Study Guide For Final ExamLecture 20 – Hunger and Eating Behaviors- Know the different hypothalamic Nuclei involved in regulating hunger and satiety and which they are involved in regulatingo Hunger – Lateral Hypothalamus (LH)o Satiety – Ventromedial Hypothalamus (VMH) and the Paraventricular Nucleus (PVN)o Both – Arcuate Nucleus (AN)- Know the neurotransmitters associated with the satiety pathway and theneurotransmitters associated with the hunger pathwayo Hunger Pathway Arcuate nucleus releases melanocyte stimulating neurons (MSHexcitatory neurons) onto satiety center neurons in the VMHand PVN activating them Another Arcuate nucleus neuron releases neuropeptide Y (NPYexcitatory neurons) onto LH hunger neurons and activatesthem NPY neurons inhibit satiety center VMH and PVN satiety neurons release the hormone CRH LH hunger neurons release Orexin- Know the different hunger and satiety signals and what increases their levelso Satiety Signals Cholecystokinin (CCK) – peptide released when the stomachhas food in it Glucose – blood levels rise during absorption Insulin – released by pancreas during absorption Serotonin – increased by absorption of tryptophan (amino acid) Leptin – released by fat cells when they are taking up fato Hunger Signals Ghrelin – peptide released by the stomach when it is empty Glucose – levels lower when there are no nutrients Endocannabinoids – endogenous cannabinoids (production is inhibited by leptin)- Be able to describe the consequences of defects in leptin signaling and how this is related to human obesityo Leptin gene defects/mutations (Ob/ob) cause hyperphagia (huge increase in eating) and thus obesityo Leptin receptor defects (Db/db) cause hyperphagia (huge increase in eating) and thus obesity Human obesity mainly caused by environmental factors rather than defects in genes- List and define the factors influencing when and how much we eat besides the hunger and satiety circuitso Memoryo Work Scheduleso Family traditions or routineso Cultural normso Personal preferences and habitso FOOD AVAILABILITY (most determinate for developed countries)- List and define the factors influencing when and how much we eat besides the hunger and satiety circuitso Social influences – people consume 60% more when eating with others but also decrease consumption so they do not appear gluttonouso Cafeteria Effect – eating one food decreases desire for that food, but then having other foods available makes you eat more of the other foodso Appetizer Effect – eating a small amount of food first often increases your hunger for more foodo Cultural norms – how long our meals are, eating until we are not hungry anymore (Europeans) vs eating until we’re full (Americans)o External/Visual cues – plate/portion size (eating until the plate is clean), super sizing, economy size, etc.o Taste and Enjoyment of food- Know the role of the mesolimbic pathway in eating behaviors and how it may be defective in obesityo Dopaminergic pathway Neurons in the ventral tegmental area release dopamine in response to pleasurable experiences onto neurons in the nucleus accumbens Dopamine stimulation of neurons in the nucleus accembens increases in anticipation of the actual stimulus- “Goldilocks Principle” of dopamine – too much or too little may lead to overeating- There is evidence that obese individuals (especially ones that binge eat) release TOO MUCH dopamine in response to food cues- There is evidence to suggest that TOO LITTLE dopamine release is also associated with weight gain, in association with trying to compensate the low level of pleasure- Know the additional brain regions that influence eating behaviors discussed in class and how they influence themo Amygdala – regulates emotions – provides input to hypothalamus about food aversions, emotional states, stress, etc.o Hippocampus and Medial Temporal Lobe – memory storage – provides input to hypothalamus about how recently we ate, how filling it was, how nutritious and good tasting it was, and learned cravings, etx.o Inferior Frontal Lobe – receives input from the olfactory bulb about smells and taste, provides input to hypothalamus about pleasurable sensory information related to foodo Reward Centers – provides input to the hypothalamus about pleasureLecture 21 – Sleep and Circadian Rhythm- Know the EEG, EOG, and EMG patterns of wakefulness, NREM sleep, and REM sleep and be able to recognize what state of sleep/wakefulness someone is in if given a description of their EEG, EOG, and EMG patternso EOG – Electrooculography – measures movement of eyeso EMG – Electromyography – measures electrical activity of muscles (especially in the neck)o EEG – Electroencephalography – measures electrical activity in the brain Wakefulness – small and rapid EEG waves -- high EOG activity -- high EMG activity “slow wave” sleep (NREM sleep) – larger and slower EEG waves -- no EOG activity -- less EMG activity “fast wave” sleep (REM sleep) –return to small and rapid EEG waves -- high EOG activity -- no EMG activity- Know the different characteristics of REM sleep vs NREM sleepo NREM sleep Accounts for 6-8 hours of sleep Stage 3 and 4 sleep is deepest and hardest to wake from  Characterized by a ton of movement We do dream, but they are fragmented Children have night terrors hereo REM sleep Muscles occasionally twitch (motor activity is inhibited) Accounts for 2 hours of sleep (increases as the sleep lasts longer) More dreaming and more vivid dreams- Know the arguments for and against the need for REM sleepo For REM sleep Nearly all mammals and many birds appear to have REM sleep If deprived of REM sleep, a person experiences REM rebound (increased tendency to go into REM sleep and have more REM sleep per sleep sessiono Against REM sleep Some animals (whales and dolphins) seem to have very little or no REM sleep Nearly all anti-depressant medications suppress REM sleep - Know the different characteristics of dreaming and its hypothesized functions, and how activity of specific brain regions is changed in ways consistent with these different functionso Freudian Interpretations – dreams are a manifestation of our subconscious wishes, desires, and fears Activity in the dorsolateral prefrontal cortex decreases Activity in the amygdala