Exam 3 (Chapters 8-11)

Made by @agreyr

Testes

Produce sperm cells

Ovaries

Produce ova

Steroid hormones produced by both gonads

Androgens (Testosterone), Estrogens (Estradiol), Progestins (Progesterone)

Gonadotropin releasing hormone (GnRH)

Produced by hypothalamic neuroendocrine cells, secreted into the blood vessels and carried to the anterior pituitary via hypothalamic-pituitary portal system (see Neuroendocrine System: Regions)

Gonadotropins

Released by anterior pituitary following GnRH

Follicle Stimulating Hormone and Luteinizing Hormone

Drive the release of gonadal steroid hormones

Two major effects of sex hormones

Organizational (developmental) and activational

Organizational effects on gonads

Indifferent (primordial) gonads

Presence of a Y chromosome triggers the synthesis of SRY protein at about 6 weeks of development; allows growth of the medulla into the testes while the cortex shrinks away

Organizational effects on internal organs

At 6 weeks, zygote contains two precursor duct systems (Wolffian system and Müllerian system)

Once formed, fetal testes release testosterone and Müllerian-inhibiting hormone (8 weeks of gestation)

Wolffian system

One of the two precursor duct systems present zygote at 6 weeks

Potential to develop into epididymis, vas deferens, and seminal ducts

Müllerian system

One of the two precursor duct systems present zygote at 6 weeks

Potential to develop into fallopian tubes, uterus, and inner vagina

Male reproductive organ development

XY chromosome; Y chromosome being testis-determining factor

Primordial gonads develop into testes; anti-Müllerian hormone and androgens are produced

Defeminization and masculinization occur

Defeminization

Triggered by anti-Müllerian hormone

Müllerian system withers away

Masculinization

Triggered by androgens

Wolffian system develops into vas deferens, seminal vesicles, prostate

Primordial external genitalia develop into penis and scrotum

Female reproductive organ development

XX chromosome

Primordial gonads develop into ovaries; no hormones are produced

Müllerian system develops into fimbriae, fallopian tubes, uterus, inner vagina

Wolffian system, without androgens, withers away

Primordial external genitalia develop into clitoris, labia, outer vagina

Activational effects

Puberty, a time period during which fertility is achieved, growth spurt occurs, and secondary sex characteristics develop; marked by surge in hormone release from the anterior pituitary

Pituitary

Anterior and posterior

Hypothalamus

Supraoptic and paraventricular

Posterior pituitary

Major hormones (Vasopressin and Oxytocin) signaled via neural connections and released into the blood; negative feedback signaling

Controls the secretion of anterior pituitary hormones via its own set of hormones; releasing and inhibitory factors

Vasopressin

Facilitates water reabsorption in the kidney

Oxytocin

Parental behavior

Releasing factors

Stimulate the release of an anterior pituitary hormone

Inhibitory Factors

Inhibit the release of an anterior pituitary hormone

Anterior pituitary

Considered to be the master gland because it releases tropic hormones

Part of the hypothalamic-pituitary portal system

Releases gonadotropins (see Neuroendocrine System: Gonads)

Hypothalamic-pituitary portal system

Carries GnRH from the hypothalamus to the anterior pituitary (see Neuroendocrine System: Gonads)

Tropic hormones

Primary function is to influence the release of other hormones

Prolactin, gonadotropic hormones (FSH and LH), thyroid-stimulating hormone, ACTH, growth hormone

Neuroendocrine cells

Special category of cell

Hormones

Chemicals released by endocrine glands into blood circulation

Act on target tissues throughout the body (including the brain) to produce physiological effects

Three main categories of hormones

Peptides, Amines, Steroids

Peptide hormones

Small protein molecules made of a string of amino acids

Bind to receptor proteins on the surface; activate second messengers; fast, but not as fast as synaptic signals

Amine hormones

Modified versions of single amino acids; smaller and simpler

Bind to receptor proteins on the surface; activate second messengers; fast, but not as fast as synaptic signals

Steroid hormones

Derived from cholesterol; most important for sexual development and behavior

Bind to receptors inside the target cell; binds to DNA and controls expression of other genes

Hypothalamus

Control of hormone secretions

Pineal gland

Reproductive maturation; body rhythms

Anterior pituitary gland

Part of the pituitary gland

Hormone secretion by thyroid, adrenal cortex, and gonads; growth

Posterior pituitary gland

Part of the pituitary gland

Water balance; salt balance

Thyroid

Growth and development; metabolic rate

Adrenal cortex (outer bark)

Part of the adrenal glands

Salt and carbohydrate metabolism, inflammatory reactions

Adrenal medulla (inner core)

Part of the adrenal glands

Emotional arousal (epinephrine)

Pancreas

Sugar metabolism

Gut

Digestion and appetite control

Gonads (testes/ovaries)

Body development; maintenance of reproductive organs in adults

Homeostasis

Relatively stable internal environment optimized for cellular activity

Factors of homeostasis

Acidity, salt, water, oxygenation, temperature, energy availability

Example of homeostasis

Thermoregulation

Mammals are endotherms, meaning we make hear inside our bodies using metabolism and muscular activity; there is a dedicated, precisely regulated system for creating warmth

Set point

Desired homeostatic value (98.6°F or 37°C)

Negative feedback

Deviation leads to compensatory action of the system

Restoring the set point turns off the response

Redundancy

Each system has multiple mechanisms for monitoring stores, conserving remaining supplies, obtaining new resources, and shedding excesses

Example: pre-optic and lateral areas of the hypothalamus controlling temp

Behavioral Compensation

Behaviors that change the exposure of the body surface, external insulation, and/or surroundings

Allostasis

Dynamic process whereby the system shifts responses depending on prior experience and the environment

DSM-identified eating disorders

Anorexia Nervosa, Bulimia Nervosa, Binge-Eating Disorder

Anorexia Nervosa

Voluntary self-starvation despite more response to the presence of food than controls

Complex combination of genetic, endocrine, personality, cognitive, and environmental factors

Similar symptoms to Bulimia Nervosa, often difficult to distinguish

Bulimia Nervosa

Bingeing and purging

Similar symptoms to Anorexia Nervosa, often difficult to distinguish

Binge-Eating Disorder

Tendency to gorge oneself way past the point of fullness

Causes not well understood but thought to involve over activation of dopamine reward mechanisms

Obesity

Determined based on Body Mass Index (BMI)

Body Mass Index (BMI) calculation

kg/mxm OR 703(lb/inxin)

Starvation BMI category

Under BMI 15

Underweight BMI category

BMI 15 to 18.5

Normal BMI category

BMI 18.5 to 25

Overweight BMI category

BMI 25 to 30

Obese BMI category

BMI 30 or higher

Weight loss treatment

Is often extremely difficult; minimal success rates

Should ideally involve both diet and exercise

Requires permanent, substantial lifestyle changes; minimal evidence of long term success

Utility of drugs/supplements or surgery; strictly complementary to lifestyle changes

How can drugs promote weight loss?

Decreasing appetite, increasing metabolism, inhibition of fat tissue, blocking absorption of calories, reducing reward/cravings for specific foods, decreasing meal size (make you feel fuller faster)

To perform these functions, drugs may act in the CNS or the digestive tract

Health at Every Size (HAES)

Weight loss doesn’t have to be a goal; instead, the idea is to support people in adopting healthy habits for the sake of health and well-being (rather than weight control)

Recognizes that health and fitness can exist at all sizes

Hypothalamus

Complex effects on ingestive behavior

Regulation of energy balance; regulation of metabolism; motor behaviors

Depends critically on interconnections with other brain regions

Two regions of hypothalamus implicated

Ventromedial hypothalamus (VMH) and Lateral hypothalamus (LH)

Two types of peptide hormones

Satiety peptides and Hunger peptides

Satiety peptides

Decreases appetite

Cholecystokinin (CCK), α-MSH, Somatostatin, Leptin, PYY_3-36, GLP-1

Hunger peptides

Increase appetite

Neuropeptide Y, Galanin, Orexin-A, Ghrelin

Basal metabolism

The majority of food energy is spent on things like heat, cellular activity, and maintenance of membrane potentials

Energy metabolism is under strict homeostatic control and can be adjusted

Short term storage

Insulin converts glucose to glycogen to store as reserve fuel

Glucagon converts glycogen back into glucose when stores are low

Long term storage

Insulin triggers lipid (far) storage in adipose tissues, liver, and muscles

Glucagon produces free fatty acids and ketones

Three phases of energy metabolism

Cephalic phase, Absorptive phase, Fasting phase

Cephalic phase

Preparatory phase, which is initiated by the sight, smell, or expectation of food

Insulin levels high; glucagon levels low

Absorptive phase

Nutrients from a meal meeting the body’s immediate energy requirements, with the excess being stored

Insulin levels high; glucagon levels low

Insulin levels high; glucagon levels low

Promotes utilization of blood glucose as a source of energy

Promotes conversion of excess glucose to glycogen and fat

Promotes conversion of amino acids to proteins

Promotes storage of glycogen in liver and muscle, fat in adipose tissue, and protein in muscle

Inhibits conversion of glycogen, fat, and protein into directly utilizable fuels (glucose, free fatty acids, and ketones)

Fasting phase

Energy being withdrawn from stores to meet the body’s immediate needs

Glucagon levels high; insulin levels low

Glucagon levels high; insulin levels low

Promotes conversion of fats to free fatty acids and the utilization of free fatty acids as a source of energy

Promotes conversion of glycogen to glucose, free fatty acids to ketones, and protein to glucose

Inhibits utilization of glucose by the body but not by the brain

Inhibits conversion of glucose to glycogen and fat, and amino acids to protein

Inhibits storage of fat in adipose tissue

Insulin

Required by glucose transporters in the body to allow use of glucose in the body

Diabetes Mellitus

Lack of insulin production or reduced sensitivity to insulin

Theories of hunger

Set point theory and Positive-incentive theory

Set point theory assumption

Hunger is a response to an energy need; we eat to maintain an energy set point

Set point theory problems

Not everyone is the same size

It doesn’t fit evolutionary pressures; energy storage necessary for survival

Reductions in blood glucose or body fat do not reliably induce eating

It doesn’t account for the influence of external factors on eating and hunger (taste, learning, social cues)

Positive incentive theory

We are drawn to eat by the anticipated pleasure of eating

We have evolved to “crave” food

Eating has a positive-incentive value; multiple factors interact to determine this

Accounts for the impact of external factors on eating behavior

Water Balance

A precise balance of fluids and dissolved salts surround all of the cells of the body to allow proper functioning; approximately like diluted seawater

Important to maintain a decent ratio of water in the intracellular compartment vs the extracellular compartments; happens via diffusion and osmosis

Diffusion

Passive spread of the salt components (ions) to evenly space them in the water

Osmosis

Movement of water molecules to equalize the concentration of two solutions on either side of a semi-permeable membrane

Two types of water imbalance (thirst)

Osmotic thirst and Hypovolemic thirst

Osmotic thirst

Volume of extracellular fluid is slightly decreased due to obligatory losses

Concentration of salt in the extracellular fluid increases

Results in water being drawn out of the cells

Detected by osmosensory neurons

Hypovolemic thirst

Caused by a more significant decrease in the overall volume of extracellular fluid

Due to vomiting, hemorrhage, or sustained diarrhea; detected by baroreceptors

Doesn’t change concentration, just volume

How the brain controls sleep

1. Forebrain system that generates SWS

2. Brainstem system that activates the sleeping forebrain to wakefulness (reticular activating system of the brainstem)

3. Pontine system that triggers REM sleep (REM sleep nuclei in the pons)

4. Hypothalamic system that coordinates the others

Sleep disorders

Insomnia, hypersomnia, sleep apnea, unreliable respiration, nocturnal myoclonus, narcolepsy, nightmares, night terror, REM behavior disorder, sleep paralysis

Sleep apnea

Unreliable respiration

Nocturnal myoclonus

Restless leg syndrome

Nightmares vs night terror

Nightmares are frightening dreams; night terror is arousal from SWS, intense fear

Narcolepsy

Daytime sleep attacks, cataplexy, sleep hallucinations

REM behavior disorder

Act out a dream while sleeping

Sleep paralysis

Inability to talk/move upon waking or falling asleep

Drugs that affect sleep

Hypnotic drugs and anti-hypnotic drugs

Hypnotic drugs

Benzodiazepines, Ambien, Melatonin

Anti-hypnotic drugs

Stimulants and tricyclic antidepressants