Preface

As a hormone, oxytocin is closely related to human social behavior, and it has been widely studied in the fields of biology, psychology, and sociology. In recent years, with the development of research on human social behavior, the relationship between oxytocin and social function has also attracted more and more attention. This book provides a comprehensive introduction to the research on oxytocin and social function, including the relationship between oxytocin and human social behavior, the mechanism of oxytocin in regulating social function, and the application of oxytocin in improving social function. The book includes contributions from leading experts in the field of oxytocin research, as well as relevant research results and findings. This book will be of interest to researchers in biology, psychology, and sociology, as well as to people who are interested in human social behavior and want to learn more about the role of oxytocin in social function. We hope that this book will help readers deepen their understanding of oxytocin and its role in human social behavior, promote the research and application of oxytocin in the field of social function, and contribute to improving human social behavior and social development.

Chapter 1 discusses the role of depolarization-induced oxytocin vs. vasopressin secretion in the absence of external calcium, and calcium release from ryanodine-sensitive internal stores as a significant physiological contributor to neuropeptide secretion from hypothalamic neurohypophysial system terminals. This has important therapeutic implications given that exogenous administration of oxytocin to children with autistic spectrum disorders has shown some success in improving social behavior and lessening anxiety.

Chapter 2 outlines the current knowledge of oxytocin and epilepsy, including the potential mechanisms of oxytocin's antiepileptic effects, the limitations and challenges of clinical studies, and future research directions and implications. The chapter also discusses the broader impact of oxytocin research on understanding social behavior and neurological disorders.

Chapter 3 overviews studies of transcranial direct current stimulation on social cognition and discusses optimal brain regions to be targeted for ameliorating symptoms and cognitive disturbances of schizophrenia.

Chapter 4 discusses the regulation of oxytocin on empathy and its neural mechanism. Empathy plays a vital role in social communication, and it is very important for establishing harmonious relationships, trust, and mutual understanding. Oxytocin can enhance emotional and cognitive empathy, as well as trust and cooperative behavior.

Chapter 5 discusses the oxytocin receptor gene polymorphisms and event-related potentials in humans. It has been found that genetic variations of the oxytocin receptor significantly influence neural activity related to emotional and social processing, except for the early phases of face recognition.

Chapter 6 discusses oxytocin and its congeners in obstetrics practice. Carbetocin, an analogue of oxytocin, has more pronounced pharmacological effects. Heat-stable carbetocin is a promising alternative to oxytocin.

Chapter 7 reviews the social and behavior change communication framework in addressing stunting. This framework integrates principles of communication theory and social psychology to create more effective messages for behavior change. The social and behavior change communication framework can help increase public awareness of health issues, motivate them to change unhealthy behaviors, and encourage healthier behavior.

Chapter 8 discusses the morphofunctional characteristics of rythmogenic regions in the rat myometrium, as well as the identification of driver pacemaker areas under the influence of oxytocin.

The completion of this book was supported by the National Key R&D Program of China (2022YFC2702900), National Natural Science Foundation of China (82273662). Many individuals made this book a reality. The completion of this book would not have been possible without the efforts of numerous contributors. I would like to thank Mrs. Maja Bozicevic at IntechOpen for her strong support from the inception to the completion of this book. I would also like to acknowledge my coauthors for their efforts.

> **Wei Wu** Department of Toxicology, School of Public Health, Nanjing Medical University, Nanjing, China

> > **1**

**Chapter 1**

**Abstract**

release in ASD patients.

**1. Introduction**

Modulation of Oxytocin Release by

This chapter elucidates the role of depolarization-induced oxytocin (OT) vs. arginine vasopressin (AVP) secretion in the absence of external calcium, and calcium release from ryanodine-sensitive internal stores as a significant physiological contributor to neuropeptide secretion from hypothalamic neurohypophysial system (HNS) terminals. This has important therapeutic implications, given that exogenous administration of OT to children with autism spectrum disorders (ASD) has shown some success in improving social behavior and lowering anxiety. However, this nonspecific treatment has side effects, including seizures, increased heart rate variability, and psychotic symptoms. Alternatively, facilitating the physiological neuronal release of OT but not AVP from the HNS via modulation of ryanodine vs. inositol triphosphate receptor (IP3R) calcium stores would specifically facilitate central vs. peripheral OT

**Keywords:** oxytocin, vasopressin, neurohypophysis, ryanodine receptor, inositol trisphosphate receptor, autism spectrum disorders, ADP-ribosyl cyclase/CD38

The main mechanism for neuropeptide release from neurohypophysial terminals (NHT) acts via depolarization-secretion coupling. This refers to the relationship between neuronal depolarization and the subsequent release of hormones, specifically oxytocin (OT) and arginine vasopressin (AVP), from the posterior pituitary gland (**Figure 1**). This hypothalamic-neurohypophysial system (HNS) plays a critical role in regulating various physiological processes, including social behavior, reproduction, and water balance. Within the HNS, specialized neurons located in the hypothalamus synthesize and package OT and AVP into vesicles. These magnocellular neurons (MCNs) extend their axons through the pituitary stalk and terminate in the posterior pituitary (also known as (aka) neurohypophysis) gland, where the hor-

mones are stored and released into the capillary bed for systemic delivery.

The classic understanding of neuropeptide release involves depolarization of the hypothalamic neurons which receive excitatory input which activates action potentials to their terminals. This depolarization leads to the opening of voltage-gated

**1.1 Hypothalamic neurohypophysial system (HNS)**

Internal Calcium Stores

*Cristina Velázquez-Marrero and José R. Lemos*
