Oxytocin

Abstract

Social interactions are critical for well-being and survival. Oxytocin neurons in the paraventricular nucleus of the hypothalamus help regulate social behaviors in many species, and respond to social stimuli to promote pro-social interactions. Here, we show that chronic social isolation reduced production of oxytocin peptide, and led to a delay in the onset of huddling behavior upon resocialization in male mice. Exogenous oxytocin treatment prevented both the behavioral and molecular effects of social deprivation. Using conditional knockouts, we found that oxytocin-induced oxytocin expression was mediated by local hypothalamic astrocytes. Oxytocin signaling in astrocytes upregulated the expression of a retinoic acid-synthesizing enzyme Aldh1a1, and retinoic acid increased oxytocin expression. These findings reveal a mechanism in which astrocytes can sense and control neuropeptide levels to influence social behaviors.

Abstract

Circular RNAs (circRNAs) are stable epigenetic regulators of various biological processes, yet the functional role of ciR-02852 remains unknown. This study aimed to characterize the influence of ciR-02852 on the fundamental functions of porcine ovarian granulosa cells.

Abstract

Surge release of luteinizing hormone (LH) from the pituitary is essential for fertility, as it triggers ovulation. Secretoneurin (SN), a conserved peptide derived from secretogranin-2, stimulates LH release, but its relationship to periovulatory changes in classical reproductive hormones remains unclear.

Abstract

Neuropeptides represent a heterogeneous class of signalling molecules whose release has initially been described in the hypothalamus. Their release often follows a circadian rhythm and basal release may be enhanced by internal and external stressors. Research on the cellular actions of neuropeptides began in the hypothalamus but progressed to the entire brain following observations of neuropeptide and neuropeptide receptor expression throughout the brain. Recent research suggests that the prefrontal cortex (PFC) exhibits particularly high levels of neuropeptides and neuropeptide receptors suggesting that they may modulate cognitive processes necessary for executive function. However, most data on the cellular actions of neuropeptides are derived from non-cortical cells and their relevance to PFC-dependent behaviour is currently not understood. This review aims to bridge the gap between cellular and network actions of neuropeptides and their relevance to behaviour and mood disorders. Therefore, this review summarises the function of the PFC and highlights the effects of selected neuropeptides on cortical processing and PFC-dependent behavioural output. Where available, we compare the actions of neuropeptides in the rodent brain to the human brain and review potential therapeutic benefits of neuropeptides in PFC-dependent neuropsychiatric disorders.

Abstract

Evidence suggests a role for oxytocin in language development and cognitive functions in humans. However, there is a lack of research investigating the role of oxytocin in childhood-onset fluency disorder (stuttering). The aim of this study is to compare blood oxytocin levels between children diagnosed with stuttering and healthy controls.

Abstract

Vasopressin (VP) magnocellular neurosecretory neurons of the hypothalamic supraoptic nucleus (SON) are critical regulators of renal water retention and vascular tone. VP neurons undergo detrimental plastic changes in cardiovascular diseases such as heart failure (HF), resulting in hyperexcitability and thus altered fluid/electrolyte balance. A major intrinsic mechanism that regulates the firing activity of VP neurons is the slow afterhyperpolarization (sAHP), a phenomenon underlain by a calcium-dependent K+ current (IsAHP). The sAHP is activated by Ca2+ and results in an efflux of K+ from the cell, hyperpolarizing it and throttling firing. Importantly, we previously reported that a blunted sAHP contributes to hyperexcitability of VP neurons in heart failure rats. While the features of the sAHP are well characterized, the identity of the channel underlying the IsAHP remains unknown. Combining patch clamp electrophysiology, pharmacology and immunohistochemistry in Wistar rats, we investigated Intermediate conductance Ca2+-dependent K+ (IK) channels as a potential candidate responsible for carrying the IsAHP. We generated and measured the IsAHP in voltage clamp via 20 Hz trains of 20 square voltage pulses (from -50 to +10) once per minute. After 4 min of baseline recording, we bath applied TRAM-34 (1 μM), a specific IK channel blocker. Blocking IK with TRAM-34 failed to inhibit IsAHP peak amplitude, amplitude at 1 s after stimulus end, or area. Post hoc immunohistochemistry was performed to identify the phenotype of the recorded cell. We observed no inhibitory effect of TRAM-34 on the IsAHP in either VP or OT neurons. We also saw no inhibition of IsAHP (voltage clamp) or sAHP (current clamp) in slices preincubated in TRAM-34 for at least 1 h prior to recording. Conversely, we found that TRAM-34 inhibited isolated whole cell K+ currents, supporting the presence of functional, TRAM-34-sensitive IK channels in SON neurons. Taken together, our results indicate that despite the expression of IK in SON neurons and astrocytes, we observed no evidence of a significant contribution to the sAHP in either OT or VP SON neurons. Future studies will be needed to determine other potential K+ channel candidates contributing to the sAHP in SON neurons.

Abstract

The neuropeptide oxytocin (OT) plays a crucial role in regulating homeostatic responses and complex behaviors, including social interaction. OT can be released from somatodendritic regions, enabling communication through retrograde, autocrine, and volume transmission. However, the mechanisms governing somatodendritic OT dynamics and their impact on neuronal function and behavior are not yet fully understood. Our study identifies SNAP-47, a member of the SNAP-25 protein family highly expressed in the soma of peptidergic neurons in the mouse hypothalamus, where it exhibits a close interaction with OT-containing compartments localized at the plasma membrane. Knocking down SNAP-47 diminishes the recruitment of OT to the plasma membrane in the cell body under both basal conditions and following neuronal stimulation. Reducing endogenous SNAP-47 expression in vivo results in altered spontaneous synaptic transmission in oxytocinergic neurons of the paraventricular nucleus (PVN) and decreases sociability, likely due to disrupted somatic trafficking. These findings provide new insights into the molecular mechanisms governing somatic OT dynamics, its influence on hypothalamic neuromodulation, and its role in OT-dependent behaviors such as social interaction.

Abstract

Chronic pain remains a major clinical challenge, with current treatments often providing insufficient relief. Oxytocin, classically recognized for its roles in reproduction and social bonding, has gained increasing attention for its potential involvement in pain modulation. Evidence suggests that oxytocin influences both nociceptive processing and broader dimensions of pain, including stress regulation, cognitive-affective processing and social context. Despite this promise, clinical findings remain mixed. In this opinion paper, we summarize and discuss the rationale and current clinical evidence for the role of oxytocin in chronic pain (management), highlighting key research gaps and outlining future directions focused on: endogenous oxytocin system variability, biological modulators of its effects, dosing and timing strategies, and the role of psychosocial context. We propose that oxytocin should be reconceptualized not as a straightforward analgesic, but rather as a biopsychosocial adjuvant that acts across interacting biological, psychological, and social domains of pain. Positioning oxytocin within this framework may clarify for whom, when, and under what conditions oxytocin can be most effective, and ultimately guide its translational potential in chronic pain management.

Abstract

The paraventricular nucleus of the hypothalamus (PVN) orchestrates neuroendocrine and autonomic output to maintain systolic blood pressure (SBP). Emerging evidence suggests that the PVN utilizes paracrine signals to modulate neighboring neurons. Here, we test the hypothesis that OXT (oxytocin)-synthesizing neurons of the PVN (PVNOXT) release paracrine signals that regulate SBP via modulation of AVP (arginine vasopressin)-synthesizing neurons of the PVN.

Abstract

The elegant work by Maejima et al. recently published in Aging Cell reveals a previously unrecognized mechanism linking age-related oxytocin (OXT) decline to epigenetic remodeling, mitochondrial dysfunction, and systemic inflammation (Maejima et al. 2025). Beyond documenting this relationship, the authors demonstrate its remarkable reversibility through nasal OXT administration. These findings provide the first molecular evidence supporting what has long been proposed: that the OXT system functions as a fundamental long-term regulator of health across the entire lifespan, from early development through aging (Moberg 2024, 2003; Uvnas-Moberg 1998). The current work now gives a tantalizing glimpse into the epigenetic mechanism behind this life course regulation.

Abstract

Oxytocin (OT), the peptide hormone whose release from the pituitary is essential to induce milk ejection, has been measured in blood plasma of dairy cows for decades. In the present study we tested the possible use of saliva instead of blood sampling to record OT release by using a commercially available ELISA for salivary OT measurement both in saliva and blood plasma. Measurements were performed to detect the expected OT increase in response to intravenous OT injections and during machine milking. Three dairy cows were injected with increasing dosages (0.5, 1, 5, and 10 IU i.v.) of OT, and blood and saliva samples were repeatedly taken during 1 h after injection. Furthermore, 5 cows were milked and blood and saliva samples were taken during and until 20 min after milking. To verify the expected release of OT during milking, we used our established RIA for measurements in plasma in parallel to ELISA measurements. Our results showed that the commercial ELISA kit used was able to detect the OT concentrations in both saliva and plasma. The massive increase of OT concentration after OT injection and during milking could be detected in plasma with both RIA and ELISA. However, we did not observe any change of salivary OT within the duration of the experiments. Our results showed that short-term increases in blood plasma OT, such as in response to OT injection or milking, were not reflected by increasing salivary OT concentrations.

Abstract

People with autism spectrum disorders (ASD) show a relative suppression of the melatonergic pathway across CNS and systemic cells. The differential regulation of the mitochondrial melatonergic pathway may therefore be an important core aspect of ASD pathophysiology in all its manifestations. Recent data across diverse human cells show that the melatonergic pathway is powerfully regulated by interactions between signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), with the composition of the NF-κB dimer determining whether the melatonergic pathway is upregulated or downregulated. Diverse aspects of ASD pathoetiology and pathophysiology, including the aryl hydrocarbon receptor (AhR), microRNAs, suboptimal mitochondrial function, pro-inflammatory cytokines, glucocorticoid receptor, vagal nerve, and oxytocin, are all intimately linked to pineal and/or local melatonin regulation, indicating the relevance of the mitochondrial melatonergic pathway regulation in the pathoetiology and pathophysiology of ASD. This article reviews and integrates diverse aspects of ASD pathoetiology and pathophysiology, with implications for future research and treatment.

Abstract

Reaching term gestation requires a complex interplay between the uterus and hormonal signals regulating its contractile profile. Most pregnancy-associated hormones vary in their overall level of release throughout pregnancy, but also have a circadian release pattern, including progesterone, oxytocin, and melatonin. It remains poorly understood how the circadian release of hormones impacts uterine function. To determine how time-of-day, mouse strain, and melatonin proficiency were associated with the uterotonic efficacy of oxytocin, the primary hormone promoting uterine contractions, we used melatonin-deficient C57BL/6 and melatonin-proficient CBA/C57BL/6 (CBA/B6) female mice on gestation day 18. Through RNAscope, we found that oxytocin receptor (Oxtr) mRNA exhibited a time-of-day variation that differed between the uterine endometrium and myometrium. This uterine layer-specific, time-of-day difference in Oxtr was associated with a shift in phase of the molecular clock reporter PER2::Luciferase. A strain-specific effect of PER2::Luciferase rhythms were observed in the uterus, where CBA/B6 had a shorter PER2::Luciferase period than C57BL/6. In addition, CBA/B6 uteri had lower spontaneous uterine contraction force compared to C57BL/6. Despite the difference in spontaneous contractions and circadian period, the capacity of oxytocin to induce contractions varied by time-of-day, independent of mouse strain. Together, these findings reveal that uterine responsiveness to oxytocin is gated by circadian time, with Oxtr expression and uterine contractions showing diurnal variation. At the same time, mouse strain was associated with PER2::Luciferase period and baseline uterine contractility. These results underscore the relevance of circadian timing in uterine physiology and that strain differences impact basal uterine function.

Abstract

Participation in arts-related activities has been shown to positively influence the well-being and social connectedness of young people. However, few studies have explored the neuroendocrinological changes that might contribute to these benefits. In this exploratory study, we assessed oxytocin (OT) and cortisol (CORT) responses in children experiencing facilitated drum circle activities for the first time. These activities involve imitation and coordinated movement, which are known to increase OT levels. Additionally, OT levels are associated with behavioral synchrony and affiliative behaviors in close preexisting relationships, with higher baseline levels observed in individuals who exhibit more affectionate and coordinated interactions. We hypothesized that children participating in facilitated drum circles with their friends would show higher levels of OT than those participating with strangers.

Abstract

The optimal strategy for induction of labour (IOL) in cases of prelabour rupture of membranes (PROM) with an unfavourable cervix is elusive. No study conducted in nulliparous women has shown any one induction method to be superior to any other. In this project, we seek to determine whether IOL with balloon catheter and oxytocin can (1) increase rate of delivery <24 hours and (2) increase patient satisfaction, compared with a low dose of oral misoprostol.

Abstract

Oxytocin (OT) quantification in biological samples is vital for understanding its role in social behavior, emotion, and brain development in humans and animals. Urinary OT analysis has gained attention but is challenging due to variability in matrix effects, background interference, low concentrations, and stability concerns. This study developed an efficient LC-MS/MS method using mixed-mode solid-phase extraction (SPE) for sample preparation and serially coupled columns for separation. It achieved a lower limit of quantification (LLOQ) of 1 pg/mL, surpassing the sensitivity of previous methods. The method was fully validated per FDA guidance. The extraction recovery was > 80% in human urine. The precision was < 9%, and accuracy was between 101% and 109%. Partial validation for rhesus macaque urine showed accuracy ranged between 93% and 109%, with precision under 11%. Stability studies confirmed that OT in urine remains stable at room temperature for 4 h and at -80°C for 30 days. SPE-extracted samples were stable at 4°C for 24 h, and OT was unaffected by up to three freeze-thaw cycles. These results indicate that the LC-MS/MS method is accurate, consistent, and reliable for measuring OT in human and rhesus macaque urine and provide guidance for proper sample handling and storage.

Abstract

Induction of labour (IoL) aims to initiate labour when the risks of continuing pregnancy outweigh the benefits. Over 10 methods are currently available, yet the most effective and safest method remains unclear.

Abstract

Selective TDP-43 overexpression in oxytocin neurons in the paraventricular nucleus of the hypothalamus causes a decrease in oxytocin-immunopositive cells compared to uninjected mice. AAV-mediated TDP-43 overexpression in oxytocin neurons does not appear to be a major driver of behavioural and metabolic phenotypes in mice.

Abstract

Globally, obesity is a serious health issue, and oxytocin may help regulate appetite and reduce food intake, particularly in obese individuals. One promising treatment option for controlling appetite and lowering food intake is oxytocin among the people living with obesity or overweight. Based on the relevant clinical studies, this systematic review article explored the role of oxytocin and its connection with obesity.

Abstract

Oxytocin plays a critical role in modulating social cognition and enhancing human memory for faces. However, it remains unclear which phase of memory oxytocin affects to enhance face memory. Our study explored oxytocin's potential to selectively enhance the consolidation of social memories, specifically human faces, and whether this effect varies between genders. In three preregistered, randomized, double-blind, placebo-controlled trials with heterosexual participants (total N = 445, comprising 227 males and 218 females), we explored how oxytocin affects memory consolidation. We administered oxytocin immediately after encoding (i.e., Study 1), before retrieval (i.e., Study 2), and before encoding (i.e., Study 3) in three parallel studies. This design allowed us to confirm that oxytocin's effects were indeed due to consolidation rather than retrieval or encoding. We found that administering oxytocin post-encoding, but not before-retrieval or before-encoding, significantly improved female participants' ability to recognize male faces 24 h later, with no similar enhancement observed in males recognizing opposite-gender faces. Together with our analyses of the social placebo effect-where the belief in receiving oxytocin produces effects similar to those of actual intranasal oxytocin administration-and the approachability ratings during encoding, we concluded that oxytocin specifically enhances the consolidation of long-term social memories in women recognizing male faces. These findings imply that oxytocin selectively enhances the consolidation of human social memory, potentially deepening our understanding of the mechanisms underlying social memory processes.

Abstract

Research on the effects of intranasal oxytocin (IN-OXT) on social behavior has often yielded contradictory results, likely due to variability in sample characteristics and research methodologies. To understand oxytocin's influence on neurophysiology and the associated social behaviors, this review synthesizes findings from the past decade on oxytocin's impact on brain physiology, mainly measured by functional magnetic resonance imaging (fMRI) Blood Oxygenation Level Dependent (BOLD) signals. This includes studies on resting-state connectivity, task-based functional connectivity during social cognition tasks.

Abstract

Gastrointestinal motility is regulated primarily by the enteric and the central nervous systems. Our previous studies revealed that central circuits regulating colorectal motility partially overlap with those involved in pain modulation, suggesting functional interactions between the nociceptive modulatory pathway and the autonomic regulatory pathway of colorectal motility. Here, we examined whether peripheral inflammatory pain alters the neural components of the descending pathway regulating colorectal motility. Complete Freund's adjuvant (CFA) was administered unilaterally into the hind paw of rats to induce inflammation. Colorectal motility was assessed in vivo under anesthesia with α-chloralose and ketamine. In sham-treated rats, intraluminal administration of capsaicin, a noxious stimulus to the colorectal lumen, enhanced colorectal motility. In contrast, the capsaicin-induced colorectal motility response was suppressed in rats 3 days after CFA treatment. This suppression was rescued by the intrathecal administration of a GABAA receptor antagonist or an oxytocin (OXT) receptor antagonist. Furthermore, spinal OXT administration and chemogenetic activation of OXT neurons in naïve rats elicited a marked inhibition of capsaicin-induced motility responses of the colorectum. Notably, the inhibitory effect of activated OXT neurons was abolished by the intrathecal administration of a GABAA receptor antagonist. These results indicate that the descending OXT pathway becomes operative in response to persistent pain caused by peripheral inflammation and that the inhibitory effect on colorectal motility may involve local GABAergic transmission within the spinal cord. These changes may reduce parasympathetic outflow to the colorectum and contribute to defecation disorders involving central neural mechanisms.NEW & NOTEWORTHY This study focused on the remodeling of the neural pathways regulating colorectal motility and examined whether peripheral inflammation outside the gastrointestinal tract affects this process. In rats administered a complete Freund's adjuvant into their hind paw, colorectal motility responses induced by intracolonic administration of capsaicin were suppressed. This suppression involved oxytocinergic and GABAergic transmission in the spinal cord. These results demonstrate that inflammatory pain in the hind paw induces remodeling of the neural pathways regulating colorectal motility.

Abstract

Arginine vasopressin (AVP) and oxytocin (OT) are peptide hormones critical for various physiological processes. Vasopressin receptor 1 A (V1aR), a primary AVP target, is promising for central nervous system (CNS) disorders therapies, yet the mechanisms of antagonism and oligomerization remain poorly understood. Here, we present structures of human V1aR in its apo state and in complexes with antagonists: atosiban, balovaptan, and SRX246. Structural analyses reveal a dimeric V1aR assembly, validated by functional assays and imaging in cells. The apo structure shows a flat extracellular loop 2 (ECL2) with unpaired cysteines, undergoing significant conformational changes upon ligand binding. Antagonist-bound structures, combined with mutagenesis and radioligand binding assays, uncover distinct binding modes and key determinants for antagonism and selectivity. These findings provide a comprehensive understanding of V1aR assembly and dynamic regulation, offering valuable insights for structure-guided development of new antagonists targeting dimeric V1aR for CNS disorders.

Abstract

Alcohol has a notable negative impact on global health. Understanding its physiological regulation is crucial to addressing alcohol use. Here, we show that FGF21-oxytocin neurons in the paraventricular nucleus of the hypothalamus (PVHOXT)-dopamine neurons in the ventral tegmental area (VTADA) negatively regulate the drive to drink alcohol. Alcohol induces FGF21 signaling, which activates PVHOXT and induces oxytocin release in the VTA. The VTADA neurons are activated hours after alcohol ingestion, which reduces the drive to drink alcohol, extends the interdrink interval, and thereby reduces alcohol consumption. The system is downregulated in a mouse model of alcohol dependence, and activating the system with FGF21-inducing sugars reduces alcohol ingestion and prevents binge drinking and alcohol dependence. Therefore, FGF21-inducing nutraceuticals can substitute for alcohol by supplementing the FGF21-PVHOXT-VTADA negative feedback signal to attenuate alcohol-related behaviors in mice.

Abstract

Alterations in the oxytocin system, accompanied by cognitive and behavioral deficits, are common in several neurodevelopmental conditions, including Autism Spectrum Disorder. Oxytocin, a neuropeptide produced in the hypothalamus, plays a pivotal role in modulating social cognition and complex social behaviors. Recently, increasing attention has been given to the therapeutic potential of oxytocin in the treatment of neurodevelopmental disorders. However, many aspects of oxytocin signaling and its effects remain to be fully elucidated. Given its pronounced social behaviors and conserved neurochemical pathways, the zebrafish (Danio rerio) has emerged as a model for investigating the neural and behavioral effects of oxytocin. This species exhibits a wide behavioral repertoire, making it suitable for modeling oxytocin-related neurodevelopmental alterations. Here we provide an overview of the key mechanisms underlying oxytocin signaling and discuss current findings supporting the use of zebrafish as an Autism Spectrum Disorder model.

Abstract

Social behaviour is fundamental to survival and adaptation, relying on complex, interacting neurobiological systems in which the neuropeptide oxytocin (OT) and the neurotransmitter dopamine (DA) play pivotal roles in regulating social bonding, motivation, and reward processing. This review synthesises recent advances in understanding the bidirectional interactions between OT and DA within key nodes of the brain's reward circuitry, including the nucleus accumbens, ventral tegmental area, amygdala, and medial prefrontal cortex. We examine how these interactions support a wide range of social behaviours in humans and animals, from reproductive bonds such as pair bonding and parental care to non-reproductive interactions like social exploration, cooperation, and aggression. A central focus is the disruptive impact of psychostimulants (e.g., cocaine, amphetamines) on OT-DA balance in rodents. These substances alter DA signalling, shifting reward valuation and reducing the prioritisation of natural social rewards while increasing the drive for psychostimulant-seeking behaviour. This imbalance impairs social motivation and bonding. Importantly, positive social interactions can serve as competing natural rewards that prevent, and in some cases reverse, psychostimulant-seeking behaviours, highlighting the therapeutic potential of targeting OT-DA pathways. By integrating findings from animal models and human studies, this review proposes a framework for understanding how the brain arbitrates between social and pharmacological rewards, and how this balance is modulated by internal states, environmental factors, and the pathological effects of addictive substances.

Abstract

Peptides play crucial roles in pain regulation. Following tissue injury or insults, many endogenous excitatory peptides, such as calcitonin gene-related peptide, substance P, nerve growth factor, bradykinin, hemokinin-1, cholecystokinin, and endothelin, are generated, which are eventually responsible for pain sensation. To alleviate pain physiologically, many endogenous inhibitory peptides are generated, including opioid peptides, neuropeptide Y, oxytocin, and orexin A. As peptides can induce pain, the use of pain-alleviating peptides is like fighting fire with fire. Although increasing evidence has revealed new mechanisms of peptides in the transmission and perception of pain, comprehensive descriptions regarding how endogenous peptides modulate pain are lacking. This review describes the role of endogenous peptidergic pathways in pain processing, persistence, and resolution. Targeting endogenous peptides by activating inhibitory pathways or antagonizing excitatory pathways might be a promising natural way to alleviate pain. This review also focuses on peptide-associated pathways and the therapeutic applications of peptides that reduce pain in the treatment of various diseases. Additionally, we sought to investigate peptide-based target-specific drug discovery to treat pain-related disorders.

Abstract

Exercise training reduces metabolic dysfunction and improves neural function; however, its cortical molecular effects in diabetic-obese conditions remain unclear. Here, we aimed to identify transcriptional pathways by integrating physiological evaluation with an in silico analysis of cortical RNA-seq data from Zucker Fatty Diabetes Mellitus rats following a 12-week swimming training program. Exercise training reduced body weight and improved glucose control and blood pressure. RNA-seq analysis revealed 814 differentially expressed genes, with pathway enrichment highlighting glutamatergic synapse, retrograde endocannabinoid signaling, and oxytocin signaling pathways. These coordinated transcriptional shifts involved genes related to excitatory neurotransmission, neuromodulatory feedback, and calcium-dependent regulation. As hypothesis-generating models, these pathway-level patterns suggest that exercise training may modulate cortical signaling properties in diabetic-obese states and provide a conceptual framework for future mechanistic investigation.

Abstract

The underpinnings how nasal oxytocin (OXT) treatment may affect brain-controlled motivations and behaviors remain scarcely explored. This study was undertaken to assess the presence of volatilized OXT exposure and its rapid effects in altering motivational behaviors and stress-dampened neural stem cell proliferation. Heterozygous Venus knock-in (OXTR Venus-Neo/+) mice designed for locating oxytocin receptor (OXTR)-neurons and oxytocin receptor knockout (KO) mice were used to identify nasal epithelial OXTR-expressing neurons. We demonstrated mice' nasal epithelium harbored OXTR-expressing neurons. Volatilized OXT exposure caused a heightened Fos expression in epithelium, main olfactory bulb mitral cells, piriform cortex (PIR) and cortical amygdala (CA). Mice displayed sex-dimorphic differences in their volatilized OXT-zone choice behaviors. Lavage with a oxytocin receptor antagonist prevented volatilized OXT-produced zone preference in male mice. Volatilized OXT exposure rendered male mice' rapid decreases in active approach and investigation. Inactivating CA-projecting mitral glutamatergic neuron seemed to prevent these decreases. Volatilized OXT presentation prevented tandem stressors-induced decrease in dorsal dentate gyrus (dDG) neural stem cell proliferation. Such OXT effect was not noted in mice with oxytocin receptor KO and PIR-dCA3 circuit ablation and inhibition. Finally, tandem stressors produced a rapid decline in dCA3 cytoplasmic phosphorylated signal transducer and activator of transcription 5 (pSTAT5) levels, while volatilized OXT prevented these changes. Such volatilized OXT-produced protection was prevented by intra-dCA3 STAT5 phosphorylation inhibitor infusion. These findings prompt us to conclude nasal epithelial OXTR-expressing neurons may be involved the encoding of volatilized OXT and its rapid motivation-altering effects and neural stem cell's stress responses.

Abstract

The characteristics of spontaneous electrical activity forming bursts of action potentials in the main rhythmogenic areas of the myometrium (ovarian area, cervical area, uterine corpus) were investigated. The results were analyzed by determining the values of the following parameters of action potentials: amplitude (A), mean rise-rate (V), rise-time (T/2), and half-width (t). The obtained data indicate that the ovarian horn area represents a distinct rhythmogenic site, characterized by generation of bursts of discharges with properties unique to this area, in contrast to the activity patterns observed in the cervical horn area and uterine corpus. Oxytocin, through its excitatory action, induces a synchronous increase in the measured parameters across the studied areas to the same extent. Comparable alterations in the main activity characteristics were observed under conditions of complete isolation of each uterine horn locus. Administration of oxytocin following isolation of loci resulted in a marked increase in spike amplitude and rise rate of action potentials in the ovarian area, approaching values observed in norm. Thus, these findings indicate that the ovarian horn area serves as a leading rhythmogenic site. Morphochemical results demonstrated the presence of different "functional" states in the examined myometrial areas, which is consistent with the presented electrophysiological data.