMP was suppressed. These data suggest a model in which CRMP2 and CRMP4 form complexes to bridge microtubules and actin and thus work cooperatively to regulate growth cone development and axonal elongation.

Incorporation of beta-sitosterol into the membrane increases resistance to oxidative stress and lipid peroxidation via estrogen receptor-mediated PI3K/GSK3beta signaling.

BACKGROUND: Brain lipid peroxidation has long been considered a potential therapeutic target for Alzheimer's disease (AD). beta-sitosterol (BS), a plant sterol that is prevalent in plant plasma membrane, has been suggested to have antioxidant activity. Previous studies have demonstrated that dietary BS can enter the brain and accumulates in the plasma membrane of brain cells. However, it is unknown whether and how BS exerts its antioxidant activity in plasma membrane. METHODS: To incorporate BS into the plasma membrane in vitro, HT22 cells and primarily cultured hippocampal cells were supplemented with BS using 2-hydroxypropyl-beta-cyclodextrin (HPbetaCD) as a carrier. The present study then tested the antioxidant effect of membrane BS against glucose oxidase (GOX)-induced oxidative stress and lipid peroxidation, and whether the antioxidant effect of membrane BS was associated with estrogen receptor (ER)-mediated phosphatidyl inositol 3-kinase (PL3K)/glycogen synthase kinase 3 (GSK3beta) signaling. RESULTS: Incorporation of BS into cell membrane prevented GOX-induced oxidative stress and lipid peroxidation, which could be suppressed by the ER antagonists and PI3K inhibitor. Additional experiments showed that incorporation of BS into cell membrane induced an up-regulation of PI3K activity and a recruitment of PI3K to lipid rafts, which could be inhibited by the ER antagonist. Membrane BS also increased the expression of p-GSK3beta, which could be suppressed in the presence of the ER antagonist and PI3K inhibitor. GENERAL SIGNIFICANCE: Given that BS is prevalent in foods such as plant oil, the results provide a better understanding of the beneficial effects of these BS-enriched nutrients on neurodegenerative diseases such as AD.

Genetic and immune identification and functional analysis of TRPM8 as a potential biomarker for pancreatic adenocarcinoma proliferation.

BACKGROUND: Pancreatic adenocarcinoma (PAAD), a member of highly lethal malignant tumors, has a poor outcome and extremely poor prognosis. The transient receptor potential (TRP) superfamily, a group of nonselective cation channels, is capable of influencing cellular functions by regulating calcium homeostasis. In addition, it has been shown that TRP channels can also affect various cellular phenotypes by regulating gene transcription levels and are involved in the development of a variety of malignant tumors. AIMS: In order to find new therapeutic targets and biomarkers to improve the clinical prognosis of pancreatic cancer, we performed genetic and immunological characterization of TRP channels in PAAD, as well as related functional and prognostic analyses. METHODS AND RESULTS: We investigated the expression, genetic alterations, methylation levels, and immune infiltration levels of TRP channels in PAAD, and further also analyzed the function of TRP channels in PAAD and their prognostic value for PAAD patients. Our results suggest that TRPM8 may contribute to tumor proliferation by controlling the PI3K-AKT-mTOR signaling pathway in PAAD. CONCLUSION: After careful evaluation of the accumulated data, we concluded that TRPM8 has potential as a prognostic indicator and prospective therapeutic target in PAAD.

Ultrastructure and Spectral Characteristics of the Compound Eye of Asiophrida xanthospilota (Baly, 1881) (Coleoptera, Chrysomelidae).

In this study, the morphology and ultrastructure of the compound eye of Asi. xanthospilota were examined by using scanning electron microscopy (SEM), transmission electron microscopy (TEM), micro-computed tomography (µCT), and 3D reconstruction. Spectral sensitivity was investigated by electroretinogram (ERG) tests and phototropism experiments. The compound eye of Asi. xanthospilota is of the apposition type, consisting of 611.00 ± 17.53 ommatidia in males and 634.8 0 ± 24.73 ommatidia in females. Each ommatidium is composed of a subplano-convex cornea, an acone consisting of four cone cells, eight retinular cells along with the rhabdom, two primary pigment cells, and about 23 secondary pigment cells. The open type of rhabdom in Asi. xanthospilota consists of six peripheral rhabdomeres contributed by the six peripheral retinular cells (R1~R6) and two distally attached rhabdomeric segments generated solely by R7, while R8 do not contribute to the rhabdom. The orientation of microvilli indicates that Asi. xanthospilota is unlikely to be a polarization-sensitive species. ERG testing showed that both males and females reacted to stimuli from red, yellow, green, blue, and ultraviolet light. Both males and females exhibited strong responses to blue and green light but weak responses to red light. The phototropism experiments showed that both males and females exhibited positive phototaxis to all five lights, with blue light significantly stronger than the others.

Lateral hypothalamus orexinergic projection to the medial prefrontal cortex modulates chronic stress-induced anhedonia but not anxiety and despair.

Chronic stress-induced anxiodepression is a common health problem, however its potential neurocircuitry mechanism remains unclear. We used behavioral, patch-clamp electrophysiology, chemogenetic, and optogenetic approaches to clarify the response of the lateral hypothalamus (LH) and the medial prefrontal cortex (mPFC) to stress, confirmed the structural connections between the LH and mPFC, and investigated the role of the LH-mPFC pathway in chronic stress-induced anxiodepression symptoms. Unpredictable chronic mild stress (UCMS) caused anxiodepression-like behaviors, including anxiety, anhedonia, and despair behaviors. We discovered that the activity of the LH and mPFC was both increased after restraint stress (RS), a stressor of UCMS. Then we found that the orexinergic neurons in the LH predominantly project to the glutamatergic neurons in the mPFC, and the excitability of these neurons were increased after UCMS. In addition, overactivated LH orexinergic terminals in the mPFC induced anhedonia but not anxiety and despair behaviors in naive mice. Moreover, chemogenetically inhibited LH-mPFC orexinergic projection neurons and blocked the orexin receptors in the mPFC alleviated anhedonia but not anxiety and despair behaviors in UCMS-treated mice. Our study identified a new neurocircuit from LH orexinergic neurons to mPFC and revealed its role in regulating anhedonia in response to stress. Overactivation of LHOrx-mPFC pathway selectively mediated chronic stress-induced anhedonia. In normal mice, the LHOrx-mPFC pathway exhibits relatively low activity. However, after chronic stress, the activity of orexinergic neuron in LH is overactivated, leading to an increased release of orexin into the mPFC. This heightened orexin concentration results in increased excitability of the mPFC through OX1R and OX2R, consequently triggering anhedonia.

Hyperexcitation of the glutamatergic neurons in lateral hypothalamus induced by chronic pain contributes to depression-like behavior and learning and memory impairment in male mice.

Chronic pain can induce mood disorders and cognitive dysfunctions, such as anxiety, depression, and learning and memory impairment in humans. However, the specific neural network involved in anxiety- and depression-like behaviors and learning and memory impairment caused by chronic pain remains poorly understood. In this study, behavioral test results showed that chronic pain induced anxiety- and depression-like behaviors, and learning and memory impairment in male mice. c-Fos immunofluorescence and fiber photometry recording showed that glutamatergic neurons in the LH of mice with chronic pain were selectively activated. Next, the glutamatergic neurons of LH in normal mice were activated using optogenetic and chemogenetic methods, which recapitulates some of the depressive-like behaviors, as well as memory impairment, but not anxiety-like behavior. Finally, inhibition of glutamatergic neurons in the LH of mice with chronic pain, effectively relieved anxiety- and depression-like behaviors and learning and memory impairment. Taken together, our findings suggest that hyperexcitation of glutamatergic neurons in the LH is involved in depression-like behavior and learning and memory impairment induced by chronic pain.

High-quality reference genome of cowpea beetle Callosobruchus maculatus.

Callosobruchus maculatus is one of the most competitive stored grain pests, which causes a great loss to agricultural economy. However, due to an inadequacy of high-quality reference genome, the molecular mechanisms for olfactory and hypoxic adaptations to stored environments are unknown and require to be revealed urgently, which will contribute to the detection and prevention of the invasive pests C. maculatus. Here, we presented a high-quality chromosome-level genome of C. maculatus based on Illumina, Nanopore and Hi-C sequencing data. The total size was 1.2 Gb, and 65.17% (797.47 Mb) of it was identified to be repeat sequences. Among assembled chromosomes, chromosome 10 was considered the X chromosome according to the evidence of reads coverage and homologous genes among species. The current version of high-quality genome provides preferable data resources for the adaptive evolution research of C. maculatus.

Ginsenoside Rg1 promotes nonamyloidgenic cleavage of APP via estrogen receptor signaling to MAPK/ERK and PI3K/Akt.

BACKGROUND: The pathogenic accumulation of amyloid ß peptide (Aß), a natural occurring peptide processed from beta-amyloid precursor protein (APP), is considered to play a key role in the development of Alzheimer's disease (AD). Ginsenoside Rg1, an active component in ginseng, has been identified as a phytoestrogen and also found to be neuroprotective. However, it is unknown whether Rg1-induced estrogenic activity intervenes in APP processing, and improves memory performance. METHODS: Using HT22 cells and SH-SY5Y cells stably expressing the Swedish mutant APP (APPsw), this study investigated whether Rg1 intervened in APP metabolism through estrogenic activity. Using the ovariectomized (OVX) rats to mimic age-related changes in postmenopausal females, this study also tested the long-term effect of Rg1 on APP metabolism. RESULTS: The in vitro study demonstrated that Rg1 increased extracellular secretion of soluble amyloid precursor protein α (sAPPα), enhanced α-secretase activity and decreased extracellular release of Aß. These effects of Rg1 could be prevented by inhibitors of protein kinase C (PKC), Extracellular-Signal Regulated Kinase/Mitogen-Activated Protein Kinase (ERK/MAPK) and Phosphoinositide-3 kinase (PI3K)/Akt pathways. Inhibition of endogenous estrogen receptor (ER) activity abrogated Rg1-triggered release of sAPPα, increase of α-secretase activity, and activation of ERK and Akt signaling. In addition, Rg1 promoted phosphorylation of ERα at Ser118 residue. The in vivo study demonstrated that 8-week Rg1 treatment of OVX rats increased sAPPα levels and decreased Aß content in the hippocampi, and improved the spatial learning and memory. GENERAL SIGNIFICANCE: Rg1 might be used to slow or prevent AD, in particular in postmenopausal females.

Incorporation of ß-sitosterol into mitochondrial membrane enhances mitochondrial function by promoting inner mitochondrial membrane fluidity.

Recent findings suggest that mitochondrial membrane fluidity could influence mitochondrial energy metabolism. ß-sitosterol (BS) is a common plant sterol that is prevalent in plant oils, nuts, cereals and plant food products. Its chemical structure is very similar to that of cholesterol. As a cholesterol analog, BS is highly lipid soluble and largely resides in the membranes of cells or organelles where it may have an influence on the membrane fluidity. The present study reports that, with the cholesterol chelator 2-hydroxypropyl-ß-cyclodextrin (HPßCD) as its carrier, BS is able to increase the fluidity of the inner mitochondrial membrane (IMM) without affecting the fluidity of the outer mitochondrial membrane (OMM), and consequently to increase the mitochondrial membrane potential (∆Ψm) and mitochondrial ATP content. It has been previously proposed that a therapeutical boost in adenosine triphosphate (ATP) levels in mitochondria may be beneficial for neurodegenerative diseases such as Alzheimer's disease (AD). Given that dietary administration of plant sterols could increase brain BS concentrations, these results may provide a better understanding of the beneficial effects of plant sterol-enriched nutrients on neurodegenerative diseases such as AD.

Function of TRPC1 in modulating hepatocellular carcinoma progression.

The liver is the main organ of metabolism in the human body, and it is easy to suffer from hepatitis, cirrhosis, liver cancer, and other diseases, the most serious of which is liver cancer. Worldwide, liver cancer is the most common and deadly malignant tumor, the third leading cause of cancer death in the world. Based on TCGA and ICGC databases, our research discovered the important role of TRPC1 in liver cancer through bioinformatics. The results showed that TRPC1 was over-expressed in hepatocellular carcinoma, and the higher the expression level of TRPC1, the worse the OS and the lower the survival rate. TRPC1 was a risk factor affecting the overall survival probability of hepatocellular carcinoma patients. By analyzing the function of the TRP family in liver cancer, TRPC1 might promote the occurrence of liver cancer by up-regulating common signal pathways in tumors such as tumor proliferation signature, and down-regulating important metabolic reactions such as retinol metabolism. In addition, TRPC1 could promote the development of liver cancer by up-regulating the expression of ABI2, MAPRE1, YEATS2, MTA3, TMEM237, MTMR2, CCDC6, AC069544.2, and NCBP2 genes. These results illustrate that TRPC1 is very valuable in the study of liver cancer.

Effects of lithium on aggression in Drosophila.

Lithium is a common medication used to treat mania and bipolar disorder, but the mechanisms by which lithium stabilizes mood and modifies aggression are still not fully understood. Here we found that acute but not chronic lithium significantly suppresses aggression without affecting locomotion in Drosophila melanogaster. Male flies treated with acute lithium are also less competitive than control males in establishing dominance. We also provided evidence that glycogen synthase kinase-3 (GSK-3), a well-known target of lithium, plays an important role in the anti-aggressive effect of lithium in Drosophila. Our genetic data showed that acute knockdown of GSK-3 in neurons can mimic the inhibitory effect of acute lithium on aggression, while specific overexpression of GSK-3 in a subset of P1 neurons profoundly promotes aggression which can be partially rescued by acute lithium application. Thus, these findings revealed the inhibitory effect of lithium on aggression in Drosophila and laid a groundwork for using Drosophila as a powerful model to investigate the mechanisms by which lithium reduces aggression.

A Neural Circuit Controlling Virgin Female Aggression Induced by Mating-related Cues in Drosophila.

Females increase aggression for mating opportunities and for acquiring reproductive resources. Although the close relationship between female aggression and mating status is widely appreciated, whether and how female aggression is regulated by mating-related cues remains poorly understood. Here we report an interesting observation that Drosophila virgin females initiate high-frequency attacks toward mated females. We identify 11-cis-vaccenyl acetate (cVA), a male-derived pheromone transferred to females during mating, which promotes virgin female aggression. We subsequently reveal a cVA-responsive neural circuit consisting of four orders of neurons, including Or67d, DA1, aSP-g, and pC1 neurons, that mediate cVA-induced virgin female aggression. We also determine that aSP-g neurons release acetylcholine (ACh) to excite pC1 neurons via the nicotinic ACh receptor nAChRα7. Together, beyond revealing cVA as a mating-related inducer of virgin female aggression, our results identify a neural circuit linking the chemosensory perception of mating-related cues to aggressive behavior in Drosophila females.

A neurotransmitter histamine mediating phototransduction and photopreference in Callosobruchus maculatus.

BACKGROUND: The biogenic amine histamine plays a critical role in the phototransduction and photopreference of most insects. Here, we study the function of histamine in Callosobruchus maculatus, a global storage pest. RESULTS: In our experiment, we initially identified the histidine decarboxylase (hdc) gene through bioinformation analysis. We subsequently investigated effects of hdc and histamine on the photopreference of C. maculatus using a combination of RNA interference (RNAi), electroretinograms (ERG), immunostaining, and photopreference behavior approaches. Our results showed that histamine was required for visual signal transduction of C. maculatus, and increased its photopreference regardless of the wavelength. CONCLUSION: This is the first study analyzing the molecular characteristics of C. maculatus photopreference, which forms the basis for a molecular mechanism for the effects of histamine on its visual transduction and preference. In practice, better understanding the photopreference patterns contributes to IPM (integrated pest management) for this storage pest. © 2023 Society of Chemical Industry.

Neural circuit mechanisms linking courtship and reward in Drosophila males.

Courtship has evolved to achieve reproductive success in animal species. However, whether courtship itself has a positive value remains unclear. In the present work, we report that courtship is innately rewarding and can induce the expression of appetitive short-term memory (STM) and long-term memory (LTM) in Drosophila melanogaster males. Activation of male-specific P1 neurons is sufficient to mimic courtship-induced preference and memory performance. Surprisingly, P1 neurons functionally connect to a large proportion of dopaminergic neurons (DANs) in the protocerebral anterior medial (PAM) cluster. The acquisition of STM and LTM depends on two distinct subsets of PAM DANs that convey the courtship-reward signal to the restricted regions of the mushroom body (MB) γ and α/ß lobes through two dopamine receptors, D1-like Dop1R1 and D2-like Dop2R. Furthermore, the retrieval of STM stored in the MB α'/ß' lobes and LTM stored in the MB α/ß lobe relies on two distinct MB output neurons. Finally, LTM consolidation requires two subsets of PAM DANs projecting to the MB α/ß lobe and corresponding MB output neurons. Taken together, our findings demonstrate that courtship is a potent rewarding stimulus and reveal the underlying neural circuit mechanisms linking courtship and reward in Drosophila males.