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Neurobiology of Eating > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What do short-term satiety signals cause?

A

meal termination

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2
Q

What type of signals cause meal termination?

A
  • short -term satiety signals

- anorexigenic

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3
Q

CCK causes a(an) ______ in food intake

A

decrease

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4
Q

What does CCK respond more sensitively to?

A

protein and fat

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5
Q

What is the criteria for an endogenous satiety signal?

A

1) the signal is generated after food was ingested (CCK)
2) It acts within a meal – short term
 If given increasing doses of CCK the meal size consistently decreases
 It decreases but does not block a meal because some eating must occur before CCK is released
3) Exogenous administration should decrease meal size (without causing illness)
 Should be effective in physiological dose
 Removing or antagonizing the endogenous factor should increase meal size

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6
Q

Where are CCK receptors located?

A

in the periphery

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7
Q

What does administration of exogenous CCK cause?

A

reduces food intake

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8
Q

What is a CCK receptor antagonist?

A

MK 329

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9
Q

What does MK 329 do?

A
  • MK 329 is a CCK receptor antagonist that is specific to peripheral receptors (doesn’t cross blood brain barrier) (CCK-A receptors)
  • Blocking CCK receptor (with MK-329) induced hunger which is evidence that CCK-A receptors normally mediate satiety
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10
Q

Does CCK have therapeutic potential for obesity treatment?

A
  • Short half-life (1-2min)
  • CCK has short half-life so it is not an ideal drug
  • When injected continuously it rapidly becomes ineffective
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11
Q

What happened when CCK was administered to rats each time they began a meal?

A
  • decreased size of each meal (relative to placebo)
  • But: the number of meals increased – therefore CCK was not considered a viable weight loss strategy
  • Rats compensated for the reduction in meal size by increasing the number of meals
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12
Q

Does the effect of CCK on individual meals translate to an effect on body weight?

A

CCK is critical for regulation of short-term food intake but may not be essential for maintaining body weight

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13
Q

Describe the study that examined the relationship between CCK and body weight.

A

Part 1: Evidence from inbred line of rats that do not have CCK-A receptors because of spontaneous mutation OLETF rats. Not having CCK-A receptors in OLETF rats resulted in a satiety deficit leading to increases in meal size and obesity.
Part 2: Targeted deletion of CCK-A receptor in mice. These mice do not respond to CCK administration. They don’t have the receptor, but they are able to maintain their body weight
Conclusion: CCK is critical for regulation of short-term food intake but may not be essential for maintaining body weight

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14
Q

What are OLETF rats?

A
  • a inbred line of rats, lack CCK-A receptors because of a spontaneous deletion of the corresponding gene.
  • These rats develop obesity and type II diabetes
  • OLETF rats were completely resistant to exogenous CCK.
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15
Q

Is the absence of CCK-A receptors & hyperphagia the sole cause of obesity in OLETF rats?

A
  • OLETF is an inbred line of rats, missing CCK-A receptors (and possibly additional genetic deficits) that become obese & develop Type II diabetes
  • Mice with targeted deletion of only CCK-A receptors do not get obese
    and do not develop Type II diabetes
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16
Q

How does CCK reach the CNS?

A

Vagus nerve

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17
Q

What are the manipulations to test if the vagus nerve is the pathway and the NTS is the first relay for CCK to communicate to the brain?

A
  • Vagotomy (cutting vagus nerve) or neurotoxin application (Application of neurotoxin (Capsaicin) Block action of peripherally administered CCK)
  • Lesions of NTS interfere with CCK-induced satiety
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18
Q

Can CCK pass the blood brain barrier?

A

CCK does not pass through blood brain barrier, but binds to CCK-A receptors

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19
Q

What would a vagotomy, application of a neurotoxin (capsaicin), or lesions of the NTS interfere with?

A

CCK induced satiety

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20
Q

Where are the signals integrated/summed up? Where does the integration between short and long term energy signals occur?

A

The brain

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21
Q

What are the two types of peripheral regulatory signals?

A
  • Adiposity (long-term) signals

- Short-term hunger & satiety signals

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22
Q

What is the role of the vagus nerve?

A

Innervates the thoracic and abdominal vicera, visceral sensory information, visceromotor information

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23
Q

What are some key short term hunger and satiety molecules and what do they signal to?

A

Leptin and insulin arrive through the blood, ghrelin and CCK signal through the vagus nerve, all eventually reaches the brainstem, hypothalamus

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24
Q

What is the role of the NTS?

A

sensory input

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25
Q

What is the role of the DMX?

A

motor output

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26
Q

What is a reflex?

A
  • involuntary process

- Reflex is a fast reaction, then your brain tells you what you did after

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27
Q

What are some examples of reflexes?

A

knee, touch something hot

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28
Q

Dorsal

A

top (of brain) / back (of spine)

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29
Q

Ventral

A

bottom (of brain) / front (of spine)

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30
Q

Midline

A

middle of body, split in half down the front

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31
Q

Each aspect of brain location/nomenclature comes….

A

in pairs

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32
Q

What is medial?

A

closer to the midline

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33
Q

What is lateral?

A

farther from the midline

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34
Q

Rostral/anterior

A

(front of the brain)

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35
Q

Caudal/posterior

A

back of the brain

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36
Q

Compare an alligator and a human’s brain set up.

A
  • Alligator – brain and spinal cord on same plane

- Humans – brain is 90 degrees to the spine

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37
Q

What is the gustatory system?

A

taste

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38
Q

Any sensory information has the potential to do what?

A

to inform the entire brain

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39
Q

What does the brainstem receive and put out?

A

The brainstem receives sensory inputs and has motor outputs (motor neurons and motor pattern generators are located in the brainstem)

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40
Q

What model was used to investigate the function of the brainstem?

A

The decerebrate rat model - used to investigate what the brainstem can accomplish without the forebrain

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41
Q

Where is the cut in a decerebrate rat?

A
  • Cut between forebrain and brainstem

- transecting the brainstem

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42
Q

How does decerebration affect ingestive behavior?

A

This operation disconnects the forebrain from the hindbrain so that the muscles involved in ingestive behavior are controlled solely by hindbrain mechanisms

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43
Q

What does the hindbrain control in a decerebrate rat?

A

Hindbrain – control of muscles involved in ingestive behavior

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44
Q

What does the forebrain control in a decerebrate rat?

A

Forebrain – neural circuit in the forebrain cannot affect behaviors controlled by motor neurons caudal (posterior to) to the transection

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45
Q

Describe the behavior of a decerebrate rat.

A
  • Maintains posture and grooms spontaneously
  • Does not spontaneously walk, run, and jump but can if stimulated
     (They don’t have the motivation to walk)
  • Does not approach food and must be fed (by gavage) to survive
    • Sort of like how we feed babies
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46
Q

Decerebrate rats were evaluated for their ability to regulate the following three things:

A

o Short term control – control of meal size
o Long-term control – integration of energy intake and expenditure
o Learning – associative learning

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47
Q

What determines a short-term meal size in intact rats?

A

Taste, (Ghrelin) and GI satiety signals (post-ingestive feedback) codetermine a meal size in intact rats (that have brainstem-forebrain communication)

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48
Q

What test was used to examine ability to recognize and respond to taste?

A

The “Taste Reactivity” Test

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49
Q

What test evaluated ability of rats to ingest/control variable amounts of liquid?

A

“Intraoral Intake” Test

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50
Q

What aspects of meal size control were evaluated in intact and decerebrate rats?

A

.Ability to recognize and respond to taste
Ability to ingest/control variable amounts of liquid
Ability to respond to GI signals

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51
Q

What foods cause reactions in rats, primates, and babies?

A
  • Hedonic reactions (sweet) – sweet is something
  • Adverse reactions (bitter) – bitterness is associated with poison so it causes a reflex reaction, you only like something bitter when it is learned
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52
Q

What are the two responses to the taste reactivity test?

A

sweet - sugar solution - acceptance

bitter - quinine solution - rejection

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53
Q

What are acceptance and rejection patterns in the taste reactivity test?

A
  • acceptance (rhythmic tongue protrusions, lateral tongue licks and ingestion)
  • rejection (“Averse profile” chin rubs, head shakes, face washes, paw shakes, paw wipes, and rejection of liquid)
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54
Q

How did decerebrate rats respond to the taste reactivity test and the intraoral infusion test?

A
  • Decerebrate rats show ingestive behaviors similar to those of intact rats
  • Based on taste reactivity test oral motor responses are intact/fully functioning in decerebrate rats
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55
Q

What did the response of rats to the taste reactivity test and the intraoral infusion test indicate about their brains?

A
  • Decerebrate rats show fundamentally normal oral motor organization of meal taking (licking; swallowing)
  • Decerebrate have intact taste and oral-motor responses related to licking and swallowing, but they are a reflex
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56
Q

How did decerebrate rats respond to the intraoral infusion test?

A

With an increase in oral infusion both intact and decerebrate rats responded by an increase in both swallow frequency and swallow volume

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57
Q

What was the third component of short-term meal control evaluated in decerebrate rats?

A
  • GI signals

- Sham feeding, nutrient preload, and CCK were tested

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58
Q

What is sham feeding?

A
  • Eat food then take it out of their stomach
  • Gastric fistula is a tube that takes the nutrients out
  • Ingested food is prevented from accumulating in the stomach and small intestine by surgical intervention
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59
Q

What does sham feeding investigate?

A

Sham feeding permits the investigation of the orosensory controls of a meal size in the absence of post-ingestive controls

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60
Q

How did decerebrate rats respond to sham feeding?

A
  • Like intact rats, decerebrate consumed more food during sham feeding
  • This shows that decerebrate rats respond to GI satiety signals
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61
Q

What is nutrient preload?

A

Eat a meal and then have another meal, would the preload impact the amount eaten at the second meal?

62
Q

How did decerebrate rats respond to nutrient preloading?

A
  • Like intact rats, decerebrate consumed less food after nutrient preload
  • This shows that decerebrate rats respond to GI satiety signals
63
Q

How did decerebrate rats respond when given CCK?

A

Decerebrate rats are responsive to CCK (they consumed less sucrose after given CCK)

64
Q

What was the conclusion about short term meal control in decerebrate rats?

A
  • Sensory/satiety information from the gut and taste are all still responded to by decerebrate rats
  • Brainstem in neural isolation from the forebrain is sufficient for simple, reflex, short term regulation of food intake
65
Q

What does long term control of food intake require?

A

integration of energy intake and expenditure

66
Q

What three tests were preformed to evaluate the long-term regulation of food intake in decerebrate rats?

A

o Effect of Food Deprivation on Energy Intake
o Effect of Meal Omission on Energy intake
o Effect of Food Deprivation on Energy Expenditure

67
Q

Describe how decerebrate rats responded to food deprivation.

A
  • Food deprivation causes next meal to be larger in intact rats
  • Hypothalamus manages integration of time
  • For Decerebrate rats 24h deprivation did not cause them to intake larger amounts
  • The decerebrate rats did not show hyperphagic responses to food deprivation.
68
Q

Describe how decerebrate rats responded to meal omission.

A
  • Experiment: First week rats are given 3 meals/day, then the second week the second meal was omitted. The rats could eat as much as they liked (ad libitum) for each meal.
  • When rats went from 3 meals to 2 meals a day intact rats compensated by increasing the average meal size while the decerebrate rats did not
  • Indicates that decerebrate rats do not have the ability to connect that they haven’t had a meal
69
Q

Describe how food deprivation of decerebrate rats effects energy expenditure.

A
  • After 48hr deprivation, both intact and decerebrate rats reduced metabolic energy expenditure and mobilized fat (they also had decreased serum leptin, and insulin)
  • This demonstrates that energy metabolism is more of a reflex
  • We cannot control metabolism, but behavior we can control
  • The decerebrate rats couldn’t change their behavior but could modify their energy expenditure
70
Q

Can decerebrate rats exhibit long-term regulation of food intake?

A

No.
Do not compensate in energy intake (behavior)
Do compensate in energy expenditure (metabolic)

71
Q

What is associative learning (basic)?

A

We learn to avoid the food (taste) that made us sick

72
Q

When is associative learning the most efficient and why?

A
  • This learning is the most efficient if the taste is novel

- This is because there are no prior biases

73
Q

What is conditioned taste aversion?

A
  • A form of associative learning
  • An experimenter was able to manipulate people to believe that they had been sick from something
  • One trial learning
74
Q

How is conditioned taste aversion performed in experiments? Induced?

A
  • A novel tasting food is consumed; the taste is a conditioned stimulus (CS).
  • After eating, animal is injected with LiCl to induce malaise, which mimics stomach illness normally induced by spoiled food.
  • (LiCl is an unconditioned stimulus)
75
Q

What is the set up of a learning/conditioning experiment?

A

o Innate responding (without learning):
Palatable food taste induces eating: CS (taste) -> eating
LiCL induces illness: US (LiCl) -> illness
o Learning (conditioning):
novel taste consumption is followed by LiCl injections
CS -> eating + US -> illness
o After learning (conditioning)
CS alone -> food avoidance/aversion (Conditioned Response, CR)

76
Q

What are the oral motor responses of rats, chimps, and babies?

A 
Hedonic reactions (sweet)
Aversive Reactions (bitter)
77
Q

How do intact rats respond to CTA experiements?

A

Trial 1: Given sucrose solution. They show acceptance pattern. Immediately after consumption of sucrose solution, rats given LiCl injections, which made them ill.
Trial 2: Given the same sucrose solution, as in Trial 1. Intact rats show rejection pattern; they respond as if they were given a bitter (e.g., quinine) solution.

78
Q

How do decerebrate rats respond to CTA experiments and what can we conclude from that?

A

Trial 1: Decerebrate rats show acceptance when given sucrose solution in Trial 1.
Trial 2: Given the same sucrose solution, as in Trial 1. The decerebrate rats did not learn an association of a taste with illness produced by LiCl.
Decerebrate rats show the same response to the sucrose solution in Trials 1 and 2.
Conclusions: The communication between the Brainstem & Forebrain is necessary for Learning (conditioned taste aversion)

79
Q

What is the brainstem sufficient for? What is integration between the forebrain and the brainstem necessary for?

A
  • sufficient for Reflex responses to taste & GI satiety signals
  • sufficient to mediate Metabolic responses to food deprivation
  • necessary for behavioral responses to food deprivation and meal omission
  • is necessary for learning (e.g., CTA)
80
Q

What are the limitations of the decerebrate rat model?

A

Impairments from experiments with decerebrated animals provide important evidence about what the brainstem can do on its own BUT they do not provide evidence about how the brainstem functions within the network with forebrain in an intact animal.

81
Q

What is glucoprivation?

A

depriving cells of glucose

82
Q

How can glucoprivation be induced?

A

Hypoglycemia can be experimentally induced with Insulin injections 2-DG which interferes with glucose metabolism

83
Q

What is lipoprivation?

A

depriving cells of lipids

84
Q

How can lipoprivation be induced?

A

Experimentally can be induced with Mercaptoacetate (MA), which interferes with the ability to metabolize fatty acids.

85
Q

Name a study that involved the NTS, glucose, lipids, and decrebration.

A

A comparison of effects of NTS lesions (bilateral) vs decerebration on lipoprivation and glucoprivation induced feeding

86
Q

Compare NTS lesions and decerebration.

A
  • An NTS lesion (blocks communication between the NTS and the brainstem by damaging the NTS (nucleus of the solitary tract) (the NTS is located within the brainstem)
  • Decerebration blocks communication between the brainstem and the forebrain
87
Q

How does lipoprivation impact intact rats, rats with NTS lesions, and decerebrate rats?

A
  • Depriving cells of lipids (lipoprivation) or depriving cells of glucose (glucoprivation) stimulates feeding in controls (without brain manipulations) compared to how much they eat when given a placebo drug.
  • Subjects with NTS lesions do not respond to lipoprivation or glucose glucoprivation; they eat similar amounts as when given a placebo drug.
     NTS is critical for both lipo- and glucoprivation
  • Decerebrated rats were able to respond to glucoprivation (increase food intake) but not lipoprivation
     Brainstem alone can only respond to glucoprivation
88
Q

What were the main conclusions from the following study: A comparison of effects of NTS lesions (bilateral) vs decerebration on lipoprivation and glucoprivation induced feeding.

A
  • This study demonstrates that the NTS is critical for Lipoprivation- and Glucoprivation-induced food intake. (Rats w NTS lesions responded to neither
  • Decerebrate rats could respond to glucoprivation)
  • BUT it does not provide evidence whether the NTS is functioning only within the brainstem or within a network with the forebrain.
89
Q

Where is the hypothalamus located?

A

in the forebrain

90
Q

What is the dual centers hypothesis?

A

The hypothalamus contains centers for initiation and cessation of responses/behaviors (model system: feeding)

91
Q

What are the two centers in the hypothalamus?

A
  • Lateral Hypothalamic Area (LHA) “Feeding/Hunger Center”

- Ventromedial Nucleus of the Hypothalamus (VMH) “Satiety Center”

92
Q

What type of peptides are released in the LHA? What are 2 examples?

A

Orexigenic peptides: appetite inducing

  • Melanin-concentrating hormone (MCH)
  • Orexin/Hypocretin (ORX)
93
Q

What are MCH and ORX?

A

neuropeptides that stimulate eating

94
Q

How are ORX and MCH related?

A
  • MCH and ORX are expressed within the same region but they are in different neurons
  • These two peptides are not colocalized
95
Q

What is interesting about orexin?

A
  • Two names because two groups discovered it at the same time
  • Important for state of arousal
  • Also stimulates eating
96
Q

What is dale’s principle?

A
  • Each neurotransmitter produced by a neuron is released from all terminals (endings of an axon) of that neuron
  • The functioning of the neurotransmitter depends on the presence of a receptor
97
Q

Describe neuron structure.

A

o Neurons have dendrites – tree branches -> cell bodies -> axon

  • Neurons have multiple inputs and multiple receptors
  • Axons with endings (terminals)
  • Synapses are the specialized endings of axons
  • Output is to the axon
98
Q

How does information flow along neurons?

A

by way of electrical signals conducted via the plasma membrane of the dendrites, cell body, and axon

99
Q

How is information transferred to another cell?

A

This information is transferred to another cell (neuron or muscle) via the release of neurotransmitter from axon’s specialized endings: synapses

100
Q

How many axons do each neuron have?

A

A neuron only has one axon, but each axon has many branches/terminals (endings) with synapses

101
Q

What should happen under food deprivation to a brain substrate that stimulates eating?

A
  • Production should be increased
  • Melanin- Concentrating Hormone (MCH)
  • If you see a lot of mRNA it is producing a lot of the neuropeptide
  • More MCH mRNA present in the northern blot of fasted mice
102
Q

What is the blot for mRNA?

A

northern blot

103
Q

What is it called when you can eat as much as you want?

A

ad libitum

104
Q

What do ob/ob mice lack?

A

o DO not have a gene for leptin – cannot produce leptin

105
Q

How would brains substrates that stimulate eating be impacted by lack of leptin (ob/ob)?

A
  • Brain substrates that stimulate eating would be increased in ob/ob compared to normal mice
  • Ob have overall more, and still responds to food deprivation (have even more when fasted)
106
Q

How would MCH/ORX be injected into the brain?

A

Intracerebroventricular injection of orexin or mch stimulates food consumption

107
Q

What are MCH/ORX stimulated by and what are they decreased by?

A
  • stimulated by food deprivation

- decreased by leptin

108
Q

What is orexin related to? What would degeneration of orexin neurons cause?

A

o Orexin and relationship between eating and sleep/wakefulness
o Degeneration of orexin neurons leads to narcolepsy – suddenly falling asleep
- Arousal/Wakefulness and degeneration of orexin neurons leads to narcolepsy (suddenly falling asleep)
- Food deprived animals have to have energy to eat
- After you eat a really big meal you fall asleep

109
Q

What happens with targeted mutation of MCH gene in mice?

A
  • Food intake drops but doesn’t stop

- This indicates that MCH isn’t the only driver of food intake

110
Q

Describe the results of the study: Hypocretin/orexin (H/O; ORX) neurons regulate arousal according to energy balance (in mice), What was the control?

A
  • Wild type mice can increase activity when they are supposed to be sleeping if they are fasted
  • Transgenic mice in which orexin neurons are ablated fail to respond to fasting with increased wakefulness and activity
  • indicating that orx plays a role in increasing the activity levels in these mice
  • Wild type was weight matched to control
111
Q

What are Tg/+ mice?

A

Transgenic mice without ORX neurons (postnatal ablation)

112
Q

What is ghrelin? Where is it released? What does it induce?

A
  • a peptide hormone released in the stomach that stimulates feeding
  • induces adiposity in rodents
113
Q

What type of injections of ghrelin stimulate feeding?

A

peripheral and central

114
Q

Describe the pathway for ghrelin.

A
  • Neurons in the NTS also contain ghrelin and send axons to the hypothalamus where they release ghrelin which induces feeding
  • Ghrelin (stomach cells) -> Vagus Nerve -> NTS Ghrelin Neurons -> HY
115
Q

How were ghrelin targets identified?

A
  • To identify ghrelin targets they examined co-expression of Ghrelin Receptor and specific peptides (their mRNA) which identifies specific neurons
  • They found co-expression of Ghrelin Receptor and Neuropeptide Y (NPY) mRNA in the Hypothalamic neurons
116
Q

What neurons does ghrelin act via?

A

Neuropeptide Y

117
Q

How was Neuropeptide Y studied in mice?

A
  • Increased food intake by neuropeptide Y is due to an increased motivation to eat
  • NPY was administered to mice ICV
  • Lever presses increased with higher NPY dose
  • NPY – injected mice tolerated shocks to the tongue during milk- drinking (better than control mice)
  • Although they don’t like quinine, NPY dosage causes an increase in consumption of milk with quinine – more hungry
118
Q

NPY is an extremely potent stimulant of _____

A

food intake

119
Q

How did Tg/+ mice respond to fasting?

A
  • they lack orx neurons

- Transgenic mice did not respond to fasting with increased wakefulness and activity

120
Q

How does NPY effect energy metabolism and weight?

A
  • It decreases energy expenditure

- Chronic NPY stimulation causes weight gain

121
Q

NPY summary:

A

o Extremely potent stimulant of food intake
o Decreases energy expenditure
o Chronic NPY stimulation causes weight gain
o NPY is regulated by food deprivation and leptin

122
Q

Where are NPY neurons located?

A

o Arcuate nucleus of the Hypothalamus

o Cell Bodies of neurons in the Arcuate Nucleus of the Hypothalamus make Neuropeptide Y (NPY)

123
Q

Where does NPY act? Where is it released from axons of NPY neurons?

A

NPY is the most potent in the Lateral Hypothalamus

124
Q

Describe the structure and the major players in the LHA.

A

Orexigenic peptides (MCH & ORX)?

  • Structural evidence indicates that NPY axons can stimulate both MCH and ORX cell bodies and dendrites (in the LHA)
  • NPY neurons cell bodies are in the ARC however
125
Q

What is related to NPY? (Also exists in the ARC)

A
  • Neurons in the Arcuate nucleus that express NPY also coexpress AGRP
  • NPY and AGRP are co-localized (co-expressed in the same neurons)
  • This is important because of Dale’s principle
  • When ghrelin stimulates these neurons there are two peptides that stimulate feeding
126
Q

What is the ARC?

A
  • Arcuate Nucleus (ARC/ARH) - NPY neuron’s cell bodies located here
  • The same neurons in the arcuate hypothalamus express/make NPY and Agrp
  • CART expressing neurons also located here
127
Q

What stimulates NPY and what inhibits NPY?

A
  • Decrease in fat stimulates NPY

* Increase in fat causes leptin to inhibit the neurons

128
Q

What are two methods to observed neuronal activity?

A

Chemogenetics:

  • use optogenetics for cell-specific manipulations: channels respond to light, cell specific - stimulate or silence
  • Ca imaging as a proxy for neuronal activity
129
Q

Do the NPY/AgRP neurons express/make other neurotransmitters of neuropeptides?

A
  • AgRP neurons release GABA as well

- They are NPY/AgRP/GABA neurons

130
Q

What are anorexigens? What is an example?

A

“appetite suppressing”

CART

131
Q

What does CART stand for?

A

Cocaine and Amphetamine Regulated transcript

132
Q

Where are CART expression neurons located?

A

the Arcuate nucleus of the hypothalamus

133
Q

Would you expect the levels of CART (mRNA) to be higher or lower under food deprivation compared to baseline/sated state?

A

Food-deprivation decreases CART mRNA in the Arcuate Nucleus

134
Q

Describe CART expression in ob/ob.

A
  • Expression of CART mRNA (therefore the molecule CART) is not present in Ob mice
  • They are hungrier than WT
  • If there is no leptin (ob/ob mice), there is no CART in the Arcuate nucleus in the ob/ob
  • If there is no leptin (ob/ob mice), there is not a significant difference between the amount of CART in DMH
135
Q

Describe an experiment to test whether CART mRNA is regulated by circulating Leptin. (What were the controls? What was observed where?)

A

Injected ob/ob mice with leptin daily for 10 days (Re-normalizing leptin in ob/ob mice)
- Control 1: ob/ob mice received Saline
- Control 2: ob/ob mice were Pair-fed
• Feed mice the same amount of food that the ob/ob ate
• Controls for the possibility that eating doesn’t stimulate CART production, just eating less doesn’t stimulate CART production
- Administration of leptin stimulated CART production in the brain in ob/ob mice (in the ARC)
- Administration of leptin was also effective in decreasing body weight
- The pair fed are not losing as much weight because leptin impacts metabolic side
- Leptin administration to obese mice (ob/ob) stimulates CART mRNA expression
- Leptin treatment was injected by IP (systematically)

136
Q

Provide evidence for CART function in the brain.

A
  • CART peptide was administrated centrally (intracerebralventricularly ICV) to non-fasted rats
  • It is fast acting and will shut down eating within the first hour
137
Q

What happens if both NPY and CART are injected?

A

CART peptide ICV injections inhibited feeding in animals food-deprived for 24 hours and completely blocked NPY-induced feeding

138
Q

What brain substrates stimulate feeding?

A

Ghrelin, NPY, MCH, ORX

139
Q

How was CART’s endogenous central action as feeding behavior demonstrated?

A
  • Blocked endogenous (endogenous = naturally occurring) CART with antibody against CART (anti-CART)
  • CART antiserum administration increased night-time (when they are normally active) food intake
  • Impacting their normal feeding
  • If cart is blocked they are eating more because they are not as satiated
  • Conclusion: Administration of the antibody against CART increased feeding, indicating that CART is an endogenous inhibitor of food intake
  • This work provided evidence that CART is an endogenous inhibitor of food intake and that it is controlled by Leptin and Neuropeptide Y
140
Q

What does endogenous mean?

A

naturally occuring

141
Q

What is CART expressed with

A
  • CART is co-expressed with another anorexigenic peptide alpha-MSH
  • Alpha-MSH (Melanocyte-Stimulating Hormone)
142
Q

What family of peptides is alpha - MSH a part of?

A
  • Melanocortins are a family of peptides such as alpha MSH that are
  • Cleaved from pro-opiomelanocortin (POMC) precursor molecule
  • Being satiated and drug abuse are related through this reward part
143
Q

CART and alpha-MSH are classic _________ in the _______

A

Classic homeostatic (catabolic) signaling molecules in the brain

144
Q

What does alpha-MSH bind to?

A

MC4-R

Melanocortin 4 Receptor

145
Q

What two peptides bind to MC4- R?

A

o Alpha-MSH binds to MC4-R: (this is an agonist) this inhibits eating
o AGRP also binds to MC4-R: (this is an antagonist – binds and blocks action) this stimulates eating

146
Q

What is the primary function of the MC4 receptor?

A
  • Agonists for melanocortin receptor can induce weight loss by increasing energy expenditure and decreasing food intake
  • Targeted Disruption of the Melanocotin-4 Receptor Results in Obesity in Mice
  • The Primary function of the MC4-receptors is to inhibit feeding, since eliminating these receptors results in obesity
147
Q

How are NPY/AgRP and POMC/CART impacted by leptin?

A

o Leptin inhibits NPY/AGRP

o Leptin stimulates POMC/CART

148
Q

Where do NPY/AgRP and POMC/CART send their axons?

A

o Both send their axons to PVN and LHA/PFA

149
Q

What upregulates NPY/AgRP? Downregulates?

A
  • Ghrelin/ Food deprivation upregulates

- Leptin downregulates

150
Q

What upregulates POMC/CART? Downregulates?

A
  • Leptin upregulates

- Ghrelin/ Food deprivation down regulates

151
Q

Summarize MC4-R

A

o Alpha-MSH binds to MC4-R and inhibits eating

o AGRP binds to MC4-R and stimulates eating

152
Q

Hyperphagia is

A

Hyperphagia definition is - abnormally increased appetite for consumption of food frequently associated with injury to the hypothalamus.

Neurobiology of Eating (4 decks)

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