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Behavioral Neuroscience: Exam 2 > Behavioral Neuroscience: Exam 3 > Flashcards

Behavioral Neuroscience: Exam 3 Flashcards

1
Q

Neural Development

A

An ongoing process ; the nervous system is plastic.

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2
Q

The Case of Genie

A

At the age of 13, Genie was discovered in a dark room tied to a chair. She weighed 62 pounds and was unable to chew solid food. She could not speak because she was never introduced to speech. She was beaten, starved, restrained, kept in a dark room, and denied normal human interactions.

Even with special care and training after her rescue, her behavior never become normal.

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3
Q

Zygote

A

Ovum + Sperm

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4
Q

Developing Neurons Accomplish Things in Five Phases (5 Phases of Development) Essay Question

A
  1. Induction of the neural plate
  2. Neural proliferation
  3. Migration and aggregation
  4. Axon growth and synapse formation
  5. Neuron death and synapse rearrangement
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5
Q

Induction of the Neural Plate

A

Starting off with a collection of cells. The new zygote is plate shaped. The collection of cells will start to fold on itself and form a valley (neural groove). This process begins shaping the nervous system (neural tube).

A patch of tissue on the dorsal surface of the embryo becomes the neural plate. Neural plate cells are often referred to as embryonic stem cells. Development is induced by chemical signals from the mesoderm. The neural plate is visible 3 weeks after conception.

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6
Q

Neural Proliferation

A

The mass growing of neural stem cells.

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7
Q

Migration and Aggregation

A

The moving of neural stem cells throughout the body. Migrating cells are immature, lacking axons and dendrites. The clotting of cells together and then they begin to specialize (aggregation).

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8
Q

Axon Growth and Synapse Formation

A

Once cells are specialized they seek out other compatible cells and make a connection, and then build a synapse. These then become functional neural circuits and additional specialization.

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9
Q

Neuron Death and Synapse Rearrangement

A

After the first several years of life, the brain starts pruning away neurons that did not make a connection or form a functional synapse. So the brain kills off these cells through starvation or the will be genetically triggered to kill themselves. This allows the remaining neurons to become stronger, and they form stronger synaptic connections (rearrangement).

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10
Q

Three layers of embryonic cells:

A

Ectoderm
Mesoderm
Endoderm

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11
Q

Endoderm

A

(Innermost Layer) Will become all of our guts and organs.

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12
Q

Mesoderm

A

(Middle Layer) Will become our muscles. The “organizer”.

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13
Q

Ectoderm

A

(Outermost Layer) Will become all of our peripheral nerves and all of our central nervous system.

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14
Q

Embryonic Stem Cells

A
  • AKA Neural Plate Cells
  • Have unlimited capacity for self renewal
  • Can become any kind of mature cell
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15
Q

Totipotent

A

The earliest embryonic stem cells have the ability to become any type of body cell.

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16
Q

Multipotent

A

With development, neural plate cells are limited to becoming one of the range of mature nervous system cells.

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17
Q

Two Types of Neural Tube Migration

A
  • Radial Migration (moving out)

- Tangential Migration (moving up)

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18
Q

Two Methods of Migration

A
  1. Somal - an extension develops that leads migration, cell body follows
  2. Glial - mediated migration (the cell moves along a radial glial network)

*Most cells engage in both types of migration

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19
Q

Neural Crest

A
  • Formed from neural tube cells
  • Develops into the cells of the peripheral nervous system
  • Cells migrate long distances
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20
Q

Cell-Adhesion Molecules (CAMs)

A
  • Aid both migration and aggregation

- CAMs recognize and adhere to molecules

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21
Q

Pioneer Growth Cone

A

The first to travel a route, interact with guidance molecules.

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22
Q

Fasiculation

A

The tendency of developing axons to grow along the paths established by preceding axons.

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23
Q

Synapse Formation

A
  • High levels of cholesterol are needed which is supplied by astrocytes
  • Depends on the presence of glial cells
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24
Q

Neurotrophins

A

Promote growth and survival. They guide axons and stimulate synaptogenesis (the formation of additional synapses).

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25
Q

Necrosis

A

Passive cell death.

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26
Q

Apoptosis

A

Active cell death.

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27
Q

Postnatal Growth

A

Is a consequence of:

  • Synaptogenesis
  • Myelination
  • Increased dendritic branches

*Overproduction of synapses may underlie the greater plasticity of the young brain

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28
Q

Development of the Prefrontal Cortex

A
  • Believed to underlie age-related changes in cognitive function
  • No single theory explains the function of this area
  • Prefrontal cortex plays a role in working memory, planning and carrying out sequences of actions, and inhibiting inappropriate/ dangerous responses.
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29
Q

Permissive Experiences

A

Experiences that are necessary for information in genetic programs to be manifested. Give the brain permission to grow a specific structure. Must happen during the critical period of development,

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30
Q

Instructive Experiences

A

Those that contribute to the direction of development.

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31
Q

Nuerogenesis

A

Growth of new neurons. Adult neural stem cells are created in the epedymal layer lining in ventricles and adjacent tissues.

*Enriched environments can promote neurogenesis

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32
Q

Tinnitus

A

Ringing in the ears. Produces major reorganization of primary auditory cortex.

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33
Q

Autism

A

Three core symptoms:

  1. Reduced ability to interpret emotions
  2. Reduced capacity for social interaction
  3. Preoccupation with a single subject or activity
  • Autism is heterogenous (the level of brain damage and dysfunction varies)
  • Often considered a spectrum disorder
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34
Q

William’s Syndrome

A
  • Mental retardation, and an uneven pattern of abilities and disabilities
  • Opposite of autism
  • Profound impairments in spatial cognition
  • Mutation on chromosome 7
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35
Q

H.M Case Study

A

H.M. was a man suffering from severe epilepsy. He could no longer live independently or manage his own self-care. He had his temporal lobes removed in 1953. His seizures were dramatically reduced, but so was his long-term memory. H.M is unable to form most types of new long-term memories, but his short-term memory is still intact.

-Mild retrograde amnesia and severe anterograde amnesia.

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36
Q

Retrograde Amnesia

A
  • Backward acting

- Unable to remember the past

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37
Q

Anterograde Amnesia

A
  • Forward acting
  • Unable to form new memories
  • You can remember things from the past
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38
Q

Digit Span

A

H.M. can repeat digits provide the time between learning and recall is within the duration of short-term memory

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39
Q

Block-Tapping Memory-Span Test

A

This test demonstrated that H.M.s amnesia was global - not limited to one sensory modality

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40
Q

3 Major Contributions of H.M.s Case

A
  1. Medial temporal lobes are involved in memory
  2. Short term memory, remote memory and long term memory and distinctly separate
  3. Memory may exist but not be recalled (explicit vs. implicit)
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41
Q

Explicit

A

-Conscious memories

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42
Q

Implicit

A

-Unconscious memories, as when H.M. shows the benefits of prior experience

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43
Q

Medial Temporal Lobe Amnesia

A

-These people may have trouble imagining future events

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44
Q

R.B. Case Study

A
  • R.B. suffered damage to just one part of the hippocampus and developed amnesia
  • R.B.s case suggest that hippocampal damage alone can produce amnesia
  • H.M.s damage and amnesia was more severe than R.B.s
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45
Q

Korsakoff’s Syndrome

A
  • Most commonly seen in severe alcoholics
  • Tyiamine deficiency
  • Characterized by amnesia, confusion, personality changes and physical problems
  • Damage in the medial diencephalon: medial thalamus + medial hypothalamus
46
Q

Amnesia of Alzheimer’s Disease

A

-Begins with a slight loss of memory and progresses to dementia

General deficits in predementia Alzheimer’s:

  • Major anterograde and retrograde amnesia in explicit memory tests
  • Deficits in short term memory and some types of implicit memory - verbal and perceptual
47
Q

Posttraumatic Amnesia

A

Concussions may cause retrograde amnesia for the period before the blow and some anterograde amnesia after

  • The same is seen in comas
  • Concussions disrupt consolidation (storage) of recent memories
48
Q

Hebb’s Theory

A

Memories are stored in the short term by neural activity

  • Interference with this activity prevents memory consolidation
  • Ex: blows to the head, electroconvulsive shock
49
Q

Reconsolidation

A
  • Each time a memory is retrieved from the long term memory, it is temporarily held in the short term memory
  • Memory in the short term memory is susceptible to post-traumatic amnesia until it is reconsolidated
  • Anisomycin, a protein synthesis inhibitor, prevents reconsolidation of conditioned fear in rats
50
Q

Removal of the Rhinal Cortex

A

Results in object-recognition deficits.

51
Q

Removal of the Hippocampus

A

Results in no or moderate effects on object recognition.

Removing the hippocampus results in a moderate deficit, but small lesions of the hippocampus results in a severe deficit. Why? The lesions damage neurons outside the of the hippocampus.

52
Q

Removal of the Amygdala

A

Results in no effect on object recognition.

-If you have a fear of something and you remove the amygdala, the fear goes away with it. Emotional memory.

53
Q

Rhinal cortex plays an important role in…

A

Object Recognition

54
Q

Hippocampus plays a key role in…

A

Memory for Spatial Location

Removal produces deficits in solving mazes.

55
Q

Many hippocampal cells are…

A

Place Cells - responding when a subject is in a particular place and to other cues

56
Q

Grid Cells

A

Work like a map in terms of distance. How far is a drive?

57
Q

Cognitive Map Theory

A

Hippocampus constructs and stores allocentric maps of the world.

58
Q

Where are memories stored?

A

Each memory is stored diffusely throughout the brain structures that were involved in it’s formation

  • Hippocampus: spatial location
  • Perirhinal cortex: object recognition
  • Mediodorsal nucleus: Korsakoff’s symptoms
  • Basal forebrain: Alzheimer’s symptoms
59
Q

Prefrontal Cortex

A
  • Holds memories about temporal order of events and working memory
  • Tasks involving a series of responses
60
Q

Cerebellum

A

-Stores memories of sensorimotor skills

61
Q

Striatum

A

-Habit formation

62
Q

Long-Term Potentiation

A

Synapses are effectively made stronger by repeated stimulation (this creates a long term memory).

Can be viewed as a three part process:
1. Induction (learning)
2. Maintenance (memory)
3. Expression
(recall)
63
Q

Smart Drugs

A

Substances thought to improve memory.

64
Q

Steps in Digestion

A
  1. Chewing breaks up food
  2. Saliva lubricates food and begins digestion
  3. Swallowing moves food and drink from the esophagus to the stomach
  4. Stomach = storage reservoir. The hydrochloric acid in the stomach breaks down food into small particles, and pepsin begins the process of breaking down protein molecules to amino acids
  5. The stomach gradually empties through the pyloric sphincter into the duodenum (the upper portion of the intestine) where most absorption takes place
  6. Digestive enzymes in the duodenum (from the gall bladder and pancreas) break down protein molecules into amino acids, and starch/ complex sugars into simple sugars. Simple sugars/ amino acids then pass through the duodenum wall into the bloodstream and carried to the liver
  7. Fats are emulsified by bile, which is manufactured in the liver and stored in the gall bladder. Emulsified fat is carried by small ducts in the duodenum wall into the lymphatic system
  8. Most remaining water and electrolytes are absorbed from the waste in the large intestine, and the remainder is ejected from the anus
65
Q

Is there a set point for the body’s energy reserves that determines when we eat?

A

No - because of the prevalence of eating disorders.

3% of U.S. adolescents suffer from anorexia or bulimia

66
Q

Purpose of eating…

A

Is to provide the body with molecular building blocks and energy

67
Q

Digestion

A

Breaking down food and absorbing its constituents

68
Q

Duodenum

A

The upper portion of the intestine responsible for absorption

69
Q

Liver

A

Blood’s filter

70
Q

Bile

A

Breaks down the fat that we eat

71
Q

Emulsification

A

The breakdown of large fat molecules into small fat molecules

72
Q

Large Intestine

A

Pulls out as much usable water from food as possible. In the water you also get your basic ions (sodium, potassium)

73
Q

Energy Storage in the Body

A
  • Energy is delivered to the body as lipids, amino acids and glucose
  • Energy is stored in the body as fats, glycogen and proteins
74
Q

Fats get broken down into…

A

Lipids

75
Q

Protein gets broken down to…

A

Amino Acids

76
Q

Carbohydrates/ Complex Sugars get broken down into…

A

Glucose

77
Q

Energy Storage in the Body

A
  • Lipids are stored as fat
  • Glucose is stored as glycogen
  • Amino acids are stored as protein
  • Fats are the most efficient for energy storage
  • 1 gram of fat stores twice as much energy as 1 gram of glycogen
  • Fat does not attract or hold as much water as glycogen, which is why it provides denser energy storage
78
Q

Sugar

A
  • Hydrophylic

- Loves to absorb lots of water

79
Q

3 Phases of Energy Metabolism

A

Energy Metabolism - Chemical changes that make energy available for use

  1. Cephalic Phase
  2. Absprptive Phase
  3. Fasting Phase
80
Q

Cephalic Phase

A

(Brain Phase)

Preparation for eating

81
Q

Absorptive Phase

A

Energy is being absorbed, digestion begins. We do this until we use up all of the available nutrients in the bloodstream

82
Q

Fasting Phase

A

Brain shuts down absorptive phase. Molecular building blocks that our brain needs are taken from the body’s storage/ reserves. We stay in the fasting phase until we enter the next cephalic phase.

83
Q

The 2 phases of energy metabolism rely on 2 pancreatic hormones…

A
  1. Insulin
  2. Glucagon

When insulin levels are high, glucagon levels are low and vice versa.

84
Q

Insulin

A
  • High during cephalic and absorptive phases
  • Triggers glucose use as fuel by the body
  • Triggers conversion of blood-borne energy to fat, glycogen and protein
  • Triggers energy storage in the liver and muscles
  • Blocks withdrawing energy from storage reserves
85
Q

Glucagon

A
  • High during fasting phase

- Triggers change of stored energy to usable fuel

86
Q

The Set-Point Assumption

A

-Hunger is a response to an energy need; we eat to maintain an energy set point

Typical Assumption: Eating works like a thermostat… It turns on when energy is needed, and off when the set point is reached.

87
Q

Glucostatic Theories

A

Glucose levels determine when we eat

88
Q

Lipostatic Theories

A

Fat sores determine how much we eat over long term (explaining why weight tends to be constant)

89
Q

Problems with Set-Point Theories of Hunger

A
  • Contrary to evolutionary pressures that favored energy storage for survival
  • Reductions in blood glucose or body fat do not reliably induce eating
  • Do not account for the influence of external factors on eating and hunger (seeing someone eat, smelling something tasty)
90
Q

Positive-Incentive Perspective

A
  • We are drawn to eat by the anticipated pleasure of eating
  • We have evolved to “crave” food
  • Multiple factors interact to determine the positive-incentive value of eating
  • Accounts for the impact of external factors on eating behavior
91
Q

Factors that determine what, when and how much we eat…

A
  • Sweet and fatty foods = high energy
  • Salty = sodium rich
  • Bitter = often associated with toxins
92
Q

Factors that determine WHEN we eat…

A
  • We tend to get hungry at mealtime
  • As mealtime approaches, the body enters the cephalic phase leading to a decrease in blood glucose
  • Pavlovian conditioning of hunger demonstrated experimentally
93
Q

Factors that influence HOW MUCH we eat…

A

Satiety: “being full”, may stop a meal

-Satiety signals:: Food in gut and glucose in the blood can induce satiety signals

94
Q

Appetizer Effect

A

Small amounts of food may increase hunger - it triggers a cephalic phase

95
Q

Serving Size

A

The larger the serving, generally the more consumed

96
Q

Social Influences

A

We eat more when we are in a group

97
Q

Sensory-Specific Satiety

A

(Taste Dependent Satiety)

  • Tasting a food immediately decreases the positive-incentive value of similar tastes and decreases the palatability of all foods about 30min later
  • Adaptive: encourages a varied diet

Some foods are resistant to sensory-specific satiety… rice, bread, potatoes, sweets and green salads

98
Q

Role of Blood Glucose in Hunger

A
  • Blood glucose drops prior to a meal as preparation to eat, not a cue to eat
  • Must decrease blood glucose by 50% to trigger feeding
99
Q

Gut peptides that decrease meal size…

A
  • Cholecystokinin (CCK)
  • Bombesin
  • Glucacon
100
Q

CCK causes…

A

Nausea at high doses, but suppresses food intake at doses insufficient to induce taste aversions

101
Q

The hypothalamus plays a central role in…

A

eating behaviors

102
Q

Prader-Willi Syndrome

A

-Patients with insatiable hunger

Symptoms:

  • Insatiable appetite, extremely slow metabolism, eventual death in adulthood from obesity related diseases
  • Weak muscles, small hands and feet, triangular mouth, stubbornness, feeding difficulties in infancy, tantrums, compulsivity, skin picking

*Damage or absence of a section of chromosome 15

103
Q

Body Weight Regulation

A
  • According to the set-point assumption, it should be very difficult to gain weight… but it’s not
  • Free feeding does not lead to optimum health
  • Positive effects seen with caloric restriction
104
Q

Diet-Induced Thermogenesis

A

Body temperature drops with fat loss, making weight-loss diets gradually less effective

105
Q

Body weight drifts around a settling point…

A

the level at which the various factors that influence body weight achieve an equilibrium

106
Q

The Leaky Barrel Model

A
  1. The amount of water entering the hose is similar to the amount of available food
  2. The water pressure at the nozzle is similar to the incentive value of the available food
  3. The amount of water entering the barrel is similar to the amount of consumed energy
  4. The water level in the barrel is similar to the level of body fat
  5. The amount of water leaking from the barrel is similar to the amount of energy being expended
  6. The weight of the barrel on the hose is analogous to the strength of the satiety signal
107
Q

Who needs to be concerned about obesity?

A

Everyone, as rates of obesity are increasing in most parts of the world

-Obesity is related to many other health problems

108
Q

Why is there an epidemic of obesity?

A

-Evolution favored preferring high-calorie food, eating to capacity, storing fat, and using energy efficiently

109
Q

Why do some people become obese while others do not?

A

Energy Input Differences

  • Craving for high-calorie foods
  • Cultural norms
  • Large cephalic-phase response to sight and smell of food

Energy Output Differences

  • Exercise
  • Diet induced themogenesis
  • NEAT (nonexercise activity thermogenesis)
110
Q

Why are weight-loss programs typically ineffective?

A
  • Long term weightloss will require a permanent lifestyle change
  • Exercise also can make you hungry… often people eat more calories after the workout than they burned during the workout
111
Q

Leptin

A

A negative feedback fat signal.

  • Hormone released by fat cells
  • Leptin receptors found in the brain
  • Eat more and store fat more efficiently than controls
  • Leptin and insulin in the brain have some effects on eating behavior, but are (again) not the only eating/sating signals

Behavioral Neuroscience: Exam 2 (4 decks)

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