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PSY 760 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What is adult neurogenesis?

A
  • the ability of the adult brain to generate new neurons
  • previously thought that neurogenesis only occurred in the developing brain
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2
Q

What are the brain areas we know experience adult neurogenesis?

A
  • primarily in the hippocampus
  • also in the olfactory bulb and caudate nucleus
  • some evidence that it occurs in the spinal cord
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3
Q

How can we identify neurogenesis?

A
  • We can identify neurogenesis by identifying new neurons using BrdU, a marker or stain that identifies dividing cells (aka newly born neurons).
  • When injected, BrdU incorporates itself into the DNA of these dividing cells that have not already matured/differentiated.
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4
Q

Most evidence of adult neurogenesis has been found in ______ studies.

A

animal

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5
Q

Explain the first human adult neurogenesis study and what it showed us.

A
  • in humans in cancer patients who were given BrdU to monitor tumor growth.
  • After death, their brains were examined, and the hippocampus showed presence of BrdU positive neurons.
  • Because the BrdU was administered in adulthood, it could be determined that these were newly born neurons in the hippocampus.
  • This tells us that the adult human brain has some regenerative potential.
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6
Q

What promotes neurogenesis in mice?

A
  • In mice, an enriched environment promotes neurogenesis.
  • Mice with stimulation, toys, and a running wheel, large cage, cage mates had about 60% more neurons in the hippocampus than genetically identical mice without enriched environment.
  • It is assumed similar factors promote neurogenesis in humans.
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7
Q

Explain some neurogenesis follow-up studies in mice.

A
  • Follow up studies included learner condition- water maze training; swimmer condition- just swimming; running condition- access to running wheel only.
  • Measured BrdU cells one day after injection and one month after – look at initial proliferation and survival of the cells. Running wheel alone shows increase in proliferation and survival of neurons in hippocampus.
  • Exercise drives enhanced neurogenesis in adult brain.
  • In some studies, learning tasks that engage the hippocampus also promote neurogenesis (though this study did not find that).
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8
Q

What are mechanisms that drive exercise-induced neurogenesis?

A
  • exercise increases levels of growth factors in the body and the brain, which support the survival of existing and development of new neurons.
  • Exercise also slows the progression of neurogenerative diseases.
  • Exercise also increases the production of new blood vessels, which brings more oxygen and nutrients to cells, so that may be another mechanism through which exercise has beneficial effects on supporting and generating neurons.
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9
Q

What inhibits neurogenesis?

A
  • Stress inhibits neurogenesis.
  • This is thought to be mediated by elevated levels of cortisol.
  • This inhibits the production of stem cells in the hippocampus.
  • In addition to inhibiting neurogenesis, will also cause degeneration, so kill existing neurons.
  • Glucocorticoid receptors in the hippocampus, when chronically stimulated by cortisol, kill hippocampal neurons.
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10
Q

What are stem cells?

A
  • Ability to multiply or make copies of themselves (they are mitotic or self renewing)
  • Adults have limited capacity to regenerate because we do not retain pluripotent stem cells. We DO retain multipotent stem cells, such as skin and blood cells.
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11
Q

Explain pluripotent vs. multipotent stem cells.

A
  • A week after conception, we all possess pluripotent stem cells, which are able to become any cell type in the body. They are unspecialized cells.
  • Later in embryonic development (2-3 weeks after conception), stem cells lose pluripotent capacity and become multipotent.
  • They can still differentiate into multiple cell types, but they are limited to a tissue family.
  • This “specialization” process continues until there are fully differentiated cells locked into “identities”
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12
Q

What is the principle of induced pluripotent stem cells?

A
  • Taking cells that have differentiated from an adult and reprogramming them back into stem cells that have the potential to differentiate into any type of cell (so they are pluripotent).
  • Done for the purpose of treating disease. Like “turning back the cellular clock”
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13
Q

What is the method of creating induced pluripotent stem cells (IPSC)?

A
  1. Harvest a sample of mature fully differentiated skin cells (easy to do with skin biopsy)
  2. Insert the key stem-cell associated genes into a retrovirus and then introduce the retrovirus into the skin cells
  3. the retrovirus will deliver the stem-cell associated genes to the nucleus of the mature skin cells, which initiates re-programming them to pluripotent cells (“induced” pluripotent stem cells)
  4. Then differentiate the IPSCs into healthy cells of a particular type to treat the disease and introduce those back to the organism (in the case of the cell therapy application) OR differentiate the IPSCs back into the diseased cell type to study the diseased cells in vitro (in the case of disease modeling)
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14
Q

What is sickle cell anemia?

A
  • Sickle cell anemia is a disease that’s caused by a single genetic mutation of red blood cells, making it easy to create a model for.
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15
Q

How can you use IPSCs to treat sickle cell anemia?

A
  • We can reprogram skin cells into IPSCs by introducing them with stem cell-associated genes.
  • Once you generate IPSCs from skin cells, then you differentiate them into healthy blood stem cells, and inject them into the mouse to treat the disease.
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16
Q

What is disease modeling (in the context of IPSCs)?

A
  • Disease modeling is a more basic science application of IPSCs.
  • It is difficult to study degenerative diseases because we can’t obtain brain tissue from living patients to study the diseased cells.
  • Now you can look at the structural characteristics of these cells, change over time, and can test treatments on these cells.
  • The cells are out of their normal environment, but they do still exhibit characteristics of the disease
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17
Q

How would you use IPSCs for disease modeling for patients with ALS? Parkinson’s disease?

A
  • we can take skin cells of a patient with a disease, such as ALS, and convert them into IPSCs, then you can differentiate them back into the type of cell that is afflicted with the disease.
  • In ALS: differentiate into motor neurons.
  • In Parkinson’s: differentiate into dopamine cells.
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18
Q

What are the advantages of using IPSCs in disease modeling?

A
  • using cells from an individual to treat that individual, so you can avoid issues of rejection
  • Ability to model and study disease processes
  • Don’t need embryonic tissue, which is a controversial matter.
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19
Q

What are the disadvantages of using IPSCs for disease modeling?

A
  • We still need retroviruses, which can incorporate themselves into DNA.
  • We don’t know if IPSCs are as good as true embryonic cells/if they retain memory of the type of cell they were previously
  • IPSCs may create ethical issues, such as custom babies, the fountain of youth.
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20
Q

What is the current status of the field in reference to using IPSCs?

A
  • IPSCs are already being used to generate multiple types of tissue and in disease modeling
  • It’s estimated that we will be able to use IPSCs in humans for cell therapy within 10-15 years.
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21
Q

Explain what role the amygdala has in aggression.

A
  • Stimulating the amygdala induces aggressive behavior.
  • Lesions/tumors of the amygdala can result in changes in aggressive behavior.
  • Individuals with aggressive personality disorders (e.g. BPD) show heightened amygdala activity. “Bottom up drive”
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22
Q

Explain the role of the prefrontal cortex in aggression.

A
  • The prefrontal cortex is involved in impulse control and decision making.
  • Damage to the prefrontal cortex or reduced activity is associated with aggressive bx.
  • Lack of inhibition of emotion. “Top down breaks”
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23
Q

What is a neurotransmitter system associated with aggression?

A
  • Serotonin (5-HT)
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24
Q

How is the 5-HT neurotransmitter system related to aggression?

A
  • Aggressive behavior is associated with low levels of serotonin
  • Animals and humans that are most aggressive have low levels of serotonin metabolites in their cerebral spinal fluid.
  • There are serotonergic projections that go to the prefrontal cortex, loss of input from these projections impairs its ability to regulate the amygdala
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25
Q

How does alcohol addiction induce synaptic effects?

A
  • Alcohol has biphasic effects: it produces a stimulatory effect at low levels of blood alcohol that is associated with an increase in dopamine (stimulates dopamine pathways) pleasurable or euphoric effects
  • …then as blood alcohol levels rise, it has GABAergic (potentiates activity of the GABAa receptor-coupled chloride channel, increases postsynaptic inhibition), depressive effects…sedation, motor incoordination
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26
Q

Alcohol and nicotine together have a(n) ______ effect on the dopamine system, which helps to explain why they are highly co-abused.

A

additive

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27
Q

What are the synaptic effects of nicotine addiction?

A
  • Nicotine binds to nicotinic acetylcholine receptors (ACh receptor agonist).
  • Part of it’s addictive property is due to binding to nicotinic receptors on dopamine neurons in the VTA, leading to increased dopamine in the nucleus accumbens.
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28
Q

What are the synaptic effects in methamphetamine addiction?

A
  • Highly reinforcing/addictive because they increase dopamine in multiple ways
    • Blocks dopamine receptors, leaving more in synapse
    • Cause dopamine vesicles to release dopamine into the cytosol, so there is more available to be released
    • Act as an alternative target for MAO, so less MAO that’s breaking dopamine down, so more dopamine is released
  • This is a trifecta that potently increases dopamine levels
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29
Q

How does exercise influence authophagy?

A
  • Autophagy is the mechanism by which exercise improves brain function.
  • process by which cells degrade some of their own components that accumulate as a product of metabolism – it’s like cleaning house.
  • thought to mediate the beneficial effects of exercise in protecting against diabetes, cancer, neurodegenerative diseases – all of which are diseases from cells not functioning properly.
  • Failure of autophagy contributes to accumulation of cell damage and aging.
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30
Q

How does exercise influence DNA protection mechanisms?

A
  • Exercise has benefits at the level of the chromosomes themselves.
  • There is an association between exercise and the integrity of telomeres, which are nucleotide caps on the end of chromosomes that help protect the DNA within the chromosome.
  • Damage can cause cancer and gene mutations that can be passed to offspring.
  • Exercise helps maintain the length of telomeres.
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31
Q

What is leptin?

A
  • Leptin is released by fat cells,
  • it functions to maintain body fat levels.
  • When there is too much fat tissue, leptin is secreted to decrease appetite. It is a satiety signal.
  • When fat tissue is low, leptin is low, stimulates appetite.
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32
Q

What is ghrelin?

A
  • Ghrelin is released by the stomach and regulates feeding behavior.
  • It increases appetite, is a hunger signal.
  • Levels rise when fasting and drop after eating.
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33
Q

What are the neurons that leptin acts on?

A
  • POMC-CART neurons inhibit appetite
34
Q

What are the neurons that ghrelin acts on?

A
  • NPY/AgRP neurons stimulate appetite
35
Q

What happens during the hypothalamic regulation of appetite?

A
  • Neurons in the arcuate nucleus monitor levels of hormones released from the body (e.g. from fat cells, from the gut).
  • These hormones inform the hypothalamus about the body’s energy state/work to maintain energy homeostasis.
36
Q

What are the stages of sleep?

A
  • Non-REM
    • Made up of four stages of sleep
      • Stages 1 and 2 are lighter stages
      • Stages 3 and.4 are deeper stages, delta waves
    • Slowing of the heart rate and respiration, muscles relaxed, cognitive state fairly inactive
  • REM
37
Q

What is REM?

A
  • Rapid eye movements intermittently, active EEG pattern that resembles awake brain.
  • Visual cortex is very active.
  • People awoken from REM report vivid dreams.
  • Muscles in the body are flaccid – pons inhibits motor neurons in the spinal cord.
  • Also known as paradoxical sleep.
  • happens in stage 4
38
Q

What are some consequences of sleep deprivation?

A
  • Sleepiness
  • Even mild sleep deprivation alters levels of appetite regulating hormones – it increases ghrelin levels and suppresses leptin levels, which together stimulate appetite.
  • Mood deterioration – depression
  • Cognitive impairment – LTP inhibition in the hippocampus, detrimental effects on memory
  • Changes in response to emotional stimuli. Amplified amygdala response, decrease in connectivity between amygdala and prefrontal cortex. Inhibitory function of prefrontal cortex is impaired, produces a hyperlimbic response.
39
Q

Stress mobilizes the body to respond to a _____.

A

threat

40
Q

How does stress impact the autonomic nervous system?

A
  • Release of norepinephrine from sympathetic fibers onto effector organs, and then produces an increase in heart rate, blood pressure, oxygen uptake
  • Release of epinephrine/adrenaline and norepinephrine from adrenal medulla into the bloodstream amplifies the sympathetic response on target organs
  • The effect is increased heart rate, blood pressure, dilated bronchi, glucose release (for energy), and inhibition of digestive function
41
Q

Stress activates the ________ branch of the autonomic nervous system.

A

Stress activates the sympathetic branch of the autonomic nervous system

42
Q

Stress activates a hormonal cascade as a result of a stressor in the ___________ axis

A

Hypothalamic-Pituitary-Adrenal (HPA)

43
Q

How does stress influence the HPA axis?

A
  1. Hypothalamus secretes corticotropin releasing hormone (CRH)
  2. CRH causes pituitary gland to secrete Adrenocorticotropic hormone (ACTH)
  3. ACTH causes the adrenal cortex to secrete cortisol
  4. cortisol increases glucose metabolism and suppresses immune function
44
Q

What are some adaptive responses to short-term stress?

A
  • It increases cardiovascular tone, mobilization of energy
  • it suppresses digestion, growth, reproduction, immunity/inflammatory response
  • leads to altered cognition and sensory thresholds
45
Q

What are some damaging consequences of long-term stress?

A
  • The stress system wasn’t designed to be chronically activated.
  • constantly high levels of cortisol and epinephrine that can cause damage to blood vessels, ulcers, impairment of immune function.
  • High levels of cortisol will kill brain cells in the hippocampus.
  • It leads to fatigue, hypertension, anxiety, depression, accelerated neural degeneration.
46
Q

Define social neuroscience.

A
  • Definition: interdisciplinary field devoted to understanding how biological systems are related to social processes and behavior, using biological concepts to inform/refine theories of social behavior
  • Brain mechanisms mediate social processes like social cognition, empathy, learning social norms, social comparisons
  • fMRI is really useful in these studies to understand patterns of activation
47
Q

What are some examples of research focus in social neuroscience?

A
  • Social cognition, norms, social comparison, empathy, stereotyping, emotions, etc.
  • Amygdala processes social threat
  • Reward related striatal regions respond to social reward
  • Areas of the brain, such as the dorsal anterior cingulate cortex, that activate during social pain are the same as areas that activate during physical pain
48
Q

What are some examples of social neuroscience and health research topics?

A
  • Threats to social connections elicit a similar physiological response as threats to survival
    • Activation of the sympathetic nervous system, activation of the HPA
    • Social connectedness protects against stress, while social disconnectedness is a risk factor for disease and mental illness
49
Q

What are the steps of nervous system development?

A
  1. Begins at 18 days of gestation, cells of ectoderm start proliferating to form neural plate
  2. At 22 days, neural plate folded in to form neural groove
  3. Central cavity in neural tube will become ventricular system
  4. Neurogenesis occurs at the ventricular zone of neural tube (inside border) and neurons move outward
  5. Neurogenesis at the head end (anterior) will develop into the forebrain, midbrain, hindbrain (divisions of the brain)
50
Q

Explain what happens in the stages of nervous system development?

A
  • New neurons formed and start moving outward (neurogenesis), most neurons generated at 3-5 months gestation – critical period
    • Neurons that migrate farthest form the cerebral cortex; neurons that don’t migrate far form the inner nuclei around the ventricles (like basal ganglia)
  • Cells differentiate into different cells types, controlled by gene expression
  • Axons and dendrites start to form synaptic connections; critical period for synaptogenesis is about 3rd trimester to 2 years of age. So this begins prenatally and continues after birth
  • A large number of neurons and synapses that were originally generated die or are lost
  • some synaptic rearrangement or remodeling occurs “fine tuning of the system.” Has to do with which neurons are active. So synaptic connects initially established based on location, but precision is determined by neural activity
51
Q

What is Spina bifida ?

A
  • occurs when the caudal/posterior end of the neural tube fails to close.
  • It is possible to surgically correct this depending on the severity, and can be prevented by taking folic acid supplements prior to conception
52
Q

What is Anencephaly?

A
  • very serious and occurs when the rostral end of the neural tube fails to close.
  • The brain fails to develop adequately, and this is a condition that’s not compatible with life
53
Q

Define epigenetics.

A
  • Epigenetics has to do with how the environment regulates expression of the genes we inherit.
  • This occurs even in identical twins.
  • These are non-genetic facts that cause an organism’s genes to be expressed differently.
  • Modifications to gene expression are regulated by specific chemical marks or tags that control the transcription of genes.
54
Q

What are some mechanisms that contribute to epigentics?

A
  1. DNA methylation
  2. Histone Modification
  3. Maternal Behavior
55
Q

Define DNA methylation.

A
  • It refers to the addition of methyl groups directly onto the DNA itself, which results in gene silencing/turns genes off.
  • This is a normal part of development in the nervous system and it determines differentiation of cells.
56
Q

Define histone modification.

A
  • refers to the modification of histone proteins associated with DNA.
  • Tails of histone proteins extend outside of the nucleosome. When certain enzymes bind to these tails, it can loosen or tighten the structure of the chromatin, which changes the accessibility of genes to transcription factors.
  • This is an indirect mechanism. Results in increased or decreased transcription of gene depending on which types of enzymes are bound.
57
Q
  • Explain the epigenetic effects of maternal behavior on glucocorticoid receptor expression
A
  • Offspring of high licking/grooming moms (a lot of maternal behavior) have higher density of glucocorticoid receptors in the hippocampus, leading to more efficient negative feedback function of the HPA axis, making them more resilient to stress.
  • Pups of low licking/grooming moms have fewer glucocorticoid receptors in the hippocampus and show increased stress response.
58
Q

How does depression impact brain changes?

A
  • Reduction in hippocampal volume, which is likely related to elevated levels of cortisol
  • High concentration of glucocorticoid receptors in the hippocampus, which is bad when cortisol is chronically bound to these receptors – leads to neuronal damage
  • Hyperactivity of the amygdala and reduction of prefrontal cortical activity, so disrupted connectivity in structures related to cognitive function and emotion
59
Q

What are some available treatments for depression?

A
  • Cognitive therapy
    • Imaging studies show that individuals successfully treated with cognitive therapy show increased activity in the prefrontal cortex and decreased activity in the amygdala, so there is greater normalization of that circuit
    • Psychotherapy, social support, exercise, and sleep all have direct effects on the brain, and we are just starting to understand the mechanisms behind these nondrug therapies
60
Q

How is anxiety related to depression?

A
  • high comorbidity with depression, and similar brain abnormalities show that anxiety and depression are related disorders.
61
Q

How does anxiety impact brain areas?

A
  • Hyperactivity of the amygdala
  • Deficits in prefrontal cortical functioning
  • Hyperactivity of the sympathetic nervous system (stress response is always on)
62
Q

What are some treatments for anxiety?

A
  • Overlap with treatments for depression
  • SSRIs increase serotonin levels and help maintain normal functioning of the prefrontal cortex
  • Anxiolytics, such as benzodiazepines act by facilitating GABA’s inhibitory effects, so there is an immediate reduction in anxiety, but they can produce dependence
  • Beta-blockers act by beta adrenergic receptors, so they diminish excessive physiological arousal by reducing activity of the sympathetic system
63
Q

What is Alzheimer’s disease?

A
  • Type of dementia characterized by cognitive deficits, including memory loss and disorientation.
    • Progressive memory loss, loss of executive function. Short term memory loss first, and eventually long-term memory loss, confusion
  • Incidence is increasing – number one neurogenerative disease in this country
64
Q

What structural brain changes occur within Alzheimer’s disease?

A
  • Widespread loss of neurons in several brain areas: hippocampus, entorhinal cortex (provides input to hippocampus), nucleus basalis (have projections to cortex)
  • As disease progresses, extensive loss of neurons in the cortex
65
Q

What cellular abnormalities occur within Alzheimer’s disease?

A
  • Presence of amyloid plaques: buildup of B-amyloid in frontal and tempoparietal cortex that interferes with synaptic function
  • Presence of neurofibrillary tangles within specific neurons: twisted strands of neurofilaments
66
Q

What are some risk factors of Alzheimer’s disease?

A
  • Inheritance of E4/E4 alleles, which are normally involved in the breakdown of B-amyloid
  • Head injury
  • High fat diet, obesity
  • Hypertension, diabetes
  • Smoking
  • Mild cognitive impairment
67
Q

What are some protective or factors that decrease risk for Alzheimer’s disease?

A
  • Inheritance of E2/E2 alleles
  • Maintaining normal weight
  • Omega-3 fats
  • Exercise
  • Antioxidant rich diet
  • Continuing mental challenge
68
Q

What is BDNF?

A
  • brain-derived-neurotrophic-factor
  • supports already existing neurons
  • increase production of new neurons
  • increases differentiation of new neurons
69
Q

When is genotypic sex (XX or XY) determined?

A

conception

70
Q

How do sex chromosomes determine sex?

A
  • Sex chromosomes determine sex of initially indifferent gonads
  • SRY gene on Y chromosome -> gonads produce Sry protein and develop into testes
  • absence of Sry protein -> ovaries develop
71
Q

How do gonadal hormones influence sexual differentiation?

A
  • Gonadal hormones drive sexual differentiation of the body (genitalia) AND brain
    • presence of testicular hormones -> masculinization
    • absence of testicular hormones -> feminization
72
Q

What are some structural differences in male and female brains?

A
  • Determined before birth (in humans)
  • Gonadal hormones direct sexual differentiation of initially equipotent brain
  • Hypothalamic nuclei display sexual dimorphism
  • Hormonal organization of brain determines sexual behavior
73
Q

What is congenital adrenal hyperplasia (CAH)?

A
  • Genotypic XX females exposed to high levels of adrenal androgens before birth
  • Consequences: intersex genitalia and masculinization of brain
  • More likely to report homosexual orientation than other women
74
Q

What is androgen insensitivity syndrome (AIS)?

A
  • Genotypic XY male with dysfunctional androgen receptors that don’t respond to androgen hormones
  • Consequences: external genitalia remain female and brain does not masculinize
  • Behave like females
75
Q

What is multiple sclerosis (MS)?

A
  • De-myelinating disease affecting the central nervous system
    • oligodendrocytes
76
Q

What are some key neuropathological features of MS?

A
  • Inflammation
  • Demyelination
  • Axonal degeneration
  • Myelin is destroyed, results in “sclerosis” (scar tissue)
  • Nerve signals are slowed, distorted or interrupted
77
Q

Multiple sclerosis is believed to be an _________ disease

A

autoimmune

78
Q

What are some commonly affected brain areas of MS?

A
  • cerebrum
  • optic nerve
  • cerebellum
  • brain stem
  • spinal cord
79
Q

What are some MS symptoms?

A
  • Motor (muscle weakness, spasms, poor balance, incoordination)
  • Sensory (numbness or tingling, blurred or double vision)
  • Symptoms generally reflect heaviest areas of demyelination
80
Q

What are induced pluripotent stem cells (IPSCs)?

A
  • mature body cells that have been made to change their identities and revert to an embryolike state without the help of eggs or embryos
81
Q

What is pluripotency?

A

its ability to give rise to any type of tissue in the organism’s body

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