Prepared by Grant McLaren, Department of Psychology, Edinboro University of Pennsylvania FOUNDATIONS OF BEHAVIORAL NEUROSCIENCE 9 TH EDITION This multimedia

Prepared by Grant McLaren, Department of Psychology, Edinboro University of Pennsylvania

FOUNDATIONS OF BEHAVIORAL NEUROSCIENCE 9TH EDITION

This multimedia product and its contents are protected under copyright law.The following are prohibited by law: any public performance or display, including transmission of any image over a network, preparation of

any derivative work, including the extraction, in whole or in part, of any images, any rental, lease or lending of the program

Copyright © 2014 Pearson Education, Inc. All Rights Reserved

Chapter 11

Ingestive BehaviorCopyright © 2014 Pearson Education, Inc. All Rights

Reserved


Physiological Regulatory Mechanisms

Drinking

Some Facts About Fluid Balance

Two Types of Thirst

Eating: Some Facts about Metabolism

What Starts a Meal?

Signals from the Environment

Signals from the Stomach

Metabolic Signals


What Stops a Meal?

Gastric Factors

Intestinal Factors

Liver Factors

Insulin

Long-Term Satiety: Signals from Adipose Tissue


Brain Mechanisms

Brain Stem

Hypothalamus

Obesity

Possible Causes

Treatment


Anorexia Nervosa/Bulimia Nervosa

Possible Causes

Treatment

Ingestive BehaviorsLearning Objectives

1.Explain the characteristics of a regulatory mechanism.

2.Describe the fluid compartments of the body.

3.Explain the control of osmometric thirst and volumetric thirst and the role of angiotensin.

4.Describe characteristics of the two nutrient reservoirs and the absorptive and fasting phases of metabolism.

5.Discuss the signals from the environment, the stomach, and the metabolism that begin a meal.

6. Discuss the long-term and short-term factors that stop a meal.

7. Describe research on the role of the brain stem and hypothalamus in hunger and satiety.

8. Discuss the social and physiological factors that contribute to obesity.

9. Discuss surgical, behavioral, and pharmacological treatments for obesity.

10. Discuss the physiological factors that may contribute to anorexia nervosa and bulimia nervosa. Copyright © 2014 Pearson Education, Inc. All Rights

Reserved


homeostasis (home ee oh stay sis) The process by which the body’s substances and characteristics (such as temperature and glucose

level) are maintained at their optimal level.

ingestive behavior (in jess tiv) Eating or drinking.



system variable A variable that is controlled by a regulatory mechanism, for example, temperature in a heating system.

set point The optimal value of the system variable in a regulatory

mechanism.

correctional mechanism In a regulatory process, the mechanism that is capable of

changing the value of the system variable.




negative feedback A process whereby the effect produced by an action

serves to diminish or terminate that action; a characteristic of regulatory systems.

satiety mechanismA brain mechanism that causes cessation of hunger or thirst, produced by adequate and available supplies of nutrients or water.

Copyright © 2014 Pearson Education, Inc. All Rights

Reserved


DrinkingSome Facts About Fluid Balance

intracellular fluidThe fluid contained within cells.

extracellular fluid All body fluids outside cells: interstitial fluid, blood plasma, and

cerebrospinal fluid.

intravascular fluidThe fluid found within the blood vessels.


Reserved



isotonicEqual in osmotic pressure to the contents of a cell. A cell placed in an

isotonic solution neither gains nor loses water.

hypertonicThe characteristic of a solution that contains enough solute that it will draw

water out of a cell placed in it, through the process of osmosis.

hypotonicThe characteristic of a solution that contains so little solute that a cell

placed in it will absorb water, through the process of osmosis.




hypovolemia (hy poh voh lee mee a)Reduction in the volume of the intravascular fluid.


DrinkingTwo Types of Thirst

The term thirst means different things in different circumstances.

Its original definition referred to a sensation that people say they have when they are dehydrated.

Because we do not know how other animals feel, thirst simply means a tendency to seek water and to ingest it.


DrinkingOsmometric Thirst

osmometric thirstThirst produced by an increase in the osmotic pressure of the interstitial

fluid relative to the intracellular fluid, thus producing cellular dehydration.

osmoreceptorA neuron that detects changes in the solute concentration of the

interstitial fluid that surrounds it.


Reserved



Investigators placed a micropipette against the membranes of individual osmoreceptors and found that the application of pressure or suction could alter the membrane potential of the cells.

For example, if a cell was exposed to a hypertonic solution, the cell lost water and its membrane potential fell.

If pressure was then applied, the volume of the cell increased and the membrane potential returned to normal.




A functional imaging study by Egan et al. (2003) found that the human AV3V also appears to contain osmoreceptors.

The investigators administered intravenous injections of hypertonic saline to normal subjects while their brains were being scanned.

They observed strong activation of several brain regions, including the AV3V and the anterior cingulate cortex.



DrinkingVolumetric Thirst

volumetric thirstThirst produced by hypovolemia.

Volumetric thirst occurs when the volume of the blood plasma—the intravascular volume—decreases.

Loss of blood causes pure volumetric thirst. From the earliest recorded history, reports of battles note

that the wounded survivors called out for water.



Role of Angiotensin

renin (ree nin) A hormone secreted by the kidneys that causes the conversion of angiotensinogen in the blood into angiotensin.

angiotensin (ann gee oh ten sin)A peptide hormone that constricts blood vessels, causes the retention of sodium and water, and

produces thirst and a salt appetite.




Role of Angiotensin

subfornical organ (SFO)A small organ located in the confluence of the

lateral ventricles, attached to the underside of the fornix; contains neurons that detect the presence of angiotensin in the blood and excite neural circuits that initiate drinking.



Role of Angiotensin

median preoptic nucleusA small nucleus situated around the front of the

anterior commissure; plays a role in thirst stimulated by angiotensin.



Eating: Some Facts About Metabolism

glycogen (gly ko jen)A polysaccharide often referred to as animal starch; stored in liver and muscle; constitutes the short-

term store of nutrients.

insulinA pancreatic hormone that facilitates entry of

glucose and amino acids into the cell, conversion of glucose into glycogen, and transport of fats into adipose tissue.

glucagon (gloo ka gahn)A pancreatic hormone that promotes the conversion

of liver glycogen into glucose.Copyright © 2014 Pearson Education, Inc. All Rights

Reserved



triglyceride (try gliss er ide)The form of fat storage in adipose cells; consists of

a molecule of glycerol joined with three fatty acids.

glycerol (gliss er all)A substance (also called glycerine) derived from the breakdown of triglycerides, along with fatty acids;

can be converted by the liver into glucose.

fatty acidA substance derived from the breakdown of

triglycerides, along with glycerol; can be metabolized by most cells of the body except for the brain.



Figure 11.11 reviews what I have said so far about the metabolism that takes place while the digestive tract is empty, which physiologists refer to as the fasting phase of metabolism.

A fall in blood glucose level causes the pancreas to stop secreting insulin and to start secreting glucagon.

The absence of insulin means that most of the cells of the body can no longer use glucose; thus, all the glucose present in the blood is reserved for the central nervous system.



fasting phaseThe phase of metabolism during which nutrients are not available from the digestive system; glucose, amino

acids, and fatty acids are derived from glycogen, protein, and adipose tissue during this phase.

absorptive phaseThe phase of metabolism during which nutrients are

absorbed from the digestive system; glucose and amino acids constitute the principal source of energy for cells during this phase, and excess nutrients are stored in adipose tissue in the form of triglycerides.


Reserved


What Starts a Meal?Regulation of body weight requires a balance between food intake and energy expenditure.

If we ingest more calories than we burn, we will gain weight.

Assuming that our energy expenditure is constant, we need two mechanisms to maintain a relatively constant body weight.

One mechanism must increase our motivation to eat if our long-term nutrient reservoir is becoming depleted, and another mechanism must restrain our food intake if we begin to take in more calories than we need.


What Starts a Meal?Signals from the Environment

Although an empty stomach is an important signal, many factors start a meal, including the sight of a plate of food, the smell of food cooking in the kitchen, the presence of other people sitting around the table, or the words “It’s time to eat!”


What Starts a Meal?Signals from the Stomach

An empty stomach and upper intestine provide an important signal to the brain that it is time to start thinking about finding something to eat.

Recently, researchers discovered one of the ways this signal may be communicated to the brain. The gastrointestinal system (especially the stomach) releases a peptide hormone called ghrelin (Kojima et al., 1999).


What Starts a Meal?Signals from the Stomach

ghrelinA peptide hormone released by the stomach that increases

eating; also produced by neurons in the brain.

duodenumThe first portion of the small intestine, attached directly to the

stomach.



What Starts a Meal?Metabolic Signals

glucoprivationA dramatic fall in the level of glucose available to cells; can be caused by a

fall in the blood level of glucose or by drugs that inhibit glucose metabolism.

lipoprivationA dramatic fall in the level of fatty acids available to cells; usually caused by

drugs that inhibit fatty acid metabolism.



hepatic portal veinThe vein that transports blood from the digestive

system to the liver.


Reserved



To summarize: The brain contains detectors that monitor the availability of glucose (its only fuel) inside the blood–brain barrier, and the liver contains detectors that monitor the availability of nutrients (glucose and fatty acids) outside the blood–brain barrier.


Reserved


What Stops a Meal?

There are two primary sources of satiety signals—the signals that stop a meal. Short-term satiety signals come from the immediate effects of eating a particular meal, which begin long before the food is digested.

These signals do not control the beginning and end of a particular meal, but they do, in the long run, control the intake of calories by modulating the sensitivity of brain mechanisms to the hunger and satiety signals that they receive.


What Stops a Meal?Gastric Factors

The stomach apparently contains receptors that can detect the presence of nutrients.

Of course, this study indicates only that the stomach contains nutrient receptors; it does not prove that there are not detectors in the intestines as well.


What Stops a Meal?Intestinal Factors

The intestines do contain nutrient detectors.

Studies with rats have shown that afferent axons arising from the duodenum are sensitive to the presence of glucose, amino acids, and fatty acids (Ritter et al., 1992).

In fact, some of the chemoreceptors found in the duodenum are also found in the tongue.

These axons may transmit a satiety signal to the brain.



cholecystokinin (CCK) (coal i sis toe ky nin)A hormone secreted by the duodenum that regulates

gastric motility and causes the gallbladder (cholecyst) to contract; appears to provide a satiety signal transmitted to the brain through the vagus nerve.



Investigators have discovered another chemical produced by cells in the gastrointestinal tract that serves as an additional satiety signal.

This chemical, peptide YY3–36 (let’s just call it PYY) is released by the small intestine after a meal in amounts proportional to the calories that were just ingested.


Reserved


What Stops a Meal?Liver Factors

Satiety produced by gastric factors and duodenal factors is anticipatory; that is, these factors predict that the food in the digestive system will, when absorbed, eventually restore the system variables that cause hunger.


What Stops a Meal?Liver Factors

Not until nutrients are absorbed from the intestines can they be used to nourish the cells of the body and replenish the body’s nutrient reservoirs.

The last stage of satiety appears to occur in the liver, which is the first organ to learn that food is finally being received from the intestines.


What Stops a Meal?Insulin

The absorptive phase of metabolism is accompanied by an increased level of insulin in the blood.

Insulin permits organs other than the brain to metabolize glucose, and it promotes the entry of nutrients into fat cells where they are converted into triglycerides.

Insulin is a peptide and would not normally be admitted to the brain. However, a transport mechanism delivers it through the blood–brain barrier, and it reaches neurons in the hypothalamus that are involved in regulation of hunger and satiety.


What Stops a Meal?Long-Term Satiety: Signals from Adipose Tissue

In most people, body weight appears to be regulated over a long-term basis.

If an animal is force-fed so that it becomes fatter than normal, it will reduce its food intake once it is permitted to choose how much to eat (Wilson et al., 1990).

The discovery of a long-term satiety signal from fat tissue came after years of study with a strain of genetically obese mice.



What Stops a Meal?Long-Term Satiety: Signals from Adipose Tissue

ob mouseA strain of mice whose obesity and low metabolic rate are caused by a

mutation that prevents the production of leptin.

leptinA hormone secreted by adipose tissue; decreases food intake and

increases metabolic rate, primarily by inhibiting NPY-secreting neurons in the arcuate nucleus.



Brain MechanismsBrain Stem

decerebrationA surgical procedure that severs the brain stem,

disconnecting the hindbrain from the forebrain.


Reserved


Brain MechanismsHypothalamus

Discoveries made in the 1940s and 1950s focused the attention of researchers interested in ingestive behavior on two regions of the hypothalamus: the lateral area and the ventromedial area.

For many years investigators believed that these two regions controlled hunger and satiety, respectively; one was the accelerator, and the other was the brake.



Role in Hunger

melanin-concentrating hormone (MCH)One of two peptide neurotransmitters found in a system of lateral

hypothalamic neurons that stimulate appetite and reduce metabolic rate.




Role in Hunger

neuropeptide Y (NPY)A peptide neurotransmitter found in a system of neurons of the arcuate

nucleus that stimulate feeding, insulin and glucocorticoid secretion, decrease the breakdown of triglycerides, and decrease body temperature.



Role in Hunger

arcuate nucleusA nucleus in the base of the hypothalamus that controls secretions of the

anterior pituitary gland; contains NPY-secreting neurons involved in feeding and control of metabolism.


Reserved


Role in Hunger

paraventricular nucleus (PVN)A nucleus of the hypothalamus located adjacent to the dorsal third ventricle; contains

neurons involved in control of the autonomic nervous system and the posterior pituitary gland.

agouti-related protein (AGRP)A neuropeptide that acts as an antagonist at MC-4 receptors and increases eating.




Role in Satiety

CARTCocaine- and amphetamine-regulated transcript; a peptide neurotransmitter found in a

system of neurons of the arcuate nucleus that inhibit feeding.

-melanocyte-stimulating hormone (-MSH)A neuropeptide that acts as an agonist at MC-4 receptors and inhibits eating.


Reserved


Role in Satiety

melanocortin-4 receptor (MC-4R)A receptor found in the brain that binds with -MSH and agouti-related protein; plays a

role in control of appetite.



Obesity

Obesity is a widespread problem that can have serious medical consequences.

In the United States, approximately 67 percent of men and 62 percent of women are overweight, defined as a body mass index (BMI) of over 25.

Obesity is also increasing in developing countries as household incomes rise.

For example, over a 10-year period, the incidence of obesity in young urban children in China increased by a factor of eight.



ObesityPossible Causes

It appears genetic differences—and their effects on development of the endocrine system and brain mechanisms that control food intake and metabolism—appear to be responsible for the overwhelming majority of cases of extreme obesity.

Changes in the gene pool cannot account for this increase; instead, we must look to environmental causes that have produced changes in people’s behavior.


Reserved


Body weight is the result of the difference between two factors: calories consumed and energy expended.

If we consume more calories than we expend as heat and work, we gain weight. If we expend more than we consume, we lose weight.



Differences in body weight—perhaps reflecting physiological differences in metabolism, activity levels, or appetite—have a strong hereditary basis.

Twin studies suggest that between 40 percent and 70 percent of the variability in body fat is due to genetic differences.

Twin studies have found also strong genetic effects on the amount of weight that people gain or lose when they are placed on high- or low-calorie diets.



Thus, heredity appears to affect people’s metabolic efficiency.

However, until recently, variations in only two genes were found to cause obesity in humans: the gene for the MC4 receptor and the FTO gene (fat mass and obesity related gene), which codes for an enzyme that acts in hypothalamic regions related to energy balance, such as the PVN, and the arcuate nucleus.



However, these genes are very rare, so none of them can account for the prevalence of obesity in the general population.

The high level of heritability of obesity must be explained, then, as the additive effects of a large number of genes, each of which has a small effect on BMI.

In any event, we cannot blame the current epidemic of obesity and type 2 diabetes on genetics.


Reserved


ObesityTreatment

Obesity is extremely difficult to treat; the enormous financial success of diet books, health spas, and weight reduction programs attests to the trouble people have in losing weight.

More precisely, many programs help people to lose weight initially, but then the weight is quickly regained.


ObesityTreatment

Whatever the cause of obesity, the metabolic fact of life is this: If calories in exceed calories out, then body fat will increase.

Because it is difficult to increase the “calories out” side of the equation enough to bring an obese person’s weight back to normal, most treatments for obesity attempt to reduce the “calories in.”


Reserved

ObesityTreatment

Surgeons have become involved in trying to help obese people lose weight.

The procedures they have developed (called bariatric surgery, from the Greek barys, “heavy,” and iatrikos, “medical”) are designed to reduce the amount of food that can be eaten during a meal or interfere with absorption of calories from the intestines.

Bariatric surgery has been aimed at the stomach, the small intestine, or both.


Reserved

ObesityTreatment

The most effective form of bariatric surgery is a special form of gastric bypass called the Roux-en-Y gastric bypass, or RYGB.

The jejunum (the second part of the small intestine, immediately “downstream” from the duodenum) is cut, and the upper end is attached to the stomach pouch.

Digestive enzymes that are secreted into the duodenum pass through the upper intestine and meet up with the meal that has just been received from the stomach pouch.



ObesityTreatment

Suzuki et al. (2005) found that rats that sustained a RYGB procedure (but not rats that received sham surgery) ate less, lost weight, and showed decreased ghrelin levels and increased PYY levels.

Figure 11.25 shows the effects of RYGB surgery in two strains of rats: normal rats and those from a strain that was bred for overeating and obesity (Shin et al., 2011).

As you can see, even normal rats continue to gain weight when they are housed in a cage with food always available, but the obesity surgery suppressed weight gain in both strains of animals.


Reserved



Anorexia Nervosa/Bulimia Nervosa

anorexia nervosaA disorder that most frequently afflicts young women; exaggerated concern with being

overweight that leads to excessive dieting and often compulsive exercising; can lead to starvation.

bulimia nervosaBouts of excessive hunger and eating, often followed by forced vomiting or purging with

laxatives; sometimes seen in people with anorexia nervosa.


Reserved

Anorexia Nervosa/Bulimia NervosaPossible Causes

Anorexia is a serious disorder.

Five to 10 percent die of complications of the disease or of suicide.

Many anorexics suffer from osteoporosis, and bone fractures are common.

When the weight loss becomes severe enough, anorexic women cease menstruating.



Many researchers and clinicians have concluded that anorexia nervosa and bulimia nervosa are symptoms of an underlying mental disorder.

However, evidence suggests just the opposite: that the symptoms of eating disorders are actually symptoms of starvation.


Reserved



The fact that anorexia nervosa is seen primarily in young women has prompted both biological and social explanations.

Most psychologists favor the latter, concluding that the emphasis that most modern industrialized societies places on slimness—especially in women—is responsible for this disorder.

Another possible cause could be the changes in hormones that accompany puberty.


Reserved


Anorexia Nervosa/Bulimia NervosaTreatment

Anorexia is very difficult to treat successfully.

Cognitive behavior therapy, considered by many clinicians to be the most effective approach, has a success rate of less than 50 percent and a relapse rate of 22 percent during a one-year treatment period.


Reserved

Anorexia Nervosa/Bulimia NervosaTreatment

Researchers have tried to treat anorexia nervosa with many drugs that increase appetite in laboratory animals or in people without eating disorders.

For example, antipsychotic medications, drugs that stimulate adrenergic 2 receptors, l-DOPA, and THC (the active ingredient in marijuana).

Unfortunately, none of these drugs has been shown to be helpful (Mitchell, 1989).


Reserved

Documents

Prepared by Grant McLaren, Department of Psychology, Edinboro University of Pennsylvania FOUNDATIONS OF BEHAVIORAL NEUROSCIENCE 9 TH EDITION This multimedia