HMB200H1 Study Guide - Final Guide: Chronic Traumatic Encephalopathy, Sympathetic Nervous System, Brodmann Area 32
1. What brain structures are generally considered part of the limbic system? What
brain structures are considered part of the extended limbic system?
Hypothalamus, amygdala, anterior thalamus, hippocampus and prefrontal
cortex
Extended: septum, olfactory tubercle, nucleus accumbens, entorhinal
cortex, insular cortex, dorsolateral prefrontal cortex,
parahippocampal region and bed nucleus of stria terminalis
○
-
2. Name the major parts of the prefrontal cortex that were covered in class.
Dorsolateral prefrontal cortex, orbitofrontal cortex and anterior cingulate
cortex
-
3. What are the functions of the hypothalamus?
Hypothalamus is an important drive center for regulatory behavior and a
homeostatic regulator. (4 F's)
-
4. What is the hypothalamic-pituitary-adrenal (HPA) axis? Give all structures and
signaling compounds involved. Identify sources of negative feedback to the axis.
HPA axis involves the hypothalamus, pituitary gland and adrenal cortex.
-
Hypothalamus (CRF) - pituitary gland (ACTH) -> adrenal gland -> cortisol
(negative feedback)
-
5. What glands are associated with the hypothalamus? What hormones are
associated with hypothalamus-to-pituitary signaling?
ACTH- adrenal gland / TSH - thyroid gland / FSH & LH - gonads / prolactin -
mammary glands / GH -areas of growth
-
6. What receptors respond to glucocorticoids? Where are these receptors found?
Glucocorticoid receptors and mineralocorticoid receptors
Found in almost every tissue of the body
○
-
7. Explain (with examples) how lesion to the amygdala may influence behavior.
Lesion in amygdala will lead to alternations in fear and anxiety but effect
can vary.
Bilateral amygdaloid lesion seen in S.M. due to Urbach-Wiethe
Disease
○
Monkey: lesion in medial temporal lobe results in Kluver-Bucy
Syndrome, which involved docility, visual agnosia, compulsive eating
and hyper-sexuality.
○
-
8. Explain fear conditioning. Give examples of fear conditioning in animals and
humans. What is the role of the hippocampus and amygdala in fear conditioning?
Fearing conditioning involved the pairing of a non-conditioned fear
stimulus with a conditioned stimulus and results in a conditioned fear
response. This is seen in humans with phobia and aversion along with mice
in a foot shock experiment.
-
The hippocampus is involved in the memory while the amygdala is involved
in the fear conditioning.
-
9. Give the ‘Simple Fear Circuit’ that was reviewed in class. For any part of the
circuit covered in class, be able to explain its significance to fear and anxiety.
Sensory organ -> thalamus -> sensory cortex or amygdala(fast) ->
hippocampus or amygdala(fast). In amygdala, the lateral nucleus ultimately
leads to the central nucleus which has outputs to lateral hypothalamus,
central gray and bed nucleus of stria terminalis.
-
10.What brain circuits govern fear extinction in animals and humans?
In animals: prelimbic cortex (PL): initiation fear
Infralimbic cortex (IL): block fear
§
-
In human: area 32: initiate fear
Area 25: block fear
§
-
IL may block fear via disynaptic route. mPFC neurons activate ITC neurons
of amygdala. Then ITC neurons inhibit cells in central amygdaloid nucleus.
Due to reduced activity in central amygdaloid nucleus, fear cannot be
strongly expressed.
-
11.How is fear extinction affected in anxiety disorders?
Person is repeatedly exposed to anxiety triggering stimuli which leads to
declining anxiety response over time because there is no reinforcement.
-
12.What is chronic traumatic encephalopathy (CTE)? What is its relevance to mood
disorders?
CTE is repeated injuries in athletes. Symptom: depression and aggression
-
13.Give the main anatomic and physiologic features of depression.
Reduced hippocampus and orbitofrontal cortex
-
Enlarge lateral ventricle size
-
Disrupted brain activity
-
Decrease in serotonin, norepinphrine, GABA.
-
Increase in cytokines and cortisol
-
14.Explain the main theories of depression that were reviewed in class.
Monoamine hypothesis: reduced norepinephrine and serotonin in
depressed individuals leads to depression.
-
Neurogenesis hypothesis: neurogenesis may be reduced in depression.
-
Neuroendocrine hypothesis: higher corticotrophin releasing factor and
cortisol in depressed individuals
-
GABA and Neuroinflammation (increased cytokines) based theories
-
15.What is the monoamine hypothesis of depression? Give examples of cases in
which the predictions of the monoamine theory are not supported.
Monoamine hypothesis: depressed patients show reduced level of
monoamine neurotransmitters (norepinephrine and serotonin)
Ex. Jitteriness syndrome: antidepressants increase anxiety
○
Ex. In animal, transgenic knockout of serotoninergic genes (5-HTT)
leads to increase anxiety
○
-
16.What is neurogenesis? Where is it observed?
Neurogenesis is the production of new neurons in the brain. This is primary
seen in the hippocampus and along lateral ventricles
-
17.How are young, adultborn hippocampal neurons different from older,
developmentallygenerated neurons? Why might neurogenesis be significant for
mood disorders?
Young neurons are plays a role in stress resiliency leads to greater
resistance to stress-induced depression. They also have enhanced
excitability and plasticity relative to older neurons.
-
Neurogenesis is important for mood because enhanced hippocampal
neurogenesis is correlated with improved memory as well as reduced
anxiety
-
18.Explain stress-induced epigenetic modifications and their consequences.
Early childhood stress factors such as abuse are related to epigenetic
changes in glucocorticoid receptor genes in the hippocampus (specifically a
decrease in GR which may lead to inability to regulate mood). Creates a
vicious cycle as future stressors are exaggerated.
-
19.Explain how gene x environment interactions can increase the risk for
depression.
Expressing two short alleles for 5-HTTLPR leads to low serotonin
transporter expression. However, depression results more viciously when
those containing the short alleles undergo stress (environment)
-
20.Explain the role of GABAergic transmission in anxiety disorders.
Reductions in GABAergic transmission are implicated in anxiety (GABA
signaling is necessary in inhibiting behavior, therefore, reduction in GABA
can lead to increase in behaviors like anxiety) -> anxiogenic (increase
anxiety)
-
21.Differentiate learned and unlearned fears. Give examples!
Unlearned fear is innate, represent evolutionary adaptation. In animals,
exposure to substance TMT (waste product of foxes) causes innate fear. In
human, fear of heights and loud noises are examples.
-
Learned fear is formed through conditioning (foot shock paired with bell
makes bell a learned fear)
-
22.What is TMT? What does TMT do?
TMT is 2,5-dihydro-2,4,5-trimethylthiazoline (TMT), it's a waste product by
foxes. TMT makes the mouse freeze.
-
23.Identify the three main outputs of the Central Amygdaloid Nucleus that were
identified in the simple fear circuit.
Lateral hypothalamus, central gray, bed nucleus of stria terminalis
-
24.Explain the role of the lateral hypothalamus in different types of fear.
Lateral hypothalamus is involved in autonomic fear response to learned
fear (such as arterial pressure)
Lesion will only affect learned fear not unlearned feat
○
-
25.Explain the role of the central gray in different types of fear. What are the
functions of different subregions of the central gray?
Ventrolateral periaqueductal gray -> freezing responses via
Parasympathetic nervous system.
-
Dorsolateral periaqueductal gray -> fight or flight responses via
sympathetic nervous system
-
26.Explain the treatment of anxiety and depression.
Anxiety medications like benzodiazepines increase GABA receptor activity
-
Depression medications increase serotonin activity with SSRIs, SNRIs and
MAOi. As well as psychotherapy, wake therapy, deep brain stimulation etc.
TMS, ketamine etc.
-
Study notes Lec 6
Saturday, 3 March 2018
8:45 PM
1. What brain structures are generally considered part of the limbic system? What
brain structures are considered part of the extended limbic system?
Hypothalamus, amygdala, anterior thalamus, hippocampus and prefrontal
cortex
Extended: septum, olfactory tubercle, nucleus accumbens, entorhinal
cortex, insular cortex, dorsolateral prefrontal cortex,
parahippocampal region and bed nucleus of stria terminalis
○
-
2. Name the major parts of the prefrontal cortex that were covered in class.
Dorsolateral prefrontal cortex, orbitofrontal cortex and anterior cingulate
cortex
-
3. What are the functions of the hypothalamus?
Hypothalamus is an important drive center for regulatory behavior and a
homeostatic regulator. (4 F's)
-
4. What is the hypothalamic-pituitary-adrenal (HPA) axis? Give all structures and
signaling compounds involved. Identify sources of negative feedback to the axis.
HPA axis involves the hypothalamus, pituitary gland and adrenal cortex.
-
Hypothalamus (CRF) - pituitary gland (ACTH) -> adrenal gland -> cortisol
(negative feedback)
-
5. What glands are associated with the hypothalamus? What hormones are
associated with hypothalamus-to-pituitary signaling?
ACTH- adrenal gland / TSH - thyroid gland / FSH & LH - gonads / prolactin -
mammary glands / GH -areas of growth
-
6. What receptors respond to glucocorticoids? Where are these receptors found?
Glucocorticoid receptors and mineralocorticoid receptors
Found in almost every tissue of the body
○
-
7. Explain (with examples) how lesion to the amygdala may influence behavior.
Lesion in amygdala will lead to alternations in fear and anxiety but effect
can vary.
Bilateral amygdaloid lesion seen in S.M. due to Urbach-Wiethe
Disease
○
Monkey: lesion in medial temporal lobe results in Kluver-Bucy
Syndrome, which involved docility, visual agnosia, compulsive eating
and hyper-sexuality.
○
-
8. Explain fear conditioning. Give examples of fear conditioning in animals and
humans. What is the role of the hippocampus and amygdala in fear conditioning?
Fearing conditioning involved the pairing of a non-conditioned fear
stimulus with a conditioned stimulus and results in a conditioned fear
response. This is seen in humans with phobia and aversion along with mice
in a foot shock experiment.
-
The hippocampus is involved in the memory while the amygdala is involved
in the fear conditioning.
-
9. Give the ‘Simple Fear Circuit’ that was reviewed in class. For any part of the
circuit covered in class, be able to explain its significance to fear and anxiety.
Sensory organ -> thalamus -> sensory cortex or amygdala(fast) ->
hippocampus or amygdala(fast). In amygdala, the lateral nucleus ultimately
leads to the central nucleus which has outputs to lateral hypothalamus,
central gray and bed nucleus of stria terminalis.
-
10.What brain circuits govern fear extinction in animals and humans?
In animals: prelimbic cortex (PL): initiation fear
Infralimbic cortex (IL): block fear
§
-
In human: area 32: initiate fear
Area 25: block fear
§
-
IL may block fear via disynaptic route. mPFC neurons activate ITC neurons
of amygdala. Then ITC neurons inhibit cells in central amygdaloid nucleus.
Due to reduced activity in central amygdaloid nucleus, fear cannot be
strongly expressed.
-
11.How is fear extinction affected in anxiety disorders?
Person is repeatedly exposed to anxiety triggering stimuli which leads to
declining anxiety response over time because there is no reinforcement.
-
12.What is chronic traumatic encephalopathy (CTE)? What is its relevance to mood
disorders?
CTE is repeated injuries in athletes. Symptom: depression and aggression
-
13.Give the main anatomic and physiologic features of depression.
Reduced hippocampus and orbitofrontal cortex
-
Enlarge lateral ventricle size
-
Disrupted brain activity
-
Decrease in serotonin, norepinphrine, GABA.
-
Increase in cytokines and cortisol
-
14.Explain the main theories of depression that were reviewed in class.
Monoamine hypothesis: reduced norepinephrine and serotonin in
depressed individuals leads to depression.
-
Neurogenesis hypothesis: neurogenesis may be reduced in depression.
-
Neuroendocrine hypothesis: higher corticotrophin releasing factor and
cortisol in depressed individuals
-
GABA and Neuroinflammation (increased cytokines) based theories
-
15.What is the monoamine hypothesis of depression? Give examples of cases in
which the predictions of the monoamine theory are not supported.
Monoamine hypothesis: depressed patients show reduced level of
monoamine neurotransmitters (norepinephrine and serotonin)
Ex. Jitteriness syndrome: antidepressants increase anxiety
○
Ex. In animal, transgenic knockout of serotoninergic genes (5-HTT)
leads to increase anxiety
○
-
16.What is neurogenesis? Where is it observed?
Neurogenesis is the production of new neurons in the brain. This is primary
seen in the hippocampus and along lateral ventricles
-
17.How are young, adultborn hippocampal neurons different from older,
developmentallygenerated neurons? Why might neurogenesis be significant for
mood disorders?
Young neurons are plays a role in stress resiliency leads to greater
resistance to stress-induced depression. They also have enhanced
excitability and plasticity relative to older neurons.
-
Neurogenesis is important for mood because enhanced hippocampal
neurogenesis is correlated with improved memory as well as reduced
anxiety
-
18.Explain stress-induced epigenetic modifications and their consequences.
Early childhood stress factors such as abuse are related to epigenetic
changes in glucocorticoid receptor genes in the hippocampus (specifically a
decrease in GR which may lead to inability to regulate mood). Creates a
vicious cycle as future stressors are exaggerated.
-
19.Explain how gene x environment interactions can increase the risk for
depression.
Expressing two short alleles for 5-HTTLPR leads to low serotonin
transporter expression. However, depression results more viciously when
those containing the short alleles undergo stress (environment)
-
20.Explain the role of GABAergic transmission in anxiety disorders.
Reductions in GABAergic transmission are implicated in anxiety (GABA
signaling is necessary in inhibiting behavior, therefore, reduction in GABA
can lead to increase in behaviors like anxiety) -> anxiogenic (increase
anxiety)
-
21.Differentiate learned and unlearned fears. Give examples!
Unlearned fear is innate, represent evolutionary adaptation. In animals,
exposure to substance TMT (waste product of foxes) causes innate fear. In
human, fear of heights and loud noises are examples.
-
Learned fear is formed through conditioning (foot shock paired with bell
makes bell a learned fear)
-
22.What is TMT? What does TMT do?
TMT is 2,5-dihydro-2,4,5-trimethylthiazoline (TMT), it's a waste product by
foxes. TMT makes the mouse freeze.
-
23.Identify the three main outputs of the Central Amygdaloid Nucleus that were
identified in the simple fear circuit.
Lateral hypothalamus, central gray, bed nucleus of stria terminalis
-
24.Explain the role of the lateral hypothalamus in different types of fear.
Lateral hypothalamus is involved in autonomic fear response to learned
fear (such as arterial pressure)
Lesion will only affect learned fear not unlearned feat
○
-
25.Explain the role of the central gray in different types of fear. What are the
functions of different subregions of the central gray?
Ventrolateral periaqueductal gray -> freezing responses via
Parasympathetic nervous system.
-
Dorsolateral periaqueductal gray -> fight or flight responses via
sympathetic nervous system
-
26.Explain the treatment of anxiety and depression.
Anxiety medications like benzodiazepines increase GABA receptor activity
-
Depression medications increase serotonin activity with SSRIs, SNRIs and
MAOi. As well as psychotherapy, wake therapy, deep brain stimulation etc.
TMS, ketamine etc.
-
Study notes Lec 6
Saturday, 3 March 2018 8:45 PM
Document Summary
Hypothalamus, amygdala, anterior thalamus, hippocampus and prefrontal cortex. Extended: septum, olfactory tubercle, nucleus accumbens, entorhinal cortex, insular cortex, dorsolateral prefrontal cortex, parahippocampal region and bed nucleus of stria terminalis: name the major parts of the prefrontal cortex that were covered in class. Identify sources of negative feedback to the axis. Hpa axis involves the hypothalamus, pituitary gland and adrenal cortex. Found in almost every tissue of the body: explain (with examples) how lesion to the amygdala may influence behavior. Lesion in amygdala will lead to alternations in fear and anxiety but effect can vary. Bilateral amygdaloid lesion seen in s. m. due to urbach-wiethe. Monkey: lesion in medial temporal lobe results in kluver-bucy. Syndrome, which involved docility, visual agnosia, compulsive eating and hyper-sexuality: explain fear conditioning. Give examples of fear conditioning in animals and humans. Fearing conditioning involved the pairing of a non-conditioned fear stimulus with a conditioned stimulus and results in a conditioned fear response.
