Lecture 9 - Regulation

• excess of Glucose and amino acids is stored • as glucose in blood increases, PNS is activated • Physiological changes occur, including bile released to digest lipids and gastro-intestinal system is no longer inhibited by sns • more insulated secreted by pancrease for glucose uptake in cells (not brain cells) • insulin move glucose from blood -> cells

glucose and amino acids

Make blood syrupy, doesnt work, need optimal level (diabetes)

Glucose is stored as glycogen (carb) stored in muscles and liver, to convert later back to glucose (fuel for brain(

Fat = tyrigylceride = glycerol (carb) + fatty acids - stored under skin/ around organs - harmful

• Clock/ schedules (learned) • Smells/ sight/ taste - anticipations of food lowers glucose in blood - low glucose levels make you hungry • Size of meal/ fat content - small portions = nicer, if distracted by others/ tv you eat more

• Intenstines give sinals to brain via CCK and PYY chemicals • Liver + panrease (insulin) feedback to hypothalamus • Adipose tissue growth produces LEPTIN - tells brain to stop eating

Body parts send signals to • Lateral hypothalamus (NPY) • Arcuate nuclueus hypothalamus (Leptin goes here) - when receiving leptin, this area produces NEUROPEPTIDE Y

Regulates feeding, starting feeding, its under control from Leptin and ventromedial nuclues in hypothalamus

In the hypothalamus, regualted feeding via NPY When lesioned in a rat, they couldnt stop eating. But it isnt just the VMN that controls eating, its loads of things

SNS is activated as glucose levels drop too much in blood, due to: • Adrenal medulla (adrenaline - feel jittery) • ADipose tissue (break down fats) • Pancrease (stops secreting insulin, now secretes glucagon, using glycogen stores from liver and muscles to make energy)

• Leptin deficiency/ faulty leptin receptors - Doenst cause obesity tho • Genetic differences - Maybe afircan americans passed on very slow metabolisms • learning from parents/ evolution • capitalise on high salt/sugar/ fat foods when we can • learn portions, less excercise, grazing/ snacking • Serotonin • can help suppress eating and lose weight • can help against bulimia, not anorexia

Women have: • Slighlty smaller brains • Thicker corpus callosum • Share function hemispheres • Slight difference in diencephalon/ telencephalon

• Organisational effects 2. Activational effects

• Prenatal: genetics -> sex organs -> hormones • determines which system we follow • permanant, influence brain and sex organ development

• occur later in life, after development of sex organs - e.g. puberty or menopause

• Gonads - 1st to develop - via genetics • Internal sex organs - precursers for male and female internal organs are present in embryo, default = girl • external genitalia - visibile sex organs, masculine development requires androgens

XX = male XY = female Determine different development of brain and gonads (organisational effect)

Testosterone: WOLLFIAN SYSTEM develops, causing masculination Estrogen: MULLERIAN SYSTEM develops, causnig feminisation We’re a girl by default - During prenatal phase, if gonads start to develop testosterone - we become a boy

X0 chromosome • Short stature, webbed necked, shield chest, wide nipples, rudimentary ovaries (dont work) • can happen under to foetus under infulence of genetics

• Hypothalamus - produces GNRH • Stimulates Pituitary gland produces LH and FSH (precursor hormones) • Gonads (testes - testosterone, ovaries - estrogen) - estrogen helps ova release and develop egg (otherwise system resets) - testosterone can also be inhibited, dont need it 24/7

Testes: testosterone - facial/ armpit hair, public hair, deeper voice, hairline changes, muscle growth, bone maturation, external genitalia mature Ovaries: estrogen - Breasts, fat distribution, external genitalia mature

Organisational - some structures are different in brains of men/ women Activational - may affect some behaviours (sexual, emotional and cognitive)

prenatally - anatomy, social behaviour, sexual ID