Effects of Environmental Factors on the Endocrine System
George H. Gass, Harold M. Kaplan in Handbook of Endocrinology, 2020
The endocrine system plays a crucial regulatory role in the internal environment of an organism. Some of its components had evolved to merge with the nervous system that possesses sensory detectors for external stimuli such as light and temperature. This integration of neural and endocrine tissues created a neuroendocrine interface capable of accepting neural signal inputs and secreting hormones into the blood circulation. It can transduce information from the external environment into endocrine signals.1 With the ability to receive and interpret environmental cues through the neuroendocrine system, the endocrine system is enhanced in its adaptability to the environment. In response to external environmental changes, proper endocrine adjustments can be evoked in the internal environment. The neuroendocrine system, as its name implies, is an integrated control system of both neural and endocrine functions. In this chapter, the neuroendocrine system is discussed as a part of the endocrine system, though it can be considered as a system on its own.2
Principles of Neuroendocrinology
Paul V. Malven in Mammalian Neuroendocrinology, 2019
In addition to the transduction of neural signals into endocrine signals as just described, the neuroendocrine system mediates the cooperation between the nervous and endocrine systems to regulate in an optimum manner the physiological functions of the organism. This function can be described as neuroendocrine integration and is illustrated diagrammatically in Figure 1-2. In addition to a neurosecretory neuron that transduces the information, other ordinary (i.e.,non-neurosecretory) neurons play important roles in the integration of information. Two such neurons represented in Figure 1-2 are (1) integrative neuron and (2) hormone-sensitive neuron that each have direct input to neurosecretory neurons. Figure 1-2 also illustrates that integrative neurons of the neuroendocrine system receive a variety of inputs. These may include (1) information about the ambient environment obtained through the special senses, (2) integration of current inputs with the learned or conditioned information stored in higher cortical centers, (3) endogenous free-running rhythms (e.g., circadian or ultradian), (4) neurally mediated sensory information from internal organs (e.g., reproductive tract) and sensors (e.g., blood osmolarity, pH and pressure), and (5) neural signals from specific hormone-sensitive neurons (e.g., feedback from endocrine glands).
Physical symptoms
Aurora Lassaletta, Ruth Clarke in The Invisible Brain Injury, 2019
I have also found myself, since the accident, having trouble regulating my diet. I have noticed that I eat more food and more often. At first this overconsumption was also diagnosed as a symptom of anxiety. Later, the doctors saw that the impact had affected an area of my brain specifically responsible for the sensation of satiety. This means that, when I start eating, I never get to a point where I feel full and I could keep on eating indefinitely. Sometimes I need something external, such as my belt feeling tight, to give me a sign to stop. I have also read accounts after TBI of gaining weight and changes in appetite-control mechanism, like Sheena McDonald’s (McDonald, Little and Robinson, 2019). The hypothalamus has a neuroendocrine system regulating hunger and satiety, which receives peripheral and central nervous system (CNS) signals to balance our consumption with our energy needs. It is very common that with brain injury this function is affected by damage to the hypothalamus itself or by the alteration of the transmission of the signal from the cortex to the hypothalamus.
An overview of the neuroendocrine system in Parkinson’s disease: what is the impact on diagnosis and treatment?
Published in Expert Review of Neurotherapeutics, 2020
Neuroendocrinology is the field exploring bidirectional interaction between the nervous system and the endocrine system to maintain homeostasis of the organism [1]. The neuroendocrine system used to be described as the sets of neurons, glands, and non-endocrine tissues sharing co-production and responsiveness to a wide spectrum of neurochemicals, hormones, and humoral signals which participate in an integrated regulation of a physiological and behavioral state [2]. The central neuroendocrine system consists of the main axes including the hypothalamus, the pituitary gland and the target organs such as the adrenal glands, the thyroid, and the gonads. Apart from these hierarchically functioning axes based on the negative feedback loops, there are numerous neuroendocrine cells spread all over the body almost in every organ constituting also an integral component of the neuroendocrine system. This diffuse neuroendocrine system (APUD – amine precursor uptake and decarboxylation) actively participates in the neuroendocrine interactions [1].
The effects of chronic testosterone administration on hypothalamic gonadotropin-releasing hormone regulatory factors (Kiss1, NKB, pDyn and RFRP) and their receptors in female rats
Published in Gynecological Endocrinology, 2018
Takeshi Iwasa, Toshiya Matsuzaki, Kiyohito Yano, Rie Yanagihara, Yiliyasi Mayila, Minoru Irahara
Reproductive functions are mainly regulated by the neuroendocrine system, which is known as the hypothalamic–pituitary–gonadal axis (HPG axis). Gonadotropin-releasing hormone (GnRH) functions as a central regulator of the HPG axis through its stimulatory effects on gonadotropin secretion. In the early twenty-first century, it was clarified that GnRH production/secretion is regulated by hypothalamic neuropeptides. Kisspeptin and its receptor (Kiss1r) act as positive regulators of GnRH, whereas RFamide-related peptides/gonadotropin inhibitory hormone (RFRP/GnIH) and its receptor G protein-coupled receptor (GPR)147 function as inhibitory regulators [1–3]. In addition, in 2007, it was shown that neurokinin B (NKB) and dynorphin (Dyn) co-localize with kisspeptin in the same neuronal populations, and therefore, these neurons are termed KNDy neurons [4,5]. NKB stimulates the activity of KNDy neurons, predominantly via its receptor tachykinin receptor 3 and increases GnRH secretion [6,7]. On the other hand, Dyn inhibits KNDy neurons and/or GnRH neurons via the kappa opioid receptor (KOR), which in turn reduces GnRH secretion [6,8]. Interestingly, although kisspeptin is found in two hypothalamic nuclei, the anteroventral periventricular nucleus (AVPV) and arcuate nucleus (ARC), its co-localization with NKB and Dyn is only observed in the ARC [6,9].
Subarachnoidal hemorrhage related cardiomyopathy: an overview of Tako-Tsubo cardiomyopathy and related cardiac syndromes
Published in Expert Review of Cardiovascular Therapy, 2022
Susan Deenen, Dharmanand Ramnarain, Sjaak Pouwels
Heart failure including TTS is a well-recognized complication of neurologic diseases. In normal physiology, the parasympathetic and sympathetic nervous systems have an important role in the regulation of cardiac function [5,15]. The nervus vagus mediates the parasympathetic stimulation of the heart and leads to decreased heart rate, atrioventricular (AV) conduction, and ventricular excitability. Sympathetic stimulation leads to increased heart rate, AV conduction, and ventricular excitability and contractility. Also, the higher cerebral structures such as the frontal cortex, insula, amygdala, cingulate, hypothalamus, and periaqueductal gray matter influence cardiac function [5]. Furthermore, the hypothalamic–pituitary–adrenal axis (neuroendocrine system) influences the cardiac system by creating a stress response and thereby releasing cortisol and catecholamines. Catecholamines influence adrenergic receptors (ARs), leading to increased heart rate, contraction, and changes in blood pressure [5]. How these pathways can be disrupted by neurological injury and thereby cause cardiac dysfunction is a complex process, and many theories are mentioned. However, most recent studies describe an important role for catecholamines [5,9,12,13]. This theory is generally believed to explain the pathophysiology of cardiac dysfunction in SAH patients. SAH can cause mild-to-severe cardiac dysfunction in the form of ECG changes, arrhythmias, LV dysfunction, and release of cardiac biomarkers. In SAH patients with elevated catecholamine levels, it is also described that cardiac enzymes are elevated [1,2,5,12,13].
Related Knowledge Centers
- Nervous System
- Neuroendocrine Cell
- Peptide
- Physiology
- Secretion
- Endocrine System
- Brain
- Pituitary Gland
- Hormone
- Hypothalamus