Chapter 12 Flashcards
1
Q
Does physical pain and social pain have a common neuroanatomical basis?
A
Yes. The insula, dorsal anterior cingulate cortex (daCC), somatosensory thalamus and secondary somatosensory cortex (SII)
2
Q
Why does this prey-killing circuit become active when a cat does not need food?
A
One explanation is that, to secure survival, the activity of circuits like the prey-killing circuit is in some way rewarding—it makes the cat feel good. As a result, the cat will engage often in the pleasure-producing behavior. This helps to guarantee that the cat will usually not go hungry.
3
Q
Why was Roger so hungry?
A
Neurological testing revealed that a tumor had invaded Roger’s hypothalamus at the base of his brain. He was indeed hungry all the time and in all likelihood could consume more than 20,000 calories a day if allowed to do so.
4
Q
Who first proposed the idea that behaviors such as prey killing are rewarding?
A
Steve Glickman and Bernard Schiff
5
Q
What did Butler and Harlow discover?
A
Monkeys in these conditions spent a lot of time opening the door and viewing whatever was on display, such as toy trains circling a track. The monkeys were even willing to perform various tasks just for an opportunity to look through the door. The longer they were deprived of a chance to look, the more time they spent looking when finally given the opportunity.
6
Q
What are innate releasing mechanisms?
A
activators for inborn adaptive responses that aid an animal’s survival. IRMs help an animal to feed, reproduce, and escape predators.
7
Q
What was Kolb and Nonneman’s experiment?
A
The researchers allowed a litter of 6-week-old kittens to play in a room and become familiar with it. After this adjustment period, they introduced a two-dimensional image of an adult cat in a Halloween posture, as shown in Figure 12-2A, and a “Picasso” control version, as shown in Figure 12-2B. The kittens responded to the Halloween cat image with raised fur, arched backs, and bared teeth, all signs of being threatened by the image of the adult cat. Some even hissed at the model.
8
Q
What were their results?
A
Some sort of template of this posture must be prewired in the kitten brain. Seeing the model that matched this preexisting template automatically triggered a threat response. This innate trigger is an IRM.
9
Q
How do we know the IRM concept applies to humans?
A
Through the results of Field ‘s study in 1982
10
Q
Describe Field’s study
A
She asked an adult to display to young infants various exaggerated facial expressions, such as happiness, sadness, and surprise.
11
Q
What were her results?
A
As Figure 12-3 shows, the babies responded with very much the same expressions the adults displayed. These newborns were too young to be imitating the adult faces intentionally. Rather, babies must innately match these facial expressions to internal templates, in turn triggering some prewired program to reproduce the expressions in their own faces. Such an IRM would have adaptive value if these facial expressions serve as important social signals for humans.
12
Q
What were the responses of congenitally blind children?
A
Evidence for a prewired motor program related to facial expressions also comes from study of congenitally blind children, who spontaneously produce the very same facial expressions that sighted people do, even though they have never seen them in others.
13
Q
Give an example of how IRMs can be modified by experience
A
Our cat Hunter’s stalking skills were not inherited fully developed at birth but rather matured functionally as she grew older.
14
Q
How can the IRM concept relate to the Darwinian concept of the nervous system?
A
Natural selection favors behaviors that prove adaptive for an organism, and these behaviors are passed on to future generations. Because behavior patterns are produced by the activity of neurons in the brain, the natural selection of specific behaviors is really the selection of particular brain circuits.
15
Q
What is evolutionary psychology?
A
the field that applies principles of natural selection to explanations of human behaviour
16
Q
How do evolutionary psychologists explain homicide?
A
Evolutionary psychologists assume that any behavior, including homicide, occurs because natural selection has favored the neural circuits that produce it. When two men fight a duel, one common sense explanation might be that they are fighting over grievance. Men who fought and won duels passed on their genes to future generations. Through time, therefore, the traits associated with successful dueling—strength, aggression, agility—became more prevalent among humans, as did dueling.
17
Q
How do Daly and Wilson (1988) extend this analysis of homicide?
A
In their view, homicide may endure in our society despite its severe punishment because it is related to behaviors that were adaptive in the human past.
18
Q
What were Buss’ (2014) conclusions?
A
His conclusions after nearly 30 years of study are that women around the world value dependability, stability, education, and intelligence in a long-term mate. Men, however, value good looks, health, and a desire for home and children more than women do.
19
Q
What is the current belief about where the preference for older men and younger women and vice versa come from?
A
These preferences are a product of natural selection in a Stone Age environment, when women and men would have faced different daily problems and thus would have developed separate adaptations related to mating.
20
Q
What are the pros and cons of evolutionary psychology?
A
Pro: evolutionary psychologists can generate intriguing hypotheses about how natural selection might have shaped the brain and behavior.
Con: Evolutionary theory cannot account for all human behavior, perhaps not even homicide or mate selection
21
Q
What did BF Skinner believe?
A
behaviors are selected by environmental factors.
22
Q
How do reinforcers influence behavior?
A
Certain events function as rewards, or reinforcers. When a reinforcing event follows a particular response, similar responses are more likely to occur. Skinner argued that reinforcement can be manipulated to encourage the display of complex behaviors.
23
Q
Describe Skinner’s experiment
A
The power of experience to shape behavior by pairing stimuli and rewards is typified by one of Skinner’s experiments. A pigeon is placed in a box that has a small disc on one wall (the stimulus). If the pigeon pecks at the disc (the response), a food tray opens, and the pigeon can feed (the reinforcement or reward). The pigeon quickly learns the association between the stimulus and the response, especially if the disc has a small spot on it. It pecks at the spot, and within minutes it has mastered the response needed to receive a reward.
24
Q
How did Skinner explain a phobia of planes?
A
Understanding a person’s reinforcement history could account for various phobias. Someone who once was terrified by a turbulent plane ride thereafter avoids air travel and manifests a phobia of flying. The avoidance of flying is rewarding because it lowers the person’s anxiety level, which then maintains the phobic behavior.
25
Describe Skinner's stance on free will
free will is an illusion because behavior is controlled not by the organism but rather by the environment, through experience.
26
What does the experience do?
Increasing evidence suggests that epigenetic changes regulate changes in memory circuits.
27
What is the evidence that environment does not always change the brain?
A case in point can be seen again in pigeons. A pigeon in a Skinner box can quickly learn to peck a disc to receive a bit of food, but it cannot learn to peck a disc to escape from a mild electric shock to its feet. Why not? Although the same simple pecking behavior is being rewarded, apparently the pigeon’s brain is not prewired for this second kind of association. The bird is prepared genetically to make the first association, for food, but not prepared for the second
28
What were Koelling and Garcia's observation?
Garcia observed that farmers in the western United States are constantly shooting at coyotes for attacking lambs, yet despite the painful consequences, the coyotes never seem to learn to stop killing lambs in favor of safer prey. The reason, Garcia speculated, is that a coyote’s brain is not prewired to make this kind of association.
29
What did Garcia do to teach the wolves not to eat sheep?
he connection between eating something that makes one sick and avoiding that food in the future. Garcia gave the coyotes a poisoned lamb carcass, which sickened but did not kill them. With only one pairing of lamb and illness, most coyotes learned not to eat sheep for the rest of their lives.
30
What is learned taste aversion?
learned taste aversion is acquired even when the food eaten is in fact unrelated to the later illness. As long as the taste and the nausea are paired in time, the brain is prewired to connect them.
31
How does this associative learning make sense?
Having a brain that is prepared to make a connection between a novel taste and subsequent illness helps an animal avoid poisonous foods and so aids in its survival. A curious aspect of taste aversion learning is that we are unaware of having formed the association until we encounter the taste and/or smell again.
32
How does preparedness relate to emotional behaviour?
Preparedness can help account for some complex behaviors. For example, if two rats are paired in a small box and exposed to a mild electric shock, they will immediately fight with one another, even though neither was responsible for the shock. Apparently, the rat brain is predisposed to associate injury with nearby objects or other animals. The extent to which we might extend this idea to explain such human behaviors as bigotry and racism is an interesting topic to ponder.
33
Why is odour important to mammals?
Mammals identify group members by odor; mark their territory with urine and other odorants; identify favorite and forbidden foods by taste; and form associations among odors, tastes, and emotional events.
34
What is the receptor surface for olfaction and how does it work?
1. olfactory epithelium
2. The epithelium is composed of receptor cells and support cells. Each receptor cell sends a process ending in 10 to 20 cilia into a mucous layer, the olfactory mucosa. Chemicals in the air we breathe dissolve in the mucosa to interact with the cilia. If an olfactory chemosignal affects the receptors, metabotropic activation of a specific G protein leads to an opening of sodium channels and a change in membrane potential.
35
How come dogs can smell better than humans?
. In humans, this area is estimated to range from 2 to 4 square centimeters; in dogs, about 18 square centimeters; and in cats, about 21 square centimeters.
36
How are we able to smell many different odors despite having a small number of receptor types?
The simplest explanation is that any given odorant stimulates a unique pattern of receptors, and the summed activity or pattern of activity produces our perception of a particular odor. Analogously, the visual system enables us to identify several million colors with only three receptor types in the retina; the summed activity of the three cones leads to our richly colored life.
37
What is the olfactory pathway?
Olfactory receptor cells project to the olfactory bulb, ending in ball-like tufts of dendrites—the glomeruli where they form synapses with the dendrites of mitral cells. Mitral cells send their axons from the olfactory bulb to the broad range of forebrain areas. Many olfactory targets, such as the amygdala and pyriform cortex, have no connection through the thalamus, as do other sensory systems. However, a thalamic connection (to the dorsomedial nucleus) does project to the orbitofrontal cortex (OFC), the prefrontal area behind the eye sockets (the orbits)
38
What are pheromones?
biochemicals released by one animal that act as chemosignals and can affect the physiology or behavior of another animal of the same species.
39
How does the vomeronasal organ detect pheromones?
the vomeronasal organ, which is made up of a small group of sensory receptors connected by a duct to the nasal passage. The receptor cells in the vomeronasal organ send their axons to the accessory olfactory bulb, which lies adjacent to the main olfactory bulb; this connects primarily with the amygdala and hypothalamus, via which it probably plays a role in reproductive and social behavior.
40
What is flehman?
When exposed to novel urine from a cat or human, cats raise their upper lip to close off the nasal passages and suck air into the mouth. The air flows through the duct on the roof of the mouth en route to the vomeronasal organ.
41
What were Olsson et. al's findings?
The compound delta 4,16-androstadien-3-one (androstadienone), a natural component of human sweat, plays a unique role in communication between humans. There is growing evidence that people can identify their own odor, the odor of kin versus not-kin, and the odor of friends versus strangers with an accuracy well above chance (e.g., Olsson et al., 2006).
42
How are these social odors perceived?
Hummer et. al, 2017 used fMRI to examine the effect of androstadienone on the brain’s response to emotional images (relative to neutral images) of participants who were exposed to the odor versus no odor. They found increased activity in the right dorsolateral prefrontal and orbital prefrontal regions, especially when the images were positive.
43
What were Lundstrom et. al's findings?
Another study provides evidence that smelling a stranger’s odor activates the amygdala and insular cortex, similar to activation observed for fearsome visual stimuli, such as masked or fearsome faces
44
What are the functions of the insula?
The insula contains regions related to language, taste perception, and social perception
45
What types of tastes do humans, rats and dogs like?
Humans and rats like sucrose and saccharin solutions, but dogs reject saccharin, and cats are indifferent to both, inasmuch as they do not detect sweetness at all. The failure of cats to taste sweetness may not be surprising: they are pure carnivores, and nothing that they normally eat is sweet.
46
What was the result of Bartoshuk's study?
some perceive certain tastes as very bitter, whereas others are indifferent to them. Presumably, the latter group is more tolerant of Brussel sprouts.
47
How does genetics influence sensitivity to bitterness
It's related to genetic differences in the ability to detect a specific bitter chemical (6-n-propylthiouracil, or PROP).
PROP bitterness associates with allelic variation in the taste receptor gene TAS2R38. People able to detect minute quantities of PROP find the taste extremely bitter; they are sometimes called supertasters. Those who do not taste PROP as very bitter are nontasters. The advantage of being a supertaster is that many bitter “foods” are poisonous. The disadvantage is that supertasters avoid many nutritious fruits and vegetables, such as grapefruit, that they find too bitter.
48
How does age influence taste thresholds?
Children are much more responsive to taste than adults and are often intolerant of spicy foods because they have more taste receptors than adults have. It is estimated that by age 20, humans have lost at least 50 percent of their taste receptors. No wonder children and adults have different food preferences.
49
Where are taste receptors found?
Taste receptors are found in taste buds on the tongue, under the tongue, on the soft palate on the roof of the mouth, on the sides of the mouth, and at the back of the mouth on the nasopharynx.
50
What are the 5 types of taste receptors?
The four most familiar are sweet, sour, salty, and bitter. The fifth type, called the umami (meaning “savory” in Japanese) receptor, is especially sensitive to glutamate.
51
Why do gustatory stimuli interact with microvilli?
Gustatory stimuli interact with the receptor tips, the microvilli, to open ion channels, leading to changes in membrane potential. At its base, the taste bud contacts the branches of afferent cranial nerve 7 (facial), 9 (glossopharyngeal), or 10 (vagus).
52
What is the solitary tract?
Cranial nerves 7, 9, and 10 form the main gustatory nerve, the solitary tract.
53
Describe the gustatory pathway to the primary somatosensory cortex
Cranial nerves 7, 9, and 10 form the main gustatory nerve, the solitary tract. On entering the brainstem, the tract splits, as illustrated in Figure 12-8. One route (traced in red) travels through the posterior medulla to the ventroposterior medial nucleus of the thalamus. This nucleus in turn sends out two pathways, one to the primary somatosensory cortex (SI)
54
Describe the gustatory pathway to the primary gustatory cortex of the insula
Cranial nerves 7, 9, and 10 form the main gustatory nerve, the solitary tract. On entering the brainstem, the tract splits, as illustrated in Figure 12-8. One route (traced in red) travels through the posterior medulla to the ventroposterior medial nucleus of the thalamus. This nucleus in turn sends out two pathways, one to the primary somatosensory cortex (SI) and the other to the primary gustatory cortex of the insula, a region just rostral to the secondary somatosensory cortex (SII).
55
What is the gustatory region in the insula responsible for?
Taste
56
What is the SI responsible for?
Tactile information and possibly our reaction to food's texture
57
How do we perceive flavour?
The gustatory cortex sends a projection to the orbital frontal cortex. Neuroimaging studies suggest that the mixture of olfactory and gustatory input in the orbital cortex gives rise to our perception of flavor. It is believed that the insula identifies the nature and intensity of flavors, whereas the orbital frontal cortex evaluates the affective properties of tastes. Ambience, including music and light, also affects this region of orbital cortex, increasing blood flow and so enhancing our experience of flavor.
58
What are possibly evaluating the pleasantness and strength of flavours?
The second pathway from the gustatory nerve (shown in blue in Figure 12-8) projects via the nucleus of the solitary tract in the brainstem to the hypothalamus and amygdala. Researchers hypothesize that these inputs somehow play a part in eating, possibly evaluating the pleasantness and strength of flavors.
59
What structure plays a key role in motivation?
The neural circuits that control motivated behavior encompass regions at all levels of the brain, but the critical neural structure in producing motivated behavior is the hypothalamus. The hypothalamus receives projections from all major subdivisions of the nervous system and functions to integrate diverse adaptive behaviors. It is not an individual brain region but rather is composed of smaller neural units devoted to specific functions.
60
What were Swanson's findings?
The hypothalamus is an integrative center of a larger “behavioral control column” (or network) controlled by the cerebral hemispheres.
61
How does the behavioural control column work?
This behavioral column is composed of a rostral brainstem region devoted to social (including reproductive and defensive) behaviors and ingestion (eating and drinking), as well as a more caudal region extending into other brainstem areas related to exploration and foraging behaviors, such as the substantia nigra and ventral tegmentum. These functions are modulated by the cerebral hemispheres through descending pathways from the cerebral cortex, striatum, and pallidum. The hypothalamus acts to organize these cerebral inputs and produce feedback loops that regulate cerebral information to orchestrate homeostasis and motivated behaviors; it also ensures that the cerebral regions are aroused and online when needed. In addition, outputs from the hypothalamus project to the pituitary to control the release of a broad range of hormones.
62
How does the hypothalamus produce behavior?
To produce behavior, the hypothalamus sends axons to other brainstem circuits—but not all behavior is controlled via the funnel to the hypothalamus. Many other routes to the brainstem and spinal cord bypass the hypothalamus, among them projections from the motor cortex to the brainstem and spinal cord. Thus, it is primarily motivated behaviors that require hypothalamic involvement.
63
What are regulatory behaviours?
Regulatory behaviors—behaviors motivated by an organism’s survival—are controlled by homeostatic mechanisms.
64
What is a set point?
Human body temperature is controlled in a somewhat similar manner by a thermostat in the hypothalamus that holds internal temperature at about 37°C, a temperature referred to as a set point. Even slight variations cause us to engage in various behaviors to regain the set point.
65
What are non regulatory behaviours?
nonregulatory behaviors are neither required to meet the basic survival needs of an animal nor controlled by homeostatic mechanisms (see table). Thus, nonregulatory behaviors include everything else we do—from sexual intercourse to parenting to such curiosity-driven activities as conducting psychology experiments.
66
What brain structures are active in non regulatory behaviours?
Some certain nonregulatory behaviors, such as sexual intercourse, do involve the hypothalamus, but most of them probably do not. Rather, such behaviors entail a variety of forebrain structures, especially the frontal lobes. Presumably, as the forebrain evolved and enlarged, so did our range of nonregulatory behaviors.
67
How does the hypothalamus maintain homeostasis?
The hypothalamus maintains homeostasis by acting on both the endocrine system and the autonomic nervous system (ANS) to regulate our internal environment. The hypothalamus also influences the behaviors selected by the rest of the brain, especially by the cerebral hemispheres. Although it constitutes less than 1 percent of the human brain’s volume, the hypothalamus controls an amazing variety of motivated behaviors, ranging from heart rate to eating and sexual activity.
68
What is the main function of the hypothalamus?
To control the pituitary gland
69
What is the MFB?
The lateral hypothalamus, composed both of nuclei and of nerve tracts running up and down the brain, connects the lower brainstem to the forebrain. The principal tract, shown in Figure 12-11, is the medial forebrain bundle (MFB).
70
What does the MFB do?
The MFB connects brainstem structures with various parts of the limbic system and forms the activating projections that run from the brainstem to the basal ganglia and frontal cortex. Fibers that ascend from the dopamine- and noradrenaline-containing cells of the lower brainstem form a significant part of the MFB. The dopamine-containing MFB fibers contribute to the control of many motivated behaviors, including eating and sex. They also contribute to pathological behaviors, such as addiction and impulsivity.
71
Why do the hypothalamic nuclei have different and multiple functions?
Each hypothalamic nucleus is anatomically distinct, and most have multiple functions, in part because the cells in each nucleus contain a different mix of peptide neurotransmitters. Each peptide participates in different behaviors
72
How do peptides made in the hypothalamus influence behaviour?
Neurons in the hypothalamus make peptides (for example, oxytocin and vasopressin) that are transported down their axons to terminals lying in the posterior pituitary. If these neurons become active, they send action potentials to the terminals to release the peptides stored there. But rather than affecting another neuron, as occurs at most synapses, capillaries (tiny blood vessels) in the posterior pituitary’s rich vascular bed pick up these peptides.
The peptides then enter the bloodstream, which carries them to distant targets, where they exert their effects. Vasopressin, for example, affects water resorption by the kidneys, and oxytocin controls both uterine contractions and the ejection of milk by mammary glands in the breasts. Peptides can have multiple functions, depending on where their receptors are. Thus, oxytocin not only controls milk ejection in females but also performs a more general role in several forms of affiliative behavior, including parental care, grooming, and sexual behavior in both men and women
73
What are releasing hormones and what do they do?
The hypothalamus controls the release of these anterior pituitary hormones by producing releasing hormones, peptides that act to increase or decrease hormone release. Releasing hormones, which are produced by hypothalamic cell bodies, are secreted into capillaries that transport them to the anterior pituitary, as Figure 12-12 shows.
74
Explain the TSH feedback loop
When the level of, say, thyroid hormone is low, the hypothalamus releases thyroid-stimulating hormone–releasing hormone (TSH-releasing hormone), which stimulates the anterior pituitary to release TSH. TSH then acts on the thyroid gland to secrete more thyroid hormone.
Receptors in the hypothalamus detect the thyroid hormone level. When that level rises, the hypothalamus lessens its secretion of TSH-releasing hormone. This type of system is essentially a form of homeostatic control that works as a feedback mechanism, a system in which a neural or hormonal loop regulates the initiation of neural activity or hormone release
The hypothalamus initiates a cascade of events that culminates in hormone secretion, but it pays attention to how much hormone is released. When a certain level is reached, it stops its hormone-stimulating signals. Thus, the feedback mechanism in the hypothalamus maintains a fairly constant circulating level of certain hormones.
75
Explain the oxytocin feedback loop
As stated earlier, one function of oxytocin is to stimulate cells of the mammary glands to release milk. As shown in Figure 12-13B, when an infant suckles the breast, the tactile stimulation causes hypothalamic cells to release oxytocin, which stimulates milk letdown. In this way, the oxytocin cells participate in a fairly simple reflex that is both neural and hormonal.
76
What other stimuli can cause oxytocin release?
For example, the sight, sound, or even thought of her baby can trigger a lactating mother to eject milk. Conversely, as diagrammed in Figure 12-13B, feelings of anxiety in a lactating woman can inhibit milk ejection. These excitatory and inhibitory influences exerted by cognitive activity imply that the cortex can influence neurons in the periventricular region. It is likely that projections from the frontal lobes to the hypothalamus perform this role.
77
What are experiential responses?
A third control on the hormonal activities of the hypothalamus is the brain’s responses to experience: neurons in the hypothalamus undergo structural and biochemical changes just as cells in other brain regions do. In other words, hypothalamic neurons are like neurons elsewhere in the brain in that they can be changed by heavy demands on them.
78
Give an example of an experiential response
when a woman is lactating, the cells producing oxytocin increase in size to promote oxytocin release and meet the increasing demands of a growing infant for more milk. Through this control, which is mediated by experience, a mother provides her baby with sufficient milk over time. Thus, we can see that both the neural regulation and the environmental demands can influence a single system (in this case, oxytocin and milk letdown) in different ways.
79
How do we know that the hypothalamus plays a role in generating behavior?
This function was first demonstrated by studies in which stimulating electrodes were placed in the hypothalamus of various animals, ranging from chickens to rats and cats. When a small electric current was delivered through a wire electrode, an animal suddenly engaged in some complex behavior—eating, drinking, or digging; displaying fear, attack, predatory, or reproductive behavior. The specific behavior exhibited depended on which site was stimulated. All of the behaviors were smooth, well integrated, and indistinguishable from typically occurring ones. Furthermore, all were goal directed.
80
Explain why survival and reward are the most important characteristics of behaviors generated by hypothalamic stimulation
Animals apparently find the stimulation of these behaviors pleasant, as suggested by the fact that they willingly expend effort, such as pressing a bar, to trigger the stimulation. Recall that cats kill birds and mice because the act of stalking and killing prey is rewarding to them. Similarly, we can hypothesize that animals eat because eating is rewarding, drink because drinking is rewarding, and mate because mating is rewarding.
81
What historical behaviors might cause persistent weight gain in the postindustrial world?
Until the mid-twentieth century, much of our food was only seasonally available. In a world with uncertain food availability, it makes sense for the body to store excess calories in the form of fat to be used later, when food is scarce. Throughout history, and in many cultures today, plumpness was and is desirable as a standard of beauty and a sign of health and wealth.
In postindustrial societies, people often eat as though food will be scarce, even though it is continuously and easily available. The failure to burn off the extra calories by exercising results in weight gain and health risks. Compounding the problem, the development of electronic media, which began roughly in the 1980s, has led to a more sedentary lifestyle than was common in previous generations.
82
What were Carus-Cadavieco's results?
Using an impressive range of electrophysiological, optogenetic, and molecular techniques in mice, they were able to show that a gamma rhythm (30–80 Hz) originating in the prefrontal cortex tied together the lateral septum and lateral hypothalamus to direct food seeking and eating. Optogenetic stimulation could either drive or reduce food-seeking behavior through effects on neurons in the lateral hypothalamus (see the accompanying figure).
83
What is anorexia nervosa?
Eating disorders entail being either overweight or underweight. Anorexia nervosa is an eating disorder with a huge cognitive component: self-image. A person’s body image is highly distorted in anorexia. This misperception leads to an exaggerated concern with being overweight. That concern spirals to excessive dieting, compulsive exercising, and severe, potentially life-threatening weight loss. Anorexia is especially prevalent among adolescent girls.
84
What are the 3 major inputs for the human control system?
the cognitive factors already introduced, the hypothalamus, and the digestive system
85
How does the digestive system control eating?
As food travels through the tract, the digestive system extracts three types of nutrients: lipids (fats), amino acids (the building blocks of proteins), and glucose (sugar). Each nutrient is a specialized energy reserve. Because we require varying amounts of these reserves, depending on what we are doing, the body has detector cells to keep track of the level of each nutrient in the bloodstream.
Glucose is the body’s primary fuel and virtually the only energy source for the brain. Because the brain requires glucose even when the digestive tract is empty, the liver acts as a short-term reservoir of glycogen, a starch that acts as an inert form of glucose. When blood sugar levels fall, as when we are sleeping, detector cells tell the liver to convert glycogen into glucose for release into the bloodstream.
Thus, the digestive system functions mainly to break down food, and the body needs to be apprised of how this breakdown is proceeding. Feedback mechanisms provide such information. When food reaches the intestines, it interacts with receptors in the ENS to trigger the release of at least 10 different peptide hormones, including cholecystokinin (CCK), glucagonlike peptide 1 (GLP-1), and peptide YY (PYY). Each peptide hormone, by virtue of its release as food, is absorbed and acts as a satiation or satiety signal that inhibits food intake. For example, when CCK is infused into an animal’s hypothalamus, the animal’s appetite diminishes.
86
How does the hypothalamus control eating?
But the role of the hypothalamus in controlling eating involves more than the activities of its lateral and ventromedial structures alone.
In fact, another hypothalamic region, the arcuate nucleus, contains two major classes of neurons, one that initiates eating (e.g., neurons expressing genes for neuropeptide Y) and one that reduces eating behavior, the principal transmitter being α-melanocyte–stimulating hormone (α-MSH). Changes in hormone levels reflecting glucose (insulin) and lipid (leptin) levels in the blood act to stimulate either the first class, which initiates eating, or the second class, which acts to inhibit eating. Neurons of the arcuate nucleus also connect to the paraventricular nucleus. Damage to this region produces hyperphagia, as noted in the case of Roger at the beginning of this chapter.
The summed activity of all such hypothalamic neurons constitutes a complex homeostat that controls eating. Figure 12-16 shows that this homeostat receives inputs from three sources: the enteric nervous system (such as information about blood glucose levels), the hormone systems (such as information about the level of appetite-diminishing CCK), and parts of the brain that process cognitive factors.
87
How do we know the hypothalamus plays a role in safety?
Investigation into how the hypothalamus controls eating began in the early 1950s, when researchers discovered that damage to the lateral hypothalamus in rats caused the animals to stop eating, a symptom known as aphagia (in Greek, phagein means “to eat”). In contrast, damage to the ventromedial hypothalamus (VMH) caused the animals to overeat—thus displaying hyperphagia. A VMH-lesioned rat that overate to the point of obesity is shown in the Procedure section of Experiment 12-1. The Results section reveals that the VMH-lesioned rat weighed more than 1 kilogram, three times the weight of her healthy sister, at 340 grams.
The researchers also found that electrical stimulation of the lateral hypothalamus elicits eating, whereas stimulation of the ventromedial hypothalamus inhibits eating. The opposing effects of injury and stimulation to these two regions led to the idea that the lateral hypothalamus signals turn on eating, whereas the VMH signals turn off eating. This model quickly proved too simplistic.
Not only does the lateral hypothalamus contain cell bodies, but fiber bundles also pass through it. Damage to either the cell bodies or the fibers can produce aphagia. Similarly, damage to fibers passing through the VMH often causes injury as well to the paraventricular nucleus of the hypothalamus (review Figure 12-10A).
88
What is the amygdala's role in eating?
The amygdala’s role in regulating species-typical behaviors is well established, but the role of the orbital PFC is more difficult to pin down. Rats and monkeys with damage to the orbital cortex lose weight, in part because they eat less. Humans with orbital injuries are invariably slim, but we know of no formal studies on their eating habits. The orbital prefrontal cortex receives projections from the olfactory bulb, and cells in this region respond to smells. Because odors influence the taste of foods, it is likely that damage to the orbital cortex decreases eating due to diminished sensory responses to food odor and perhaps to taste.
89
What were Seeley and Woods' results?
adult mammals do a masterful job of matching their caloric intake to caloric expenditure. Consider that a typical man eats 900,000 calories per year. To gain just 1 extra pound he would need to eat 4000 calories more than he burned in that year. This increase amounts to only 11 calories per day, equivalent to a single potato chip. But people rarely eat just one chip.
90
What are the 2 types of thirst?
Osmotic thirst results from increased concentrations of dissolved chemicals, known as solutes, in the body fluids. Hypovolemic thirst results from a loss of overall fluid volume from the body.
91
How does osmotic thirst happen?
Solutes inside and outside cells are ideally concentrated for the body’s chemical reactions. Maintaining this concentration requires a kind of homeostat, much like the mechanism that controls body temperature. Deviations from the ideal solute concentration activate systems to reestablish it.
Turning to sugar-sweetened beverages to quench thirst from eating salty foods increases the likelihood of weight gain.
When we eat salty foods, such as potato chips, the salt (NaCl) spreads through the blood and enters the extracellular fluid between our cells. This shifts the solute concentration away from the ideal. Receptors in the hypothalamus along the third ventricle detect the altered solute concentration and relay the message “too salty” to various hypothalamic areas that in turn stimulate us to drink. Other messages are sent to the kidneys to reduce water excretion.
92
What is water intoxication?
Body tissues swell with the excess fluid, essentially drowning the cells in fresh water. At the same time, the relative concentration of sodium drops, leading to an electrolyte imbalance.
93
What are symptoms of water intoxication?
Water intoxication can produce widely ranging symptoms, from irregular heartbeat to headache. In severe cases, people may show motor disorganization, as though they are drunk. The most likely way for an adult to develop water intoxication is to sweat heavily, by running a marathon in hot weather, for example, and then drink too much water without added electrolytes.
94
What causes hypovolemic thirst?
hypovolemic thirst arises when the total volume of body fluids declines, motivating us to drink more and replenish those fluids. In contrast with osmotic thirst, however, hypovolemic thirst encourages us to choose something other than water because water would dilute the solute concentration in the blood. Rather, we prefer to drink flavored beverages that contain salts and other nutrients, such as fruit juices or milk.
95
Describe the circuit that controls hypovolemic thirst
Hypovolemic thirst and its satiation are controlled by a hypothalamic circuit different from the one that controls osmotic thirst. When fluid volume drops, the kidneys send a hormone signal (angiotensin) that stimulates midline hypothalamic neurons. These neurons, in turn, stimulate drinking.
96
What were McCarthy and colleagues' findings
Hormones cause sex differences by acting during development as well as in adulthood.
There are sex differences in behavior.
There are sex differences in physiology.
There are sex differences in disease susceptibility.
There are sex differences in neural and glial structure and neural connectivity.
There are sex differences in neurochemistry.
Androgens and estrogens play a role in sexual differentiation in the brain.
Sex chromosome complement contributes to sexual differentiation.
Sex differences are context dependent.
Sexual differentiation depends on four key processes: neurogenesis, cell migration, cell death, and the differentiation of neural circuits.
97
What were Phoenix and colleagues' findings?
hormones have two general effects on brain organization: during development gonadal hormones organize the brain, and in adulthood they activate many sex-specific behaviors, such as mating behaviors.
98
What is the best known difference in humans?
the female advantage in verbal fluency, which is apparent in young children. When asked to write down words beginning with a particular letter in five minutes, females typically produce at least 10% more words than males. Karson Kung and colleagues (2016) found that higher levels of salivary testosterone at 1–3 months are related to a smaller expressive vocabulary measured at 18–30 months
99
Explain the male advantage in spatial navigation
A male advantage in spatial navigation is found not only in humans but also in most other mammals that have been studied. Male rodents typically can navigate larger territories and are better at solving problems, such as the Morris Water Task (see Figure 7-3A), in which the solution requires the mental construction of a configuration of the room cues. But if room cues must be ignored, such as in the landmark task (see Figure 7-3C), females perform better. Therefore, a major difference is seen in the strategy used by each sex rather than in the spatial cognitive ability of each sex. This strategy difference alerts us to the fact that sex differences are context dependent. In another example, the wording of instructions on a test can influence outcome by altering the strategy typically used by one sex or the other.
100
Why are neurodevelopment disorders more common in boys?
This male bias is striking because these early-onset disorders are less likely to have experiential causes but rather reflect pre- or postnatal differences in brain development. For adult-onset disorders, sex differences vary by disease. For example, females have a higher incidence of Alzheimer disease (1.5 to 3 times greater), after accounting for the sex difference in life expectancy, whereas males have a higher incidence of Parkinson disease (1.5 times greater).
101
Name some differences in the brain that males vs. females have
Differences in connectivity are reflected in the observation that females have greater interhemispheric connections and males have greater intrahemispheric connections.
102
How is sex differentiation related to sex chromosomes?
This can be seen most clearly in females, who typically have two X chromosomes. Normally, one of the X chromosomes is largely silenced, but about 15% of the genes escape inactivation. Therefore, female cells have a double dose of some genes, which creates epigenetic effects that influence gene expression (see Arnold et al., 2016, for a review).
103
What causes sex differentiation of aa trait?
due to effects on the basic processes of brain development (see Table 8-1), namely neurogenesis, cell migration, cell death, and the differentiation of neural circuits by neuronal differentiation and maturation.
104
How does a fetus become male?
During the fetal stage of prenatal development, a male’s Y chromosome controls the differentiation of embryonic gonad tissue into testes, which secrete testosterone. This process is an organizing effect of gonadal hormones. Testosterone masculinizes both the sex organs and the brain during development. A major organizing effect of gonadal hormones on the brain is in the hypothalamus, especially the preoptic area of the medial hypothalamus. Organizing effects also operate in other nervous system regions, notably the amygdala, the prefrontal cortex, and the spinal cord.
105
How do hormones influence brain development?
Gonadal hormones produce enzymes necessary for epigenetic changes such as gene methylation. One action of steroid hormones is to methylate brain regions. For example, estrogen methylates the preoptic area of females, leading to the suppression of male characteristics.
106
How do androgens influence rat development?
In the developing rat, androgens are produced during the last week of fetal development and the first week after birth. The androgens produced at this time greatly alter both neural structures and later behavior. For example, a male rat’s hypothalamus and prefrontal cortex differ structurally from those of both female rats and of males that were not exposed to androgens during development.
Male rats with little exposure to the androgen testosterone during development behave like genetically female rats in adulthood. If given estrogen and progesterone, they become sexually receptive and display typical female behaviors when mounted by males. Male rats castrated in adulthood do not act in this way.
107
How does sexual dimorphism occur?
Cells in the brain produce aromatase, an enzyme that converts testosterone into estradiol, one of the class of female sex hormones called estrogens. That is, when males produce testosterone, the brain converts it to an estrogen. Thus, a female hormone, estradiol, actually masculinizes the male brain.
108
Why aren't females masculinized by the presence of estrogens?
fetuses of both sexes produce a liver enzyme (alpha fetoprotein) that binds to estrogen, rendering it incapable of entering neurons. Testosterone is unaffected by alpha fetoprotein: it enters neurons and is converted into estradiol.
109
What were Gorski's results?
found a nucleus about five times as large in males as in females. Significantly, manipulating gonadal hormones during development can alter the sexual dimorphism of the preoptic area. Castrating male rats at birth leads to a smaller preoptic area; treating infant females with testosterone enlarges it.
110
Why are both human males and females exposed to estrogen?
It is known that alpha fetoprotein, a fetal protein, is less effective in blocking estrogen in humans, indicating that human fetuses of both sexes are exposed to estrogen. This finding suggests that androgens may play a more central role in sexual differentiation in humans.
111
What is androgen insensitivity syndrome?
After the testes have formed in a male fetus, sexual development depends on the actions of testicular hormones. In this syndrome, an XY (genetic male) fetus produces androgens, but the body cannot respond to them. Because androgen insensitivity syndrome does not affect estrogen receptors, these people are still responsive to estrogen produced by both the adrenal glands and the testes. As a result, they develop female secondary sexual characteristics during puberty, even without additional hormone treatment. A person with androgen insensitivity syndrome is therefore a genetic male who develops a female phenotype—that is, appears to be female.
112
What causes androgenital syndrome?
If no Y chromosome is present to induce the growth of testes, an XX (genetic female) fetus develops ovaries and becomes a female. If the adrenal glands of either the mother or the infant produces an excessive amount of androgens, however, exposure of the female fetus to them produces androgenital syndrome (congenital adrenal hyperplasia). The effects vary, depending on when the androgens are produced and on the level of exposure. In extreme cases, the clitoris enlarges until it can be mistaken for a small penis, as shown in the photograph on the right.
In less severe cases, no gross change in genital structure develops, but there is a behavioral effect: these girls show a high degree of tomboyishness. In early childhood, they identify with boys and prefer boys’ clothes, toys, and games. One explanation for this behavioral effect is that the developing brain is masculinized, which changes later behavior.
113
What changes occur during a female rat's estrous cycle?
When estrogen levels are high, more dendritic spines and presumably more synapses emerge. These neural differences during the estrous cycle are all the more remarkable when we consider that cells in the female hippocampus are continually changing their connections to other cells every 4 days throughout the animal’s adulthood.
114
How does testosterone activate sexual behavior?
First, testosterone’s actions on the amygdala are related to the motivation to seek sexual activity. Second, the actions of testosterone on the hypothalamus are needed to produce copulatory behavior.
115
What role does the venturemedial hypothalamus play in controlling sexual behaviour?
The ventromedial hypothalamus controls the female mating posture, which in quadrupedal animals is called lordosis: arching the back and elevating the rump while the female otherwise remains quite still. Damage to the VMH abolishes lordosis. The role of the VMH is probably twofold: it controls the neural circuit that produces lordosis, and it influences hormonal changes in the female during coitus.
116
What controls sexual motivation?
The brain structure responsible for motivation appears to be the amygdala. When Everitt trained male rats in the apparatus and then lesioned their amygdala, they would no longer press the bar to gain access to receptive females, but they would mate with receptive females provided to them.
117
What is sexual orientation?
a person’s sexual attraction to the opposite sex or to the same sex or to both sexes
118
What determines one's orientation?
Sexual orientation appears to be determined during early development, influenced by genetics and by epigenetic factors during prenatal brain development. No solid evidence points to any postnatal experience directing sexual orientation.
119
How do epigenetics play a role in sexual differentiation?
In females, for example, one of the two X chromosomes is largely silenced, but not all its genes are silenced, thereby providing a basis for sex differences. Furthermore, emerging evidence suggests that sex differences in the hypothalamus result from differences in gene methylation (again, see McCarthy et al., 2017).
120
What is gender identity?
a person’s degree of feeling male or female.
121
What does it mean to be transgender?
A person whose personal characteristics transcend traditional gender boundaries and corresponding sexual norms, believe they were born the wrong sex. Their desire to live as a member of the other sex can be so strong that they undergo gender reassignment.
122
What factors increase the likelihood of being trans?
chromosomal abnormalities, polymorphisms of the genes for the estrogen and androgen receptors, atypical gonadal hormone levels, prenatal exposure to certain anticonvulsants, and immune system activity directed toward the Y chromosome.
123
How do we know the cortex is involved in sexual activity?
In studies of rats whose entire cortex has been removed, both males and females still engage in sexual activity, although the males are somewhat clumsy. Nevertheless, the cortex must play a role in certain aspects of sexual behavior. For instance, imagery about sexual activity must include activity in the cortical ventral visual pathway. And thinking about sexual activity and planning for it must require frontal lobe participation.
124
What neural systems are responsible for the 3 types of emotion?
The autonomic component must include the hypothalamus and associated structures, as well as the enteric nervous system (the neurons in the gut). The components of subjective feelings are more difficult to localize but clearly include the amygdala and probably parts of the frontal lobes. And thoughts and plans are likely to be cortical.
125
Describe constructivist theory
The first model, labeled as constructivist theory, suggests that the brain interprets physiological changes (such as trembling and rapid heartbeat) as an emotion. This perspective implies that the brain (most likely the cortex) produces a cognitive response to autonomic information.
126
What's the James Lange theory?
Variations of this perspective have gone by many terms, beginning with the James–Lange theory, named for its originators, but all assume that the brain concocts a story to explain bodily reactions.
127
What evidence supports the James Lange theory?
One is that the same autonomic responses can accompany different emotions. That is, particular emotions are not tied to unique autonomic changes. This line of evidence leaves room for interpreting what a particular pattern of arousal means, even though particular physiological changes may suggest only a limited range of possibilities. The physiological changes experienced during fear and happiness are unlikely to be confused. The second line of evidence supporting the view that physiological changes are the starting point for emotions comes from people with reduced information about their own autonomic arousal, due, for example, to spinal cord injury. Spinal injury results in a decrease in perceived emotion, and its severity depends on how much sensory input is lost
128
How do spinal cord injuries impact emotions?
People with the greatest loss of sensory input, which occurs with injuries at the uppermost end of the spinal cord, also have the greatest loss of emotional intensity. In contrast, people with injuries to the lower end of the spinal cord retain most of their visceral input and have essentially typical emotional reactions.
129
What is appraisal theory?
Contemporary versions of appraisal theory define emotions as processes rather than states. They view emotional episodes as the activity of several biological subsystems or components: (1) an appraisal component in which there is an evaluation of the context; (2) somatic components (physiologic effects); (3) a behavioral component; and (4) a feeling component, which includes a subjective experience or feeling. Rather than process specific emotions in specific regions (such as the amygdala for fear), the appraisal component involves an extensive neural network that processes various aspects of the appraisal.
Some versions of appraisal theory also propose that emotions are dependent on an affective core, or pleasure system, that gives affective tone to emotion and interacts with appraisals (see Kringelbach & Berridge, 2017). Thus, emotions are ranked along dimensions of pleasant/unpleasant and aroused/not aroused (see Anderson & Adolphs, 2014) (see Figure 12-20).
130
What is the neuropsychological theory?
proposes that emotional control is asymmetrical. Given that there are significant asymmetries in the control of a variety of cognitive functions, this theory suggests that related emotional systems must also be lateralized.
131
Describe the limbic system
The structures are formed from a primitive three- and four-layered cortex (known as the allocortex), which lies adjacent to the six-layered neocortex. In mammals, the allocortex encompasses the cingulate (meaning “girdle”) gyrus and the hippocampal formation, as shown in Figure 12-21. The hippocampal formation includes the hippocampus—an allocortical structure important in species-typical behaviors, memory, and spatial navigation and vulnerable to the effects of stress—and the parahippocampal cortex adjacent to it.
132
What makes up the allocortex in mammals?
In mammals, the allocortex encompasses the cingulate (meaning “girdle”) gyrus and the hippocampal formation
133
What forms the hippocampal formation?
The hippocampal formation includes the hippocampus—an allocortical structure important in species-typical behaviors, memory, and spatial navigation and vulnerable to the effects of stress—and the parahippocampal cortex adjacent to it.
134
What did Papez find?
For instance, in the 1930s, James Papez observed that people with rabies display radically abnormal emotional behavior, and postmortem examinations showed that the rabies had selectively attacked the hippocampus. (Definitive proof of rabies still requires postmortem hippocampal examination.)
135
What is the Papez circuit?
He proposed a neural circuit, traced in Figure 12-22A, now known as the Papez circuit, whereby emotion could reach consciousness, presumed at that time to reside in the cerebral cortex. In 1949, Paul MacLean expanded Papez’s concept of the limbic circuit to include the amygdala and prefrontal cortex.
136
what addition did Maclean make to the Papez circuit?
The amygdala and the prefrontal cortex
137
What are the 3 subdivisions of the amygdala?
the corticomedial area, the basolateral area, and the central area.
138
What does it mean when we say that the neurons in the amygdala are multimodal?
they respond to more than one sensory modality.
139
Where do the connections go?
The amygdala sends connections primarily to the hypothalamus and the brainstem, where it influences neural activity associated with emotions and species-typical behavior.
140
What happens when an eplipetic person's amygdala is stimulated before surgery?
For example, when the amygdala of a person with epilepsy is electrically stimulated before brain surgery, that person becomes fearful and anxious. We observed a woman who responded with increased respiration and heart rate, saying that she felt as if something bad was going to happen, although she could not specify what.
141
How do we know that the amygdala plays a role in eating and drinking?
Amygdala stimulation can also induce eating and drinking. We observed a man who drank water every time the stimulation was turned on. (There happened to be a pitcher of water on the table next to him.) Within 20 minutes, he had consumed about 2 liters of water. When asked if he was thirsty, he said, “No, not really. I just feel like drinking.”
142
What is Kluver-Bucy syndrome?
- Tameness and loss of fear
- Indiscriminate dietary behavior (eating many types of formerly rejected foods)
- Greatly increased autoerotic, homosexual, and heterosexual activity with inappropriate object choice (e.g., the sexual mounting of chairs)
- Tendency to attend to and react to every visual stimulus
- Tendency to examine all objects by mouth
-Visual agnosia, an inability to recognize objects or drawings of objects
143
where does visual agnosia come from?
Visual agnosia results from damage to the ventral visual stream in the temporal lobe, but the other symptoms are related to the amygdalectomy. Tameness and loss of fear are especially striking. Monkeys that normally show a strong aversion to stimuli such as snakes show no fear of them whatsoever. In fact, amygdalectomized monkeys may pick up live snakes and even put them in their mouths.
144
What did LeDoux emphasize?
Awareness of danger and of safety has both an innate component and a learned component
145
What is the innate component?
The innate component, much as in the IRMs described in Section 12-1, is the automatic processing of species-relevant sensory information—inputs from the visual, auditory, and olfactory systems.
146
What is the learned component?
the learned component of fear consists of the avoidance of specific animals, places, and objects that the organism has come to associate with danger. The organism is not born with this avoidance behavior prewired. In a similar way, animals learn to increase contact with environmental stimuli that they associate with positive outcomes, such as food or sexual activity or, in the laboratory, drugs.
147
What behaviours does damage to the amygdala affect?
In a similar way, animals learn to increase contact with environmental stimuli that they associate with positive outcomes, such as food or sexual activity or, in the laboratory, drugs.
148
What is the prefrontal cortex?
The prefrontal cortex is a large area made up of several functionally distinct regions
149
What are the general regions of the prefrontal cortex?
The dorsolateral region; the orbitofrontal cortex (OFC), also shown from a ventral aspect in Figure 12-23B; and the ventromedial PFC.
150
What is the function of the prefrontal cortex?
The prefrontal cortex contributes to specifying the goals toward which movement should be directed. It controls the processes by which we select movements appropriate to the particular time and context. This selection may be cued by internal information, such as memory and emotion, or it may be made in response to context (environmental information).
151
How does it receive input?
Through connections from the amygdala, dorsomedial thalamus, sensory association cortex, posterior parietal cortex, and dopaminergic cells of the ventral tegmental area.
152
What is dopaminergic input + why is it important?
Dopaminergic input is important for regulating how prefrontal neurons react to stimuli, including emotional ones. Abnormalities in this dopaminergic projection may account for some disorders, including schizophrenia, in which people evince little emotional reaction to typically arousing stimuli.
153
What is the prefrontal cortex's output?
The inferior prefrontal region projects axons to the amygdala and the hypothalamus in particular. These PFC axons provide a route for influencing the ANS and ENS, which control changes in blood pressure, respiration, and other internal processes, especially those related to emotions. The dorsolateral prefrontal region sends its connections primarily to the sensory association cortex, posterior parietal cortex, cingulate cortex, basal ganglia, and premotor cortex and plays a larger role in cognitive behaviors than in emotional behaviors.
154
What is the dorsolateral frontal lobe's function?
One overall function of the prefrontal cortex is to select behaviors appropriate to the particular time and place, cued either by internal information or environmental context.
155
What happens when there is disruption to this area?
They become overly dependent on environmental cues to determine their behavior. Like small children, they can be easily distracted by what they see or hear. We have all experienced a loss of concentration to some extent, but for a patient with frontal lobe damage, the problem is exaggerated and persistent. Because the person becomes so absorbed in irrelevant stimuli, he or she cannot act on internalized information most of the time.
156
What makes JC a good example?
A good example is J. C., in whom bilateral damage to the dorsolateral prefrontal cortex resulted from having a tumor removed. J. C. would lie in bed most of the day, fixated on television programs. He was aware of his wife’s opinion of this behavior, but only the sound of the garage door opening when she returned home from work in the evening would stimulate him into action. Getting out of bed was controlled by this specific environmental cue; without it, he seemed to lack motivation. Television completely distracted him from acting on internal knowledge of things that he could or should do.
157
How do we know that adapting behavior is also a PFC function?
Most people readily change their behavior to match the situation at hand. We behave one way with our parents, another with our friends, another with our children, and yet another with our coworkers. Each set of people constitutes a different context, and we shift our behaviors accordingly. Our tone of voice, our use of slang or profanity, and the content of our conversations are quite different in different contexts.
Even among our peers we act differently, depending on who is present. We may be relaxed in the presence of some people and ill at ease with others. It is therefore no accident that the size of the frontal lobes is related to species’ sociability. Social behavior is extremely rich in contextual information, and humans are highly social animals.
158
What structures are required to control behaviour in context?
Controlling behavior in context requires detailed sensory information, which is conveyed from all sensory regions to the frontal lobes. This sensory input includes not only information from the external world but also internal information from the ANS. People with damage to the orbital prefrontal cortex, as is common in traumatic brain injuries (TBIs), have difficulty adapting their behavior to the context, especially the social context. Consequently, they often make social gaffes.
159
Describe JP's case
```
J. P.’s behavioral problems continued and expanded as he grew older, and by adolescence, he was constantly in trouble. Yet J. P. also had a positive side. When he started school, his first-grade teacher was so impressed with his polite manners that she began writing a letter to his parents to compliment them on having such a well-mannered child who was such a good influence in the class.
As she was composing the letter, she looked up to find J. P. exposing himself to the class and masturbating. This juxtaposition of polite manners and odd behavior characterized J. P.’s conduct throughout his life. At one moment he was charming; at the next, he was engaged in socially unacceptable behavior.
J. P. developed no close friendships with people of either sex, in large part because of his repeated incidents of public masturbation, stealing, excessive boastfulness, and wandering. He was a person of average intelligence who seemed unaffected by the consequences of his behavior. Police officers, teachers, and neighbors all ascribed intention to J. P.’s behavior: all believed that he was willfully misbehaving and blamed his parents for not enforcing sufficiently strict discipline.
Perhaps as a result, not until he was 19 years old was J. P.’s true condition detected. To prevent him from serving a prison term for repeated automobile theft, a lawyer suggested that J. P. undergo psychiatric evaluation. The psychiatrist who examined him ordered an X-ray (the only brain scan available at the time). The image revealed that J. P. lacked a right frontal lobe, and his left frontal lobe was about 50 percent the normal size. It is almost certain that his frontal lobes simply failed to develop.
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160
What is agenesis?
Failure of a structure to develop is known as agenesis
161
What is a frontal lobotomy?
A frontal lobotomy, which involves inserting a sharp instrument into the frontal lobes and moving it back and forth to disconnect the lobes from the rest of the brain, destroys substantial brain tissue.
162
What is psychosurgery?
neurosurgery intended to alter behavior.
163
What was one of Jacobsen's results?
In 1936, Jacobsen reported that one of the chimps was particularly neurotic before being subjected to this procedure. She became more relaxed afterward.
164
How is a leukotomy performed?
To perform a leukotomy, as illustrated in Figure 12-25, a surgeon uses a special knife called a leukotome to sever the connections of a region of the orbitofrontal cortex (see Figure 12-22).
165
What are the effects of a leukotomy?
In our conversations with Agnes, we quickly discovered her considerable insight into the changes brought about by the leukotomy. In particular, she indicated that she no longer had any feelings about things or most people, although, curiously, she was attached to her dog. She said that she often just felt empty and much like a zombie.
166
What makes the orbitofrontal area so important?
The orbitofrontal area has direct connections with the amygdala and hypothalamus. Stimulating it can produce autonomic responses, and, as we saw in Agnes, damage to the orbital region can produce severe personality change characterized by apathy and loss of initiative or drive. The orbital cortex is probably responsible for the conscious awareness of emotional states produced by the rest of the limbic system, especially the amygdala.
167
What is prosody?
Tone of voice
168
How does frontal lobe damage impact prosody?
Patients with damage to the frontal lobe are devoid of prosody, both in their own conversations and in understanding the prosody of others. The lost ability to comprehend or produce emotional expression in both faces and language partly explains those patients’ apathy. In some ways, they are similar to spinal cord patients who have lost autonomic feedback and so can no longer feel the arousal associated with emotion. These patients can no longer either read emotion in other people’s faces and voices or express it in their own.
169
What happens to individuals with damaged vmPFC?
Patients with damage to the vmPFC develop severe deficits in personal and social decision making, despite having largely preserved intellectual abilities (see Bechara, 2017). It is hypothesized that the vmPFC has a role in accessing visceral (internal) information that is related to the value (pleasant, unpleasant) of objects in the world. Noninvasive imaging studies (fMRI) have also shown that changes in the activity of the vmPFC result in changes in the subjective pleasantness of experiences with food, drugs, music, and sexual orgasm (see Berridge & Kringelbach, 2015). It is important to note, however, that imaging studies show a more extensive network of increased activity, including in the anterior cingulate cortex, the insular cortex, and subcortical regions such as the amygdala and striatum.
170
What is major depression?
Major depression, a highly disruptive emotional disorder, is characterized by some or all the following: prolonged feelings of worthlessness and guilt, disruption of normal eating habits, sleep disturbances, a general slowing of behavior, and frequent thoughts of suicide. A depressed person feels severely despondent for a long time.
171
Describe anxiety disorders
Anxiety disorders, including posttraumatic stress disorder (PTSD), phobias, generalized anxiety disorder, panic disorder, and obsessive-compulsive disorder (OCD), are estimated to affect 18 percent to 30 percent of the population
172
Describe symptoms of anxiety
persistent fears and worries in the absence of any direct threat, usually accompanied by various physiological stress reactions, such as rapid heartbeat, nausea, and breathing difficulty.
173
What is GAD
generalized anxiety disorder consists of persistently high levels of anxiety often accompanied by maladaptive behaviours to reduce anxiety; thought to be caused by chronic stress
174
What are phobias?
A phobia pertains to a clearly defined, dreaded object (such as spiders or snakes) or situation (such as enclosed spaces or crowds). Most people have a mild aversion to some types of stimuli. Such aversion becomes a phobia only when a person’s feelings about a disliked stimulus lead to overwhelming fear and anxiety.
175
What are symptoms of panic disorder?
Symptoms include recurrent attacks of intense terror that begin without warning and without any apparent relationship to external circumstances. A panic attack usually lasts only a few minutes, but the experience is always terrifying. Sudden activation of the sympathetic nervous system leads to sweating, a wildly beating heart, and trembling.
176
Describe some methods to treat anxiety disorders
Today, cognitive-behavioral therapies serve this purpose. A behavioral therapy called mindfulness, a form of meditation, is proving effective in treating anxiety disorders. Its effectiveness is correlated with suppressed activity in the anterior cingulate region (Garrison et al., 2015). The effect is greater in trained as opposed to novice meditators, which supports the value of mindfulness training programs.
Pharmacologically, anxiety disorders are most effectively treated with benzodiazepines such as diazepam (Valium), the best known. Alprazolam (Xanax) is the most commonly prescribed drug for panic attacks.
Benzodiazepines act by augmenting GABA’s inhibitory effect and are believed to exert a major influence on neurons in the amygdala.
177
What are the 3 main components of the reward system?
(1) learning about rewards and the cues that predict their availability; (2) motivation for these rewards and the cues associated with them (“wanting” the reward); and (3) affective (hedonic) responses to the actual pleasure of rewards (“liking” the reward).
178
What were Milner and Olds' results?
. They found that rats would perform behaviors such as pressing a bar to administer a brief burst of electrical stimulation to specific sites in their brain. This phenomenon is called intracranial self-stimulation, or brain stimulation reward.
179
Why would the rats engage in this behaviour?
The simplest explanation is that the brain stimulation is activating the system underlying reward. Stimulation along the MFB tract activates fibers that form the ascending pathways from dopamine-producing cells of the midbrain tegmentum, shown in Figure 12-26. This mesolimbic dopamine pathway sends terminals to sites that include especially the nucleus accumbens in the basal ganglia and the prefrontal cortex.
180
Why did Wise propose?
dopamine synapses represent a place where sensory inputs are translated into hedonic messages that we experience as pleasure.
181
What were Berridge and Robinson's results?
Berridge had been using facial expression in rats and people to measure how pleasurable or unpleasurable tastes were. As shown in Figure 12-27, exposure to palatable tastes (chocolate) elicits hedonic reactions in humans, such as licking the fingers and lips. In contrast, exposure to unpleasant tastes such as something overly salty elicits negative reactions such as grimacing, spitting, or wiping the mouth with the back of the hand. Rats, too, show distinctive positive and negative responses to pleasant and unpleasant tastes.
182
How do we know reward is comprised of multiple processes?
Such experiments show that what appears to be a single event—reward—is actually composed of at least two independent processes. Just as our visual system independently processes what and how information in separate streams, our reward system appears to process wanting and liking independently. Reward is not a single phenomenon any more than perception or memory is.
183
What transmitters are related to liking?
Berridge and his colleagues have identified small regions in the nucleus accumbens and associated ventral pallidum and ventromedial orbitofrontal cortex and insula, as well as a site in the hindbrain dorsal pons, that contribute to hedonic functions and are known to contribute to taste and pain. Each of these hotspots uses opioid (natural heroin-like transmitters) and endocannabinoid (natural marijuana-type neurotransmitters)—but never dopamine—to amplify liking (pleasure) reactions. These hedonic hotspots are relatively small in each region, but they appear to act together as a unified system to enhance pleasure. The intensity of pleasure is believed to be related to the number of regions simultaneously activated.
184
What is hedonic gloss?
Pleasure is not merely a sensation or thought but is best conceived of as an additional “hedonic gloss,” which creates the pleasure-versus-displeasure affect (see review by Kringelbach & Berridge, 2017). The hedonic gloss of objects or events is generated in the brain by activity in networks of hedonic hotspots (pleasure) or coldspots (displeasure). Berridge and his colleagues have identified these regions in the rodent nucleus accumbens and ventral pallidum, the adjacent insula in the cortex, and orbitofrontal cortex through direct neurochemical or optogenetic manipulation generating positive or negative changes in “liking” reactions to tastes (see details in Berridge & Kringelbach, 2015).
185
What are the issues with DBS being used to make people happy?
electrodes would need to be targeted at a hotspot without also stimulating an adjacent cold spot, which would produce a mixed response. There is, however, growing evidence that stimulation of the nucleus accumbens or prefrontal cortex can provide relief from anxiety or depression, which can have a significant positive impact on people’s lives.
