scholarly journals Neural and Hormonal Basis of Opposite-Sex Preference by Chemosensory Signals

2021 ◽  
Vol 22 (15) ◽  
pp. 8311
Author(s):  
Yasuhiko Kondo ◽  
Himeka Hayashi

In mammalian reproduction, sexually active males seek female conspecifics, while estrous females try to approach males. This sex-specific response tendency is called sexual preference. In small rodents, sexual preference cues are mainly chemosensory signals, including pheromones. In this article, we review the physiological mechanisms involved in sexual preference for opposite-sex chemosensory signals in well-studied laboratory rodents, mice, rats, and hamsters of both sexes, especially an overview of peripheral sensory receptors, and hormonal and central regulation. In the hormonal regulation section, we discuss potential rodent brain bisexuality, as it includes neural substrates controlling both masculine and feminine sexual preferences, i.e., masculine preference for female odors and the opposite. In the central regulation section, we show the substantial circuit regulating sexual preference and also the influence of sexual experience that innate attractants activate in the brain reward system to establish the learned attractant. Finally, we review the regulation of sexual preference by neuropeptides, oxytocin, vasopressin, and kisspeptin. Through this review, we clarified the contradictions and deficiencies in our current knowledge on the neuroendocrine regulation of sexual preference and sought to present problems requiring further study.

Genes ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 301
Author(s):  
Vishesh Kumar ◽  
Priyanka Jain ◽  
Sureshkumar Venkadesan ◽  
Suhas Gorakh Karkute ◽  
Jyotika Bhati ◽  
...  

Rice blast is a global threat to food security with up to 50% yield losses. Panicle blast is a more severe form of rice blast and the response of rice plant to leaf and panicle blast is distinct in different genotypes. To understand the specific response of rice in panicle blast, transcriptome analysis of blast resistant cultivar Tetep, and susceptible cultivar HP2216 was carried out using RNA-Seq approach after 48, 72 and 96 h of infection with Magnaporthe oryzae along with mock inoculation. Transcriptome data analysis of infected panicle tissues revealed that 3553 genes differentially expressed in HP2216 and 2491 genes in Tetep, which must be the responsible factor behind the differential disease response. The defense responsive genes are involved mainly in defense pathways namely, hormonal regulation, synthesis of reactive oxygen species, secondary metabolites and cell wall modification. The common differentially expressed genes in both the cultivars were defense responsive transcription factors, NBS-LRR genes, kinases, pathogenesis related genes and peroxidases. In Tetep, cell wall strengthening pathway represented by PMR5, dirigent, tubulin, cell wall proteins, chitinases, and proteases was found to be specifically enriched. Additionally, many novel genes having DOMON, VWF, and PCaP1 domains which are specific to cell membrane were highly expressed only in Tetep post infection, suggesting their role in panicle blast resistance. Thus, our study shows that panicle blast resistance is a complex phenomenon contributed by early defense response through ROS production and detoxification, MAPK and LRR signaling, accumulation of antimicrobial compounds and secondary metabolites, and cell wall strengthening to prevent the entry and spread of the fungi. The present investigation provided valuable candidate genes that can unravel the mechanisms of panicle blast resistance and help in the rice blast breeding program.


2021 ◽  
Vol 12 ◽  
Author(s):  
Francesca Copperi ◽  
Jung Dae Kim ◽  
Sabrina Diano

Increasing evidence indicates that the melanocortin system is not only a central player in energy homeostasis, food intake and glucose level regulation, but also in the modulation of cardiovascular functions, such as blood pressure and heart rate. The melanocortins, and in particular α- and γ-MSH, have been shown to exert their cardiovascular activity both at the central nervous system level and in the periphery (e.g., in the adrenal gland), binding their receptors MC3R and MC4R and influencing the activity of the sympathetic nervous system. In addition, some studies have shown that the activation of MC3R and MC4R by their endogenous ligands is able to improve the outcome of cardiovascular diseases, such as myocardial and cerebral ischemia. In this brief review, we will discuss the current knowledge of how the melanocortin system influences essential cardiovascular functions, such as blood pressure and heart rate, and its protective role in ischemic events, with a particular focus on the central regulation of such mechanisms.


2019 ◽  
Vol 709 ◽  
pp. 134389
Author(s):  
Hesun Erin Kim ◽  
Yeon-Ju Hong ◽  
Sunghyon Kyeong ◽  
Jae-Jin Kim

2013 ◽  
Vol 2013 ◽  
pp. 1-28 ◽  
Author(s):  
Pablo R. Brumovsky

Vesicular glutamate transporters (VGLUTs) are key molecules for the incorporation of glutamate in synaptic vesicles across the nervous system, and since their discovery in the early 1990s, research on these transporters has been intense and productive. This review will focus on several aspects of VGLUTs research on neurons in the periphery and the spinal cord. Firstly, it will begin with a historical account on the evolution of the morphological analysis of glutamatergic systems and the pivotal role played by the discovery of VGLUTs. Secondly, and in order to provide an appropriate framework, there will be a synthetic description of the neuroanatomy and neurochemistry of peripheral neurons and the spinal cord. This will be followed by a succinct description of the current knowledge on the expression of VGLUTs in peripheral sensory and autonomic neurons and neurons in the spinal cord. Finally, this review will address the modulation of VGLUTs expression after nerve and tissue insult, their physiological relevance in relation to sensation, pain, and neuroprotection, and their potential pharmacological usefulness.


2006 ◽  
Vol 39 (4) ◽  
pp. 361-396 ◽  
Author(s):  
Tamir Gonen ◽  
Thomas Walz

1. Introduction 3621.1 The elusive water pores 3621.2 CHIP28 3622. Studies on AQP-1 3632.1 Expression of AQP1 cDNA in Xenopus oocytes 3632.2 Reconstitution of purified AQP1 into artificial lipid bilayers 3642.3 Structural information deduced from the primary sequence 3652.4 Evolution and mammalian AQPs 3653. Chronological overview over AQP structures 3683.1 AQP1 – the red blood cell water pore 3683.2 GlpF – the E. coli glycerol facilitator 3713.3 AQPZ – the E. coli water pore 3723.4 AQP0 – the lens-specific aquaporin 3733.5 AQP4 – the main aquaporin in brain 3773.6 SoPiP2;1 – a plant aquaporin 3793.7 AQPM – an archaeabacterial aquaporin 3794. Proton exclusion 3805. Substrate selectivity 3826. Pore regulation 3856.1 Hormonal regulation of AQP trafficking 3856.2 Influence of pH on AQP water conduction 3866.3 Regulation of AQP pore conductance by protein binding 3876.4 Pore closure by conformational changes in the AQP0 pore 3887. Unresolved questions 3908. Acknowledgments 3909. References 391The ubiquitous members of the aquaporin (AQP) family form transmembrane pores that are either exclusive for water (aquaporins) or are also permeable for other small neutral solutes such as glycerol (aquaglyceroporins). The purpose of this review is to provide an overview of our current knowledge of AQP structures and to describe the structural features that define the function of these membrane pores. The review will discuss the mechanisms governing water conduction, proton exclusion and substrate specificity, and how the pore permeability is regulated in different members of the AQP family.


1990 ◽  
Vol 259 (6) ◽  
pp. L337-L344 ◽  
Author(s):  
I. Gross

The recent identification of the genes for the surfactant proteins has greatly facilitated the study of the regulation of fetal lung alveolar epithelial cell development at the molecular level. In general, expression of the genes for the surfactant proteins is enhanced by the same hormones that stimulate phospholipid synthesis. There are, however, some notable differences that indicate that the genes for the different components of surfactant are independently regulated. Species differences in the response of the surfactant proteins to hormones such as glucocorticoids and adenosine 3',5'-cyclic monophosphate have also been demonstrated. This review focuses on current knowledge of the hormonal regulation of the surfactant proteins against a background of previous studies of lung development.


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Alba Sansa ◽  
Ivan Hidalgo ◽  
Maria P. Miralles ◽  
Sandra de la Fuente ◽  
M. Jose Perez-Garcia ◽  
...  

AbstractSpinal muscular atrophy (SMA) is a neuromuscular genetic disease caused by reduced survival motor neuron (SMN) protein. SMN is ubiquitous and deficient levels cause spinal cord motoneurons (MNs) degeneration and muscle atrophy. Nevertheless, the mechanism by which SMN reduction in muscle contributes to SMA disease is not fully understood. Therefore, studies evaluating atrophy mechanisms in SMA muscles will contribute to strengthening current knowledge of the pathology. Here we propose to evaluate autophagy in SMA muscle, a pathway altered in myotube atrophy. We analized autophagy proteins and mTOR in muscle biopsies, fibroblasts, and lymphoblast cell lines from SMA patients and in gastrocnemius muscles from a severe SMA mouse model. Human MNs differentiated from SMA and unaffected control iPSCs were also included in the analysis of the autophagy. Muscle biopsies, fibroblasts, and lymphoblast cell lines from SMA patients showed reduction of the autophagy marker LC3-II. In SMA mouse gastrocnemius, we observed lower levels of LC3-II, Beclin 1, and p62/SQSTM1 proteins at pre-symptomatic stage. mTOR phosphorylation at Ser2448 was decreased in SMA muscle cells. However, in mouse and human cultured SMA MNs mTOR phosphorylation and LC3-II levels were increased. These results suggest a differential regulation in SMA of the autophagy process in muscle cells and MNs. Opposite changes in autophagy proteins and mTOR phosphorylation between muscle cells and neurons were observed. These differences may reflect a specific response to SMN reduction, which could imply diverse tissue-dependent reactions to therapies that should be taken into account when treating SMA patients.


2019 ◽  
Author(s):  
E. M Loizidou ◽  
A. Kucherenko ◽  
P. Tatarskyy ◽  
S. Chernushyn ◽  
G. Livshyts ◽  
...  

AbstractRecurrent pregnancy loss (RPL) affects nearly 5% of the women of reproductive age. Its heterogeneous and multifactorial nature complicate both diagnosis and treatment, as well as identification of the genetic contribution to RPL. Evidence about the aetiology of RPL is controversial; however, several biological mechanisms have been proposed. Given the current knowledge about the genetic susceptibility to idiopathic RPL, we aimed to evaluate the predictive ability of a combined variant panel to the risk of RPL in the Ukrainian sample of 114 cases and 106 healthy controls. We genotyped variants within the 12 genetic loci reflecting the main biological pathways involved in pregnancy maintenance: blood coagulation (F2, F5, F7, GP1A), hormonal regulation (ESR1, ADRB2), endometrium and placental function (ENOS, ACE), folate metabolism (MTHFR) and inflammatory response (IL6, IL8, IL10). We showed that a genetic risk score (GRS) calculated from the 12 variants was associated with an increased risk of RPL (odds ratio 1.56, 95% CI: 1.21,2.04,P=8.7×10−4). The receiver operator characteristic (ROC) analysis resulted in the area under the curve (AUC) of 0.64 (95% CI: 0.57, 0.72), indicating an improved ability of the GRS to classify women with and without RPL. In summary, implementation of the GRS approach can help defining women at higher risk to complex multifactorial conditions such as RPL. Future well-powered genome-wide association studies will help in the dissection of biological pathways not hypothesised previously for RPL and further improve the prediction and identification of those at risk for RPL.


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