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Lecture 3

PSYC 318 - Week 3 Lecture notes

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Department
Psychology
Course
PSYC 318
Professor
Wayne Sossin
Semester
Winter

Description
PSYCH 318 Behavioral Neuroscience II Professor Wayne Sossin Week 3, Class 1: Hunger and Eating (2) Eating: Not tightly regulated by nutritional needs Appetitive Mechanisms External modulated by Internal appearance time since last meal smell & taste size of last meal variety time of day social factors physical activity etc etc Hunger and Eating • Hunger and satiety signals from the periphery and the hypothalamus are integrated with reward and pleasure signals. o Reward and Pleasure signals come from other brain areas such as the Ventral Tegmental Area (VTA) and Nucleus Accumbens (NAcc) o Integration of information leads to control of food intake • Most feeding has even less to do with immediate physiological need in today’s “obesigenic environment” o Food is widely available to us • For our ancestors: food was not always available Study: Variety: Sensory Specific Satiety • Declining satisfaction generated by consumption of certain type of food, and the consequent renewal in appetite resulting from the exposure to new food. o Rats ate more with a non-varied diet. Sensory-Specific Satiety : • Firing of cells in the Lateral Hypothalamus in response to Food Stimulus • Feed monkey, observe cell firing. o Monkey’s hungry: Wide range of food stimuli increases cell firing in the lateral hypothalamus. ▪ Eating peanuts, oranges, bananas or a glucose solution increased cell firing. o If monkey sated on glucose: ▪ Glucose no longer increases cell firing but other food does. o Monkey sated with bananas: ▪ No firing from bananas, but firing from other food still occurs. • Our eating behavior: o Throughout a meal, we continuously compare the actual and expected reward value of food. ▪ The more variety the more we eat LH projects to the VTA to modulate dopaminergic cell firing in the VTA and promote reinforcement and reward. Stimulus-initiated movement: • Monkey must release key, reach hand into box to get food. o Touching food increased dopaminergic cell firing. • If there’s previous stimulus, monkeys respond to predictive stimulus. o Dopaminergic cell firing occurs before the monkey touches food. • Dopaminergic cell firing transfers from food touch to door opening. • As dopamine neurons respond to a reward predicting stimulus, they stop responding to the reward which is now predicted by the stimulus NAcc Dopamine Depletion Decreases Willingness to Work for Food • Nacc: Nucleus Accumbens. • 6-Hydroxydopamine was injected in the rats NAcc to destroy dopaminergic neurons. • When food was easy to get, the DA lesioned and control animals obtained and ate the same amount of food. • When food was hard to get , the lesioned rats were less willing to work for food. • NAcc DA transmission sustains interest in obtaining the food reward and the willingness to persist in effort to get it Dopamine & Effort Allocation • Rats had to choose between working for a preferred food (bar pressing) or walking to the other side of the cage and eat freely available but less palatable rat chow. • Normal rats preferred to work for their favorite food. o Normal rats were pressing lever a lot to eat yummy food. • The administration of a Dopamine receptor antagonist (raclopride) shifts the preference toward the easily available food. o More raclopride, less dopamine. • Rats don’t press lever as much, eat the bland food. • These results add to the evidence that Dopamine enhances the animal’s ability to sustain interest in expected rewards. Serotonin: 5-HT release in the hypothalamus increases before and during eating • Why is serotonin increasing? Study: Injection of 5HT in the Hypothalamus Decreases DA Release in the NAcc • 5HT injection to periventricular nucleus of hypothalamus • Serotonin is antagonising DA effects, inhibits “reward”. Injection of 5HT in the Hypothalamus Decreases DA Release in the NAcc 5HT: a satiety signal • Antagonists of postsynaptic 5HT receptors in the brain increase food intake. • 5HT reduces meal size and duration. • In humans, serotonergic drugs facilitate satiation o Serotonergic drugs were withdrawn from market because they caused heart problems. o Occurs because 5HT receptors are also found in heart. • 5HT seems to influence primarily the termination of feeding. Reward pathways • Dopamine and serotonin modulate reward pathways: o Dopamine signals reward and increases food intake o Serotonin antagonizes the effects of dopamine and inhibits food intake • Peptides (Leptin and Ghrelin) can also modulate reward pathways Study: Effects of Food Restriction or Leptin injection in the cerebral ventricles on the sensitivity of reward circuits • Food deprivation might increase the perceived value of food by changing the sensitivity of reward circuits. o Food deprivation increases sensitivity to electrical brain stimulation • Leptin (Feeding inhibitor) decreases the sensitivity to electrical brain stimulation (Electrical brain stimulation signals reward.) Recall: Leptin: • Signals from Fat to Brain • Produced by adipose tissue • Decreases food intake • Increases metabolic rate • Acts on the arc of the hypothalamus o (inhibits AgRP/ NPY neurons and activates POMC/CART neurons) Study: Leptin also acts on the Ventral Tegmental Area • VTA neurons respond to leptin by reducing their firing rate • Direct administration of Leptin to the VTA decreased food intake Ghrelin: • Ghrelin modulates Dopaminergic reward pathways • Ghrelin (The Hunger Hormone): o Released by the stomach o Acts on the G-protein-coupled- growth-hormone secretagog receptor o Acts on the Arc (Arcuate Nucleus) of the hypothalamus and on the hindbrain to increase feeding o Ghrelin activates AgRP/NPY neurons in the Arc of the hypothalamus Study: Ghrelin also acts on the Ventral Tegmental Area • Ghrelin acts on the VTA to increase action potential generation in Ventral Tegmental Area Dopaminergic neurons • Observed in brain Slices from Rats: o Ghrelin increases firing rate in VTA DA neurons. o Wash out ghrelin, spike frequency returns to control levels Local injections of Ghrelin in the Ventral Tegmental Area stimulates food intake in rats • Food intake was measured 2h post-injection. o Ghrelin rats ate more than saline (control) rats. Leptin & Ghrelin modulate Dopaminergic reward pathways Leptin and Ghrelin act on the arcuate nucleus of the hypothalamus to control physiological food intake. They also both act in VTA, on DA neurons to control reward pathways. • Leptin decreases food intake (negative effect) • Ghrelin increases food intake (positive effect) Study: Exposure to appetitive food stimuli markedly activates the human brain • PET-FDG study FDG: o 2-deoxy-2 [18F] fluoro-D-glucose was used to measure glucose uptake in different brain areas o A radioactive tracer was used to measure activation of brain areas. • Exposure to food cues (smell of heated food, small taste on tongue) in food deprived subjects (17-19 hrs) increased activation of SS (somatosensory cortex Correlation is seen between changes in activation of the right orbitofrontal cortex and self-report rating of hunger and desire for food • Higher activation of right orbitofrontal cortex means increased hunger. Study: Wanting Food: Dopamine • PET study was done with a dopamine tracer to measure dopamine release in the Striatum o Dopamine in striatum is involved in reward • Food deprived subjects were exposed to food stimuli but could not eat it. o The higher the self-reported “Hunger” or “Desire for Food”, the greater the Dopamine release as measured by PET. Personality Predicts the Brain’s Response to Viewing Appetizing Foods • The Neural Basis of a Risk Factor for Overeating o Eating can be triggered by the sight of food. o External Food Sensitivity (EFS): ▪ Viewing appetizing foods can induce craving and eating. ▪ This EFS varies amongst individuals o Increased EFS is associated with overeating. • Study: o Subjects (healthy volunteers) were food deprived for 2 hrs. o During fMRI scanning, subjects viewed full-color photos of foods consistently identified as highly appetizing (e.g., chocolate cake, ice cream) or bland (e.g., rice, potatoes) ▪ Personality had an effect on appetizing vs bland food cues: • EFS was positively correlated with the connectivity between the amygdala and the ventral striatum. o Attributed to the emotional and motivational states evoked by the sight of appetizing foods. • EFS was positively correlated with the connectivity between the ventral striatum and the premotor cortex. o Might enable the preparation of motor acts necessary for eating • People with high EFS show altered brain connectivity to the sight of appetizing versus bland food. o Just think of the power of food advertisement! Study: Changes in brain activity related to eating chocolate From pleasure to aversion • Self-described “Chocoholics” ate chocolate until they found it unpleasant. o Wanting more chocolate was associated with brain activity in regions related to hedonic aspects of taste: ▪ Striatum ▪ Midbrain (possibly the VTA) ▪ Insula ▪ Subcallosal region (ventral anterior cingulate plus medial OFC) ▪ Posterior cingulate. • As eating became unpleasant, activity changed in brain regions related to response inhibition: o Prefrontal cortex o Lateral orbitofrontal cortex o Parahippocampal gyrus Summary • Dopamine signals reward, expectation of reward. o Sustains the willingness to persist in effort to get the reward. • Serotonin inhibits dopamine release and inhibits eating • Leptin and Ghrelin act on the Arc of the hypothalamus to control physiological food intake and on the VTA to control reward pathways involved in eating. • People with different External Food Sensitivity show different brain connectivity to the sight of appetizing versus bland food. Week 3, Class 2: Dysregulated eating Obesity Bulimia Nervosa Anorexia Nervosa Obesity Definition: A medical condition characterized by accumulation of excess body fat to the extent that it may have adverse effects on health • The body mass index (BMI) is the measurement tool most routinely used in the clinic to diagnose obesity • Body Mass Index is a measure of body fat based on height and weight. 2 o BMI ≥ 30 kg/m signals obesity o > 40% of North American adult population obese (tripled since 1980) • Obesity is a risk factor for: o Type 2 diabetes o Hypertension o Cardiovascular diseases o Respiratory, musculoskeletal, infectious, psychiatric disorders o Cancer • Economic cost: $75 billion/year in US. o 5.7% of health costs. o 7th leading cause of death. High rates of obesity reflect: (i) Superabundance of food in present society o Obesigenic environment (ii) Decreased physical activity o Sedentary Lifestyle (iii) Aging population Role of Genetics • 30 to 40% of variance in the BMI can be attributed to genetics o Some people are genetically predisposed to accumulate fat • Twin studies: o Identical young-adult male twins were overfed by 1000 kcal/d over a 100-day period o Some twin pairs gained much more weight than other pairs o The similarity in response within pairs was evident for body weight, percentage of fat, fat mass, and stimated subcutaneous fat o Genetics impact weight gain Role of Environment • Pima Indians: o Were separated 700 to 1000 years ago ▪ Share a similar genetic predisposition o Environment: ▪ Those residing in Arizona have among the highest prevalence of obesity. ▪ Those living a traditional lifestyle in a remote section of Mexico have significantly lower BMI than those living in Arizona o Lifestyle differ in terms of both diet and energy expenditure. o Those living in Mexico eat a diet with less animal fat and caloric density and more complex carbohydrates than those in Arizona. ▪ They also have greater energy expenditure from physical labor. Causes of obesity: Most popular hypothesis: • A positive energy balance due to a combination of excessive food intake and lack of physical activity in genetically predisposed individuals Are hormones that control eating dysregulated in obesity? • Arcuate Nucleus of the Hypothalamus (Contairs central command centers): o AgRP/NPY neurons (orexigenic): ▪ When activated, release: • Neuropeptide Y signalling • Agouti-related peptide . ▪ activated by Ghr, inhibited by PYY, leptin and insulin ▪ Stimulate food intake. o POMC/CART neurons (anorectic): ▪ Release: • Proopiomelanocortin (POMC) -derived peptide (precursor) • α-melanocyte-stimulating Hormone (α-MSH) ▪ Activated by leptin and insulin Is Leptin dysregulated in obese patients? Leptin: • Produced by adipose tissue • Decreases food intake and increases metabolic rate • Genetically altered mice that do not produce leptin are obese • Some very rare cases of human obesity are due to not producing leptin o (can be cured by treatment with Leptin) Study: Obese patients who produce leptin • Subjects spent 48 hours in a lab. o Beginning the morning of day 2, plasma was sampled every 7 minutes for 24 hours. o The arrows indicate the 4 meals. • In the obese subjects, plasma leptin levels were much higher than those seen in lean subjects. • Suggests that obesity is not due to insufficient leptin release but to resistance to the effects of leptin. o Obesity may be cured if we discover the cause of leptin resistance Neuropeptide Y: • Released by the AgRP/NPY neurons of the Arc of the hypothalamus • Increases food intake • Leptin inhibits rel
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