1. Chemical Control of hunger
1.1. Artificial: Fen-phen (drug developed to try to decrease body weight and hunger)
1.2. Neuropeptide Y (NPY):Released in hypothalamus causing an increase in eating, Increase in hypothalamus=big increase in eating
1.3. Ghrelin: Hormone/Peptide released in stomach and hypothalamus and increase in hunger, Increased hunger signal to brain/hypothalamus, Effective through NPY receptors
1.4. Cholecystokinin (CCK): its job is to induce satiety, released when we are eating, Hormone/Peptide released by stomach, Delayed signal (20-30 min after we have started eating, CCK is released to get us to stop eating), Induces satiety
1.5. Leptin: Hormone/Peptide released from fat tissue, Induces satiety
2. Hunger
3. Neural control of hunger
3.1. Ventromedial hypothalamus (VMH)
3.2. Lateral hypothalamus
3.2.1. Nigrostriatal bundle
3.3. Paraventricular nucleus: involve in hunger and satiety
4. Evolution Rules: adapted to eat fats and sugars
4.1. this is what makes food taste good to us
4.2. we are adapted to eat what is available
4.3. "what the hell" phenomenon
5. Body weight maintenance
5.1. Exercise
5.2. Eat healthy, unprocessed food
5.3. eating and evolution/adaptation
6. Experimental surgery
6.1. Lesions: fried neurons in certain area chemically or electrically
6.2. Stimulation: stimulate the neurons in a certain area chemically or electrically
7. Fuel absorption
7.1. Proteins: amino acids
7.2. Carbohydrates: gluose
7.3. Fats
8. Short-term Reservoir
8.1. Hormones: released as part of endocrine system, ex:// oxytocin: bonding effect
8.2. Endorphins: neuropeptides,, very potent painkillers
9. Sleep
9.1. Stage 1: low voltage EEG, ↓ EMG, looks like beta rhythms, not very different from wake, we distinguish it based on muscle activity, has distinct drop in muscle activity (jaw opening up, headbob of nodding off
9.2. Stage 2: sleep spindles (rapid rhythmic burst), K-complexes (brain REALLY starts to slow down and at higher amplitude), slight ↓ EMG, muscle activity
9.3. Stage 3: between 20 & 50% delta waves of 30 sec epoch, slow wave sleep is taking over (delta waves) muscle activity stays the same as stage 2
9.4. Stage 4: > 50% delta waves in epoch, rhythmic, SLOW responding and high amplitude, slow frequency, muscle activity stays the same as stage 2
9.5. REM: low voltage EEG, ↓ ↓ EMG, last stage of sleep we go into, rapid, make big hourglass shapes on epoch, brain waves are basically awake, it is an awake brain in an asleep body, brain waves change rapidly to stage 4 to awake brain pattern, and a DRAMATIC IMMEDIATE drop in muscle tone/activity
9.5.1. It is dependent on the Pons (locus coeruleus - turns off muscle tone LACK OF MUSCLE TONE and starts muscle twitches) If we damage this, muscle tone does not get turned off when we sleep, we will act out our dreams
9.5.2. we tend to wake up more in REM sleep (especially when we don’t have an alarm clock waking us up)
9.6. NREM: non-REM, every stage of sleep that’s not REM sleep (stage 1, 2, 3, 4)
9.7. SWS: slow wave sleep (stage 3 & 4) not unusual to see these waves collapse together, mostly at the beginning of the night
9.8. Pons - Muscle tone: locus coeruleus, Muscle twitches
9.9. College Student Sleep:
9.9.1. ○ On average sleep 7-7.5 hours on weekdays and 8.5 to 9.5 hours on weekends
9.9.2. Major issue: irregular sleep (1 nap, 3 hours, and 20 min in each class) trains our brain that any time that we are sitting down and comfortable, our brain will try to go to sleep and will induce sleep when you're not supposed to
10. Reproduction
10.1. Genetics of Development
10.1.1. 23 pairs of chromosomes, 23rd set determines gender, female has more genetic material
10.1.2. Focusing on attention and monitoring it is important for this
10.1.3. Dosage compensation: female has more "dose" of genetics; varies from species to species; in most cases, females activate the equivalence of one X; males activate the Y and the X; most of us carry the gene for schizophrenia and it isn't activated, females have extra genetic material but choose what gets activate and seem to choose what is usually better; on every other pair we activate a little bit moms and a little bit of dad's genes, not all genes get activated
10.2. Hormones
10.2.1. Females:as the process occurs in fetus of deciding X and Y, hormones are also created
10.2.1.1. Estrogen – controller and impacts the other hormones and how they are released, can increase aggression (seductress), works with DA, 5-HT, oxytocin ( how female reacts in sexual behavior encounter)
10.2.1.2. Progesterone – allows gestation (allows fetus to develop), counter estrogen by providing calming influence
10.2.1.3. Testosterone – assertive, aggression, sex drive
10.2.1.4. Oxytocin – encourages labor/child birth & lactation; cuddler, empathy, feel good (with DA), reduce stress, increase trust
10.2.1.5. Vasopressin – subtle aggression-masculine tendencies, similar in structure to oxytocin (competitive energy to make sure you and your baby have food)
10.2.2. Males
10.2.2.1. Testosterone – dominant, assertive, competition, aggression, sex drive (highest about 16-18)
10.2.2.2. Vasopressin – Mr. Gallant, monogamy, protect turf/mate/children
10.2.2.3. Oxytocin – encourage cuddling, empathy, reduce stress, increase trust, connection on emotional level
10.2.2.4. Prolactin – Mr. Mom, connections with mate and children, increase parental caring/behavior, decrease sex drive, more caring, improving connections
10.2.2.5. Estrogen – Could be source of power
11. Sleep Motivation
11.1. Recuperative factor: the longer you are awake, the more you want to go sleep, we wake up in the morning and the drive to go to sleep immediately starts. Napping will reset this and make us more alert, napping earlier in the day is better
11.2. Circadian factor: when have less sleepiness then increased sleepiness and we will want to go to sleep
11.3. When you stay awake for more than one day, you get both of these
12. Sleep Deprivation
12.1. If you're sleep deprived enough, you will go right into REM (RARE)
12.2. Humans: don't usualy do these studies, everything was perfectly normal after 11 days of no sleep, performance, health and well-being are affected, chronic partial sleep deprivation
12.3. Rat sleep deprivation study done because you can't get long term effects from human study
13. What sleep does for us
13.1. Protein synthesis: Certain types primarily occur at night; so you can't get this from napping during the day
13.2. Memory consolidation/connection
13.3. Immune system; More likely to get sick if you aren't sleeping right, True evidence that the immune system is reset during sleep AT NIGHT
13.4. Heart health: Increased risk of cardiovascular disease and blood pressure if you don't get enough sleep
13.5. Body weight (risk of obesity; react correctly to insulin), deprives us from reacting to insulin like we should to maintain healthy body weight; also when you are awake you are more likely to eat
13.6. Muscle growth; tissue recovery (protein synthesis again), Much of the processing to maintain and increase muscle mass is done at night when we are sleeping
13.7. Reset biological clock; emotions; self-regulation
14. Human eye
14.1. Retina
14.1.1. back part of the eye that allows us to see, light comes through pupil, then lens projects it on the retina
14.2. Part of the Central Nervous System
14.3. Blinspot
14.3.1. spot on your eye where you cannot see. The layer of neurons on the most interior side send info to the brain and the blindspot is where the axons exit the brain
14.4. Fovea
14.4.1. at the very back of the eye, gives us our most acute vision. Has the best eyesight you can have.
14.5. Lens
14.5.1. job is to make sure the object we are looking at is displayed on the retina
14.5.2. Accommodation: the lens changes shape to accommodate to what they are looking at
14.5.3. Glasses assist the lenses to project images to the retina at the back of the eye
15. Transfer of Visual Input
15.1. Retina of the eye: multiple layers of neurons, information must be convert a lightwave into an action potential
15.2. Three major layers where light wavesa re converted to action potential
15.2.1. Photoreceptors: light must pass through to get to brain; all mammals have these a the back of their eye
15.2.1.1. Cones: activated when there is enough light; better in daylight, give us color vision, clearer vision, 6 million of these
15.2.1.2. Rods: not in the fovea, 120 million, black/whit vision, less well-focused vision
15.2.2. Bipolar cells: specialized for visual processing and transferring info from photoreceptors to ganglion cells
15.2.3. Ganglion cells: normal neurons, their axons form the optic nerve and send information to the brain. This is where the action potential occurs
15.3. 2 additional kinds of cells
15.3.1. Horizontal cells: between photoreceptors and bipolar cells, take information from one part of retina and impact an area in a different part of the retina
15.3.2. Amacrine cells: between bipolar and ganglion cells
16. Visual Pathway: right visual field goes to the outer edge of the left eye and vice versa
16.1. Optic nerve
16.2. Optic chiasm: crossover of information
16.3. Lateral geniculate nucleus
16.4. Superior colliculus (midbrain): branches from optic nerve and foes to the back of the brain at the same time as lateral geniculate nucleus
16.5. Primary visual cortex (occipital lobe): starts to process visual information, info is being transferred from lateral geniculate nucleus to the center of all the neurons
17. Visual Perception
17.1. Lamellae: lines of plates that are proteins
17.1.1. Photopigments imbedded within lamella: Opsin: protein, Retinal: fat, Rhodopsin: light sensitive pigments
18. Retina
18.1. Resting conditions: bipolar - hyperpolarized, ganglion: -70 mV
18.2. Light waves-retina: Bleaching of rhodopsin, hyperpolarization of photoreceptors, depolarization of bipolar cells
18.3. Lateral inhibition: allows us to see edges and find objects, inhibits nearby bipolar cells (shuts them down)
18.4. central vs peripheral: central processing in the fovea 1:1:1 ratio, peripheral processing: into multiple bipolar cells to one ganglion
18.5. Color vision: 3 types of cones: short-blue, medium-green, long-red
18.5.1. Trichromatic/compenent theory
18.5.2. Opponent processing theory: negative after-images
18.5.3. Color blindness: X-linked on chromosomes, Red/green is most common, Blue/yellow is rare