Hormones 2 Flashcards
Essay plan
Classification of hormones • Homeostatic hormones: maintain a state of internal metabolic balance and regulate physiological systems in an organism 2. • Gonadal (sex) hormones: control reproductive functions • Glucocorticoids hormones: respond to stress, challenge to control metabolism.
Classification of hormones:
.Chemical: 1. Steroids hormones: Peptide hormones, lipid (fat) soluble. Influence target cells activity by crossing cell membrane and acting on cell’s DNA to influence the production of proteins. 2. Peptide hormones: Influence target cells activity by binding to receptors on cell membrane. Functional: • General: Organizational effects Activating effects • Specific: Homeostatic hormones, gonadal (sex) hormones, glucocorticoids hormones
Where are hormones’ receptors located?
Lipid-soluble (steroid) hormones: intracellular receptors. Water-soluble (peptide) hormones: receptors on the cell surface Position of a receptor depends on the solubility of the hormone
Organizational vs activating effects:
Organizational effect: A permanent or semi-permanent change in the structure of part of the nervous system (e.g. growth of new dendrites), most often during development. When? During “sensitive periods’’ in early development. How? Hormone penetrates the cell nucleus and affects gene expression, hence the formation of new structures. • Activating effect: A transient or reversible change in the properties of cells. When? Any time an hormone occupies the receptor of a cell. How? They last for as long as an hormone is present at a cell or only for a short time after removal of the hormone. The structure of the hormone is unchanged.
A continuum rather than a clear-cut distinction: The distinction between organizational and activating effects is valid but not a clear-cut (Fitch & Denenberg, 1998).A role for ovarian hormones in sexual differentiation of the brain (Fitch & Denenberg, 1998)
Historically, studies of the role of endogenous hormones in developmental differentiation of the sexes have suggested that mammalian sexual differentiation is mediated primarily by testicular androgens, and that exposure to androgens in early life leads to a male brain as defined by neuroanatomy and behavior. The female brain has been assumed to develop via a hormonal default mechanism, in the absence of androgen or other hormones. Ovarian hormones have significant effects on the development of a sexually dimorphic cortical structure, the corpus callosum, which is larger in male than in female rats. In the females, removal of the ovaries as late as Day 16 increases the cross-sectional area of the adult corpus callosum. Treatment with low-dose estradiol starting on Day 25 inhibits this effect. Female callosa are also enlarged by a combination of daily postnatal handling and exogenous testosterone administered prior to Day 8. The effects of androgen treatment are expressed early in development, with males and testosterone-treated females having larger callosa than control females as early as Day 30. The effects of ovariectomy do not appear until after Day 55. These findings are more consistent with other evidence of a later sensitive period for ovarian feminization as compared to androgenic masculinization.
Hormones can induce structural changes in the adolescent and adult nervous system too (e.g. morphological changes in secondary sexual features, physical growth, changes in nervous system, NEW ASPECTS IN THE DIAGNOSIS AND TREATMENT OF PUBERTAL DISORDERS: Styne, 1997
Abstract: Recent developments in biochemistry, genetics, and clinical research produced a profound effect on the understanding of normal and abnormal puberty. Study of bone metabolism in puberty may explain the etiology of osteoporosis in the elderly. New ultrasensitive assays for gonadotropins demonstrate a diurnal pattern of gonadotropin secretion in prepubertal children not very different from that of puberty except for a lower amplitude of pulsation; these techniques may simplify the process of diagnosis of disorders of puberty. Studies of the development of the fetal hypothalamus explain why patients with Kallmann syndrome combine hypogonadotropic hypogonadism with anosmia. Investigation of the testicular receptors for leuteinizing hormone (LH) reveal the cause of gonadotropin independent Leydig cell and germ cell maturation. Study of the metabolism endocrine, skin, and bone cells from patients with the McCune-Albright syndrome explain the cause of this disorder of widespread abnormalities of several organ systems. Lastly, the etiology of premature thelarche is now better understood. This article is intended to point out selected new developments that affect the understanding of puberty and clinical practice in disorders of puberty.
Plasticity of some neural systems à ‘permanently transient’ (Fitch & Denenberg, 1998; Stahl, 1997) –e.g. changes in some neural connections or cortical excitability follow changes in hormone levels during the menstrual cycle, cortical excitability of male and female subjects is only similar during the follicular phase of the menstrual cycle when progesterone levels are low and estrogen levels are high (Inghilleri et al., 2004). Ovarian hormones and cortical excitability. An rTMS study in humans (Inghilleri et al., 2004).
Abstract: Objective: Ovarian steroids influence neural excitability. Using repetitive transcranial magnetic stimulation (rTMS) we investigated changes in cortical excitability during the menstrual cycle. Methods: Eight women underwent rTMS on Days 1 and 14 of the menstrual cycle. As a control group, 8 age-matched men were also tested twice, with a 14-day interval between the two experimental sessions. Repetitive magnetic pulses were delivered in trains of 10 stimuli (5 Hz frequency and 120% of the motor threshold calculated at rest) to the left motor area of the first dorsal interosseous muscle. Results: In women, the motor evoked potential (MEP) size did not increase on Day 1, but it increased progressively during the train on Day 14. The duration of the silent period progressively lengthened during the train on both days. In men the MEP increased in size, and the silent period lengthened to a similar extent on both days. Conclusions: In women, hormone changes related to the menstrual cycle alter cortical excitability. Significance: Low estrogen levels probably reduce cortical excitability because their diminished action on sodium channels reduces recruitment of excitatory interneurons during rTMS thus abolishing the MEP facilitation.
Example of no gender difference in performance following brain stimulation when female participants are tested during follicular menstrual phase when cortical excitability of males and females is similar (Fertonani et al, 2011): Random Noise Stimulation Improves Neuroplasticity in Perceptual Learning (Fertonani et al, 2011).
We investigated brain plasticity mechanisms in a learning task using non invasive transcranial electrical stimulation (tES).We hypothesized that different types of tES would have varying actions on the nervous system, which would result in different efficacies of neural plasticity modulation. Thus, the principal goal of the present study was to verify the possibility of inducing differential plasticity effects using two tES approaches [i.e., direct current stimulation (tDCS) and random noise stimulation (tRNS)] during the execution of a visual perceptual learning task. One hundred seven healthy volunteers participated in the experiment. High-frequency tRNS (hf-tRNS, 100 – 640 Hz), low-frequency tRNS (lf-tRNS, 0.1–100 Hz), anodal-tDCS (a-tDCS), cathodal-tDCS (c-tDCS), and sham stimulation were applied to the visual areas of the brain in a group of volunteers while they performed an orientation discrimination task. Furthermore, a control group was stimulated on the vertex (Cz). The analysis showed a learning effect during task execution that was differentially modulated according to the stimulation conditions. Post hoc comparisons revealed that hf-tRNS significantly improved performance accuracy compared with a-tDCS, c-tDCS, sham, and Cz stimulations. Our results confirmed the efficacy of hf-tRNS over the visual cortex in improving behavioral performance and showed its superiority in comparison to other stES. We concluded that the mechanism of action of tRNS was based on repeated subthreshold stimulations, which may prevent homeostasis of the system and potentiate task-related neural activity. This result highlights the potential of tRNS and advances our knowledge on neuroplasticity induction approaches.
Functional classification: Homeostatic hormones:
Conditions in the body are controlled, to provide a constant internal environment. This is called homeostasis. The conditions that must be controlled include body temperature, water content, carbon dioxide level, and blood sugar level. Hormones are chemicals secreted by glands. They travel through the bloodstream and affect target organs. Sexual development, the menstrual cycle and fertility in women, and blood sugar levels, are all controlled by hormones. Homeostasis: It is important that the body’s internal environment is controlled. For example, the amount of carbon dioxide in the bloodstream is carefully controlled. Maintaining a constant internal environment is called homeostasis. The nervous system and hormones are responsible for this. Essential to life because they help the body to maintain important parameters at a constant level so we can function properly. Why important? A constant internal environment has to be maintained irrespective of changes in internal and external environment, such as age, activities, conscious state etc. Examples of physiological conditions requiring homeostasis: oxygen levels in the body.
Homeostatic hormones-example 1: insulin
It promotes glucose intake, it is released in the bloodstream. Important because cells use a sugar (glucose) for their energy requirements, and they can take this up from the blood. Insulin: Why is this important: Insulin control has an important functional significance: Some cells can use glucose as well as other substances for fuel (like protein and fat). Instead neurons (cells in the brain) can only use glucose as fuel and cannot store it. So if the glucose level is low, priority of usage of any remaining glucose is given to neurons, since neurons cannot store glucose, they depend on the bloodstream to deliver a constant glucose supply. Insulin: How does it work: General process: Insulin acts as a key to unlock a cell that needs sugar, so that glucose can enter and be used for energy.
Insulin: How does it work -mechanical explanation:
Increases: –Control system (made of chemoreceptors throughout the body that constantly measure the amount of sugar in the blood) detects it –It triggers the release of insulin –Cells take up glucose. Decreases: –Control system detects it –Secretion of insulin reduced –Cells unable to take up glucose. Pancreas produces insulin as well as glucagon, which have reciprocal roles. Glucagon’s main aim is to prevent blood glucose levels dropping too low.
Insulin: How does it work -anatomical explanation
Insulin is secreted by cells in the pancreas (called ‘beta’ cells) when blood glucose level increases. Insulin stimulates the uptake of glucose from the blood stream. By increasing the transport of glucose from the blood to muscle cells and adipocytes.
How does the cephalic phase work:
Basic fact: increase in blood glucose is usually due to food intake. However, shortly after encountering food (and before glucose in the blood), the nervous system triggers insulin secretion. This is termed ‘the cephalic phase of insulin release’; it is like a conditional reflex. So insulin response anticipates the arrival of glucose. WHY? For gluco-regulation: to lower blood glucose in response to an ingested sugar load, i.e. to speed up sugar intake by cells and to avoid too much sugar in the blood. Insulin: link with nervous system: Step-by-step 1.Starting point: physiological changes 2.Picked up by the hypothalamus 3.Message sent to the nucleus of the solitary tract (medulla in brain stem) 4.Vagus nerve 5.Pancreas to induce insulin secretion.
Imbalance of glucose in blood:
Fall of blood sugar level Hypoglicemia: Low blood sugar can be severe enough to cause fainting or coma. Neurons which depend on glucose cannot function properly if not enough blood glucose is therefore below the optimum range. Symptoms usually resolve when the sugar level returns to the normal range. Rise of blood-sugar level Hyperglicemia: Deficiency in insulin or changes in insulin receptors, i.e. insulin does not instruct cells to take up glucose (Diabetes type 1 or 2). Cell function can fail through glucose starvation (even if there is a lot of sugar in the body). Chronic high blood glucose level cause damage to eyes, kidneys, nerves, heart and blood vessels.
Homeostatic hormones- example2: vasopressin:
Vasopressine is produced in the posterior pituitary gland, regulates body fluids, also known as antidiuretic hormone (ADH) or arginine vasopressin (AVP). Homeostatic hormones: Vasopressin: If body is deficient in water: A control system in the hypothalamus (called ‘osmoreceptors’) detects it and excite neurons containing vasopressin. Vasopressin is produced and released into the blood stream. Vasopressin is transported into the kidneys where the production of urine is slowed. If body exceeds in water: A control system detects it & inhibits the secretion of vasopressin and the kidneys excrete a larger amount of urine. Its two primary functions are to retain water in the body and to constrict blood vessels. Vasopressin regulates the body’s retention of water by acting to increase water reabsorption in the collecting ducts of the nephron, which is the functional component of the kidney. Vasopressin is a peptide hormone that increases water permeability of the kidney’s collecting duct and distal convoluted tubule by inducing translocation of aquaporin-CD water channels in the kidney nephron collecting duct plasma membrane. It also increases peripheral vascular resistance, which in turn increases arterial blood pressure. It plays a key role in homeostasis, by the regulation of water, glucose, and salts in the blood. It is derived from a preprohormone precursor that is synthesized in the hypothalamus and stored in vesicles at the posterior pituitary. Most of it is stored in the posterior pituitary to be released into the bloodstream. However, some AVP may also be released directly into the brain, and accumulating evidence suggests it plays an important role in social behavior, sexual motivation and pair bonding, and maternal responses to stress[citation needed]. It has a very short half-life between 16–24 minutes.
