HMB200H1 Study Guide - Final Guide: Executive Functions, Olivary Body, Medial Geniculate Nucleus
1. What is energy homeostasis? Explain energy expenditure.
Energy homeostasis is the biological response by which the body maintain
body fat stores by balancing energy intake w/ energy expenditure over time
-
Energy expenditure involved burning calories but doesn’t necessarily mean
being active
-
2. Give short-term and long-term signals regulating food intake. Where do signals
regulating food intake come from?
Short term: Cholecystokinin (CCK) and Glucagon-like peptide 1 (GLP1) (from
gut)
-
Long term: leptin and insulin (from adipose tissue)
-
3. What is leptin? How does leptin signaling work? Give some major targets for
leptin in the brain. What are the effects of leptin on food intake?
Leptin is secreted from the adipose tissue. Leptin administered in the brain
reduces food intake and weight. Leptin targets on arcuate nucleus,
ventromedial nucleus, lateral hypothalamus and nucleus of solitary tract.
-
4. How does the arcuate nucleus regulate feeding behavior? Explain the specific
neurons involved as well as the receptors and transmitters they express.
Arcuate nucleus regulates feeding via AGRP neurons and POMC neurons
AGRP neurons: increase food intake; activated by ghrelin, it inhibit
MCR4 (melanocyte receptor type 4) in paraventricular hypothalamus
which promote food intake - orexigenic
○
POMC neurons: decrease food intake; activated by leptin; release
alpha-melanocyte stimulating hormone (a-MSH) which inhibits food
intake by activating MCR4. - anorexigneic
○
-
5. How does leptin signaling change in obesity?
In obesity, there is higher level of leptin, however, the leptin signaling is less
effective in obesity due to inhibition of pSTAT3 pathway in arcuate nucleus,
which results in leptin resistance.
-
6. Explain how food is a multi-sensory experience. How might our senses change
when we are hungry? When we are satiated?
Food intake involves sight, smell, vision, taste and texture. These senses all
affect our tendency to want food by regulating drive in the orbitofrontal
cortex
-
7. How do orbitofrontal lesions affect food intake?
Orbitofrontal cortex lesions result in inability to coordinate the
multisensory food (altered sense of smell) experience and decreases
incentive learning.
-
8. What role do cannabinoids play in the olfactory system in mice? How do
cannabinoid receptors regulate food intake in mice?
Cannabinoids (anandamide and THC) increase olfactory perception and
food intake
Because cannabinoid receptor type 1 (CB1) receptors are found in
part of the olfactory system
○
-
9. Contrast the role of the ventromedial hypothalamus and lateral hypothalamus in
feeding. Give the lateral hypothalamus circuit that regulates food intake (you can
omit the NAc/VTA)
Ventromedial hypothalamus - decrease food intake
-
Lateral hypothalamus -regulates neurons in the reward circuit &
parabrachial nucleus (PBN) which promotes food intake
And receives input from the nucleus accumbens (inhibitory), BNST
(inhibitory) and involves a circulatory to stop VTA mediated inhibition
of LH
○
-
10.Explain how obesity may be the result of an abnormally functioning neural
circuit.
Increased food salience (nucleus accumbens; reward circuit) & decreased
self-regulation (PFC)
-
11.Explain the idea of food addiction.
Drugs and food act on reward circuit. Food has many drug-like effects in
terms of reward and feedback
-
12.What gene mutations are related to obesity?
Leptin mutation
-
MCR4 mutation
Likely a combination of interacting gene mutations with the
environment
○
-
13.Give traits associated with anorexia.
Negative emotion
-
Perfectionism
-
Increase cognitive control
-
Drive for thinness
-
Increase interoceptive awareness
-
Obsessive compulsive personality
-
14.How is the regulation of food intake different in anorexia?
Food intake reward is reduced in anorexia. There is increased anxiety
towards food and increased cognitive control
-
Poor compensatory response to caloric restriction
-
15.What are the neural correlates of anorexia?
Decrease activation of insula and anteroventral striatum alter responsive to
sweet taste.
-
Decrease mPFC, fusiform gyrus and parietal cortex in AN which results in
inaccurate body representation.
-
Reduced gray matter and increase ventricular size and sulci depth
-
16.What gene mutations are related to anorexia? How might these gene mutations
interact with the environment?
Genes for 5-HTT and D2/D3 are correlated with anorexia. D2 mutations
results in higher inhibitory responses o reward regions. 5-HTT (serotonin
transporter) mutations results in mood and feeding dysregulation. These
genes are linked with environmental factors such as model or actress
occupation will generate a stronger force in development of anorexia
-
17.What is the neural basis of our sensation of hearing?
Movements of basilar membrane bends cilia in contact with the overlaying
tectorial membrane. This bending generates neural activity in the hair cells
from which the cilia extend.
-
18.Give the auditory pathway.
Auditory path involves cochlear nucleus synapse to olivary complex ->
inferior colliculus -> medial geniculate nucleus -> auditory cortex
-
19.What brain areas are involved in speech, reading and hearing?
Speech: Broca's Area, motor cortex
-
Reading: Wernicke's Area (Planum Temporale), Angular Gyrus, Motor
Cortex, Visual Cortex
-
Hearing: auditory cortex, angular gyrus, Wernicke's area (Planum
Temporale)
-
20.Explain how damage or abnormal brain organization can lead to language
disorders.
Damage to
Broca's Area/Motor cortex - can't speak properly
○
Wernicke's Area/ Angular Gyrus - can’t comprehend language
○
-
21.What is the evidence for the lateralization of speech?
Lateralization of speech is evident through lesion studies, Wada test, split
brain preparation and electrostimulation studies.
-
22.What changes do we see in the bilingual brain?
Increase gray matter density in the left inferior parietal cortex
-
Study note 10
Friday, April 6, 2018
9:29 PM
Document Summary
Energy homeostasis is the biological response by which the body maintain body fat stores by balancing energy intake w/ energy expenditure over time. Energy expenditure involved burning calories but doesn"t necessarily mean being active: give short-term and long-term signals regulating food intake. Short term: cholecystokinin (cck) and glucagon-like peptide 1 (glp1) (from gut) Give some major targets for leptin in the brain. Leptin administered in the brain reduces food intake and weight. Explain the specific neurons involved as well as the receptors and transmitters they express. Arcuate nucleus regulates feeding via agrp neurons and pomc neurons. Agrp neurons: increase food intake; activated by ghrelin, it inhibit. Mcr4 (melanocyte receptor type 4) in paraventricular hypothalamus which promote food intake - orexigenic. Pomc neurons: decrease food intake; activated by leptin; release alpha- melanocyte stimulating hormone (a-msh) which inhibits food intake by activating mcr4.
