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Bio > Exam 3 > Flashcards

Exam 3 Flashcards

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Biology 101 flashcards
1
Q

What is homeostasis?

A

Balance of internal states

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2
Q

What is required for a homeostatic system to function properly? Can you provide an example?

A

Set-point (optimal level), central receptors (monitor of state), and mechanisms to change level (state is not at set-point, change balance)

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3
Q

Explain energy balance in terms of intake vs expenditure.

A

Consuming as much as we expend

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4
Q

Why do our cells need glucose?

A

To function and create ATP (measurement for energy) (Adenosine triphosphate).

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5
Q

Describe anabolic metabolism. What is glucose converted to for longer-term storage? How is insulin involved?

A

Prandial state (after a meal). Building and storing of energy

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6
Q

What is glucose converted to for longer-term storage? How is insulin involved?

A

Stored as glycogen, insulin tells the body to store glucose as glycogen after a meal.

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7
Q

Describe catabolic metabolism.

A

breakdown of complex molecules into simpler ones, releasing energy in the process.

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8
Q

What happens to glycogen and triglycerides?

A

Glycogen to glucose
Triglycerides to fatty acids

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9
Q

What is the role of the lateral hypothalamus in feeding behavior? What happens if you lesion it?

A

The feeding center of the brain, if lesioned you are less hungry.

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10
Q

What is the role of the ventromedial hypothalamus (VMH) in feeding behavior? What happens if you lesion it?

A

Supposed satiety (fullness) center, if lesioned you are very much hungry

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11
Q

What is leptin? Where is it synthesized? What does it do?

A

Released by adipocytes (fat cells). Decrease appetite and increase energy expenditure.

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12
Q

Would giving leptin to a “normal” individual help with weight loss? Why or why not?

A

No, because a normal person has a normal level of leptin.

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13
Q

How does leptin signaling affect the αMSH/CART neurons in the arcuate nucleus of the hypothalamus?

A

Detect elevated levels of leptin and activate the paraventricular nucleus. Mimics leptin

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14
Q

How does leptin signaling affect the NPY/AgRP neurons in the arcuate nucleus of the hypothalamus?

A

Project to and inhibit the paraventricular nucleus when leptin levels decrease, decrease metabolism

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15
Q

What are MCH (melanin-concentrating hormone) neurons and what is their role in feeding behavior?

A

Target of leptin-sensitive cells in the arcuate nucleus. Inform cortex of leptin levels to help coordinate goal-directed behavior

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16
Q

What are Orexin neurons and what is their role in feeding behavior?

A

The target of Leptin-sensitive cells is in the arcuate nucleus. Promotes meal initiation

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17
Q

What is Ghrelin? Where is it synthesized? What does it do? Where does it act, and what does it do there?

A

Appetite stimulant, synthesized by endocrine
cells of the stomach. Inverted relationship to leptin.

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18
Q

What are some other short-term satiety signals, and how do they work?

A

Gastric Distention: Mechanosensory axons innervate the stomach wall and send signals to the brain via the
vagus nerve.
Cholecystokinin (CCK), Release from intestines in response to stimulation

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19
Q

How is insulin involved in the regulation of hunger? Where does it act in the brain?

A

ventromedial hypothalamus. Inhibits NPY and suppresses hunger

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20
Q

What is Type 1 Diabetes?

A

Juvenile-onset, the pancreas stops producing insulin

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21
Q

What is Type 2 Diabetes? How is insulin involved?

A

Adult-onset, greatly reduced tissue sensitivity to insulin

22
Q

What is “liking”? What is “wanting”? How are they different? How can we separate out “liking” from “wanting”? Give evidence-based answers.

A

Like is because you like the flavor or feeling. Wanting is because you need.

23
Q

Describe the Olds and Milner experiments. What is electrical self-stimulation? Why does it work?

A

Implanted electrodes into the brains of rats. Stimulating wanting not liking.
Rats were allowed to press a lever to stimulate the brain with the electrode. Ventral tegmental area (VTA).

24
Q

What do microelectrode recording studies tell us about the firing of dopamine neurons in different situations? Explain this in detail using evidence from these studies.

A

Early studies of lesioned dopamine cells in the midbrain showed that rats exhibit
a liking reaction to sweetness even in the absence of motivation to consume food.
If we lesion out dopamine, there is no motivation to eat food, but there will still be
a reaction to the taste

25
Q

Is liking or wanting dysregulated to a greater extent in addiction? How do you know?

A

Wanting is more dysregulated than liking. Because liking doesn’t have anything to do with dopamine, but wanting does.

26
Q

Describe the shift in addiction from positive reinforcement to negative reinforcement. What kinds of changes are happening in the brain that correspond with this shift?

A

Positive starts with liking, which causes you to want it. Initially, positive reinforcement will go down (building intolerance). Wanting does up, and liking goes down. Increase in dopamine, the brain becomes less affected by dopamine.

27
Q

What is learning? What is memory? How do they interact?

A

Learning: Acquiring new skills
Memory: retention & recall of skills/knowledge acquired through learning

28
Q

What is declarative memory? What are the subtypes of declarative memory?

A

Explicit memory, facts and events.

29
Q

What is semantic memory? Give an example.

A

Memory for facts, such as brain areas.

30
Q

What is Episodic memory? Give an example.

A

Memory for events, such as making food

31
Q

Describe the case of patient H.M. (Henry Molaison). What does this teach us about declarative memory. Did H.M. lose all types of memory? How do we know?

A

Surgery for epilepsy. Region of hippocampus removed. Taught about how the hippocampus is involved in encoding memory. Could not form new long term memories.

31
Q

What is non-declarative memory? What are the divisions of non-declarative memory?

A

Implicit memories for actions, procedural and emotional conditioning

31
Q

What is procedural memory? Give an example.S

A

Skills and habits

31
Q

What structures are involved in the formation of declarative memory?

A

Hippocampus and prefrontal cortex

32
Q

What is retrograde amnesia?

A

Forgetting the past

33
Q

What is anterograde amnesia?

A

Can’t encode new memories

34
Q

What did Wilder Penfield’s human brain stimulation studies reveal?

A

Different parts of the brain are connected to different sensory and motor functions.

35
Q

Describe the delayed non-match to the sample task. What is it supposed to measure? Damage to what area of the brain results in a deficit in performance on this task?

A

Remember where a treat is, measuring decorative memory. Damage to the hippocampus results in deficiency.

36
Q

Striatal lesions in monkeys results in a particular type of learning deficit. What type of learning is disrupted? What type of learning is still intact?

A

Procedural memory, decorative memory is ok.

37
Q

Describe the Weather Prediction Task. What does it measure? Would Parkinson’s disease patients have trouble with this task? Would patients with medial temporal lobe damage have trouble with this task? Why?

A

probabilistic classification learning task. Patients would have a hard time. They would have a hard time at first but unknowingly get better at it.

38
Q

Describe the different timescales of declarative memory (working memory, short-term memory, and long-term memory).

A

Short-term: seconds to hours
Working memory: seconds to minutes
Long-term: days to decades

39
Q

Describe the delayed-response task. Damage to what area of the brain would result in a deficit in performance on this task?

A

The reward is hidden in a well and is shown, then after delay they have to choose the right one. The prefrontal cortex is connected.

40
Q

Describe the Wisconsin Card Sorting Task. Damage to what area of the brain would result in a deficit in performance on this task?

A

Sort cards in different ways, by either color, number of shapes, or which shape it is
Learn the sorting rules by being told of errors
Once a rule is learned, a new rule is introduced.
The prefrontal cortex: stuck on old rules.

41
Q

Describe consolidation, retrieval, and reconsolidation.

A

Consolidation: Stabilization of memory from a short-term to long-term trace
Retrieval: Brining memories to short-term
Reconsolidation: Update stored knowledge with new
information

42
Q

Describe habituation. How does it work in an aplysia?

A

Decrease in response to a stimulus after repeated stimulation. Less calcium enters per AP in sensory neurons. Hyper-polarizes, less AP.

43
Q

Describe sensitization. How does it work in an aplysia?

A

increase to all stimuli after exposure to one strong stimulus. Potassium is slower to exit, more calcium enters per AP in sensory neurons. Depolarizes the cell, more AP.

44
Q

What is LTP? Describe how we experimentally induce LPT.

A

Enhancement (potentiation) of a neuron’s sensitivity after repeated stimulation. Induced through stimulation.

45
Q

How do AMPA receptors contribute to the induction of LTP?

A

Depolarizes the postsynaptic cleft through sodium

46
Q

How do NMDA receptors contribute to the induction of LTP? What role does calcium play?

A

NMDA increases depolarization by bringing in more calcium.

47
Q

How to AMPA receptors contribute to the expression of LTP?

A

Increases the amount of AMPA receptors which further depolarizes the cell.

48
Q

Know what would happen if we blocked AMPA or NMDA receptors during induction or expression of LTP.

A

If AMPA was blocked, the cell would not be able to depolarize. If NMDA is blocked during expression, the cell will still depolarize because of the increased levels of AMPA.

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