Neuron-Endocrine Response to Stress in Animals
The physiological responses of animals to stress activate endocrine, autonomic and CNS responses along with redistribution of blood flow. Different systems act in a synergistic way in accordance to the level of stress, to sustain the homeostasis by stimulating physiological mechanisms to reduce the adverse impacts.
The stress regulating systems differ between individuals depending upon their earlier experience, physiological status, genetic predisposition, extent and severity of stress. Hence, stress brings about certain changes in the neuroendocrine reactions that stimulate different hormonal axis and secretion of hormones which promote the adaptive and behavioural responses of animals. These stress hormones regulate the energy supply for muscular and neural activities, increase the awareness of the environment, improve the glucose concentration to brain, modifications in cardiovascular and respiratory functions, modulation in immune responses and finally lead to reduction in productive and reproductive performance. The environmental stressors mainly activate two primary neuroendocrine adaptive mechanisms which include sympathetic-adrenal- medullary (SAM) and the hypothalamic-pituitary-adrenal (HPA) axis. These axes act synergistically to elicit different stress responses in combination with interplay of adaptive responses of different organs and receptors to conquer extreme stress conditions. Figure 28.1 describes the different target endocrine glands and other components involved in the different adaptive mechanisms.Neuroendocrine response is one of the principal defence mechanisms instituted by the animal to counter stress that stimulate HPA axis through sensory organs with the integration of brain centre. HPA controls the thermoregulation of animals by secreting different neurotransmitters and hormones. Further, HPA axis is activated directly or indirectly by heat stress, drought and nutritional stress and as well as disease conditions which enhances glucocorticoid secretion.
The function and regulation of HPA axis are the foremost important prerequisite in the adaptation process of animals. The activation of SAM axis establishes immediate activation of the autonomic nervous system for the release of catecholamines, adrenaline and noradrenaline. The adrenal and thyroid hormones are essential in thermoregulation and metabolic response of animals duringFig. 28.1 Overview of neuroendocrine response during heat stress in livestock. High environmental temperature stimulates brain, pituitary, adrenal glands to release various signalling molecules and hormones into circulating system. Physiological, haemato- biochemical changes occur in animals in response to heat stress to establish thermal equilibrium
stress. The corticotrophin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH) and glucocorticoids are the principal stress hormones released from HPA axis. The HPA axis enhances ACTH concentration on activation which is consequently improved the level of glucocorticoids particularly cortisol, the stress-relieving hormone. ACTH is one of the major pituitary hormones that supports growth and development of adrenal cortex and enhances the synthesis and secretion of glucocorticoids. The glucocorticoids production mainly depends on the integrity of the HPA axis and the secretory level of ACTH from the anterior pituitary. The adrenal cortex synthesizes cortisol which regulates the behavioural and neuroendocrine activities during stress. Cortisol is believed to be an important biomarker to quantify the level of stress among all the species of animals. Increased cortisol levels induce the hepatic gluconeogenesis which enhances the production of glucose from non-carbohydrate sources to establish energy homeostasis and to restore the life sustaining activities. The cortisol is the primary stress-relieving hormone that regulates the stress response in ruminants.
Glucocorticoids are the downstream effectors of the HPA axis and regulate the physiological process by stimulating the intracellular receptors. Glucocorticoids are released in the circulatory system with the carrier proteins, and the carrier protein maintains the bioavailability of glucocorticoids for the immediate response to stress. Higher level of glucocorticoids supports the animal’s survival in the extreme stress conditions. Glucocorticoids regulate the mobilization of energy expenditure in the body to sustain the energy homeostasis. However, glucocorticoids secretion is highly variable in many species during stress and also produced in a diurnal pattern that is influenced by many factors such as genetics.The association between the CNS and pituitary regulates the SAM axis stimulation which releases β-endorphin that facilitates glucocorticoids and catecholamines to interact with a wide range of cells to modify the metabolic and immune functions. Catecholamines secreted in response to stress, regulate the adaptive mechanisms such as ‘flight and fright’ responses. In addition, catecholamines coordinate the cardiopulmonary system by enhancing the cardiac output and respiration rate, sweating rate and redistribution of blood flow to the respiratory system and other vital organs to escalate different stress responses. Catecholamines act on adrenergic receptors of the visceral organs and smooth muscles to induce signalling pathways to modify different endocrine functions. Further, it alters the effects on afferent sensory nerves that impact CNS. These accelerated responses of catecholamines are highly essential for survival. However, the continued high level of catecholamines may result in pathological conditions such as cardiac hypertrophy, hypertension and post-traumatic stress disorder. The preganglionic neurons of the sympathoadrenal system secrete the neurotransmitter acetylcholine that activates the postganglionic neurons to produce nor-epinephrine.
The preganglionic neurons of spinal cord are entered into the adrenal medullary ganglia of the sympathoadrenal system, and the terminals connect the endocrine cells known as chromaffin cells. The activation of chromaffin cells by acetylcholine increases the release of catecholamines in to the peripheral blood circulatory system.The acute thermal stress activates SAM which is associated with shift in the water and electrolyte balance that is essential to support the evaporative water loss. The enhanced level of vasopressin (antidiuretic hormone) facilitates the conservation of water and increases water intake to compensate the water losses through respiratory tract and skin. The baroreceptors in the atrium and greater blood vessels, and hypothalamic osmoreceptors are activated by consistent variation in body fluids during heat stress which further increases vasopressin secretion to limit the dehydration. Whereas during cold stress polyurea, characterized by inhibition of vasopressin, facilitates more water loss through urination and prevent heat loss from tissues into water. In addition, vasopressin or antidiuretic hormone secreted from hypothalamus which enhances the effects of corticotropinreleasing factor on ACTH release from the anterior pituitary. Furthermore, vasopressin plays a vital function in the maintenance of concentration of ACTH during prolonged heat stress. The renin-angiotensin-aldosterone system also aids in maintenance of electrolyte homeostasis and hypovolemia as a result of dehydration during heat stress. Hypovolemia reduces the blood flow to the kidney and activates juxtaglomerular apparatus which increases the secretion of renin. The increased level of renin stimulates the production of angiotensin which consecutively enhances aldosterone from the adrenal cortex. The elevated aldosterone favours re-absorption of water and electrolytes especially sodium in the kidney to prevent the excretion of more water.
The hypothalamic-pituitary-thyroid (HPT) axis is most important in coordination of energy utilization by adjusting the basal metabolic rate through the actions of thyroid hormones.
The HPT axis is situated in the medial region of the paraventricular nucleus of the hypothalamus that secretes and releases thyrotropin-releasing hormone (TRH) into the pituitary. The TRH triggers the secretion of TSH from the anterior pituitary, and consequently the production and release of thyroid hormones. Thyroid hormones, triiodothyronine (T3) and thyroxine (T4) are the principal metabolic hormones in animals, and the acute and chronic stress influences the HPT axis. The activation of HPT enhances TSH due to the direct stimulatory effect of glucocorticoids on the pituitary thyrotrope. However, prolonged stress habitually lowers the HPT activity in animals to achieve lower metabolic heat production during heat stress. The decreased HPT activity is transmitted to the hypothalamus by glucocorticoids to lower the TRH production. Further, elevated level of somatostatin as an effect of increased intrahypothalamic CRH release also regulates the lower TSH secretion during heat stress. The decreased TSH production impairs conversion ratio of T4 to T3 in the stressed animal. Therefore, thyroid activity is decreased during heat stress and results in lower level of T3 and T4 and it requires many days to reach normal level. However, the reduced level of thyroid hormones is not an instant response to acute heat stress but alternatively associated in the acclimatization of animals to a continued thermal load. Similarly, the lower level of thyroid hormones is highly associated with a decrease in metabolic rate and reduction in cellular heat production.Growth hormone, produced in the anterior pituitary gland, is involved in energy partitioning along with an initiation and maintenance of lactation in animals. The concentration of growth hormone decreases during acute and chronic heat stress. However, prolactin levels, secreted by the anterior pituitary, increase during heat stress which may be involved in potassium and sodium turnover, and water metabolism. Heat stress impairs the reproductive performance of animals through the hypothalamic-pituitary-gonadal axis by inhibiting gonadotropin-releasing hormone in the hypothalamus. The secretion of gonadotropins, follicle stimulating hormone and luteinizing hormone (LH) are reduced in the anterior hypophysis which in turn affects the production of sex steroids. The decreased concentration of LH impairs the development of dominant follicle and results in decreased production of estradiol which leads to poor expression of estrus and low fertility in females.
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