Week 1-2 Flashcards

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1
Q

<p>What areneurons and synapses</p>

A

<p>Neurons</p>

<ul> <li>Cells in the nervous system</li> <li>Electrical signals (“action potentials”) are transmitted along the axons.</li></ul>

<p>Synapses</p>

<ul> <li>Where neurons meet</li> <li>Chemical signals (“neurotransmitters”) transmitted between neurons</li></ul>

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2
Q

<p>How do neurons in the CNS, PNS, ENS communicate?</p>

<p>What is the function?</p>

<ul></ul>

A

<ul> <li>All neurons in the CNS, PNS and ENS communicate through chemical signals (Neurotransmitters &amp; neuromodulators). <ul> <li>Chemicals modulate neural activity and other functions like synaptic plasticity</li> <li>Without these chemical signals, the action of one neuron would not influence any other neuron in the nervous system (no brain integration and no useful brain function).</li> </ul> </li></ul>

<p></p>

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3
Q

<p>How many neurons are there in the CNS</p>

A

<p>100 billion neurons in the CNS</p>

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4
Q

<p>What are hormones</p>

A

<p>Signaling molecules produced by glands and transported through the blood to regulate physiology (muscles, neurons etc) and behaviour.</p>

<p>Also directly modulate NT levels and function (<em>sex hormones</em>)</p>

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5
Q

<p>4 differencses between NT and hormones</p>

A

<p><u>NT</u></p>

<ul> <li>Nervous system</li> <li>Tramission between neurons (Across synapse)</li> <li>Target cells can be specific neurons or other cells</li> <li>Generally fast (ms), though sustained NT release can lead to more sustained changes in brain</li></ul>

<p><u>Hormones</u></p>

<ul> <li>Endocrine system</li> <li>Travel by blood</li> <li>Target cells can be some distance from endocrine gland</li> <li>Much slower, ranging from few seconds to days</li> <li>Also directly modulate NT levels and function</li></ul>

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6
Q

<p>What is the blood-brain barrier? (Location, Function)</p>

A

<p><u>Location</u></p>

<ul> <li>Exists within 600km of blood vessels in the CNS</li></ul>

<p><u>Function</u></p>

<ul> <li>Prevents many substances from passing betweenblood andbrain.</li> <li>Many drugs, natural chemicals and foreign infections cant pass through (but is not perfect – small amounts of many things still get through).</li> <li>However, multiple other avenues for controlled passage between blood and nervous system exist.</li></ul>

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7
Q

<p>What is the PNS (Location, Function)</p>

A

<p><u>Location</u></p>

<ul> <li>Nerves and ganglia outside of the brain and spinal cord</li></ul>

<p><u>Function</u></p>

<ul> <li>Receives sensory information about body position, pain and temperature, etc</li> <li>Sends messages from the brain to control muscles and movement.</li></ul>

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8
Q

<p>What is the ENS (Locaton - 1, how many neurons - 1 , properties - 6, function - 3)</p>

A

<p><u>Location</u></p>

<ul> <li>ENS (2nd brain) is <u>part of</u> the PNS</li></ul>

<p><u>How many neurons</u></p>

<ul> <li>Contains 100million neurons</li></ul>

<ul></ul>

<p><u>Properties</u></p>

<ul> <li>Has its own reflexes and senses and can act independently of the brain</li> <li>Does not engage in consciousness, philosophy, decision-makingdespite being so much like our “main” brain.</li> <li>Only part of the PNS that can act autonomously</li> <li>Nearly every neurotransmitter found in the brain is also found in the gut</li> <li>95% of all our serotonin is found in the gut</li> <li>90% of connections between the brain and gut go from the gut to the brain.</li></ul>

<p><u>Function</u></p>

<ul> <li>Helps digestion</li> <li>Plays a major role in emotions, stress (butterflies in our stomachs)</li> <li>Links between gut health and clinical depression / anxiety.</li></ul>

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9
Q

<p>What are the 3 systems in the gut-brain interaction (And elaborate)</p>

A

<p>1. Peripheral Serotonin</p>

<ul> <li>Cells in gut produce serotonin, affecting brain given the large amount of connectivity from gut to brain</li></ul>

<p>2. Immune System</p>

<ul> <li>Intestinal microbiome can promptimmune cells to produce cytokines, affecting neurophysiology</li></ul>

<p>3. Bacterial Molecules</p>

<ul> <li>Microbes produce metabolites (e.g. butyrate), affecting activity of cells in blood-brain barrier</li></ul>

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10
Q

<p>What is microbiome and microbiota</p>

A

<p><u>Microbiome</u></p>

<ul> <li>Combined genetic material of microbiota</li> <li>> 100 times more genes than the human genome</li></ul>

<p><u>Microbiota</u></p>

<ul> <li>Trillions of bacteria and other microorganisms that live in the gut</li> <li>Impacts brain, behaviour, cognition <ul> <li>Shy mice became "adventurous" after receiving gut microbiota transplant from social mice</li> </ul> </li></ul>

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11
Q

<p>How does the gut microbiota influence the brain</p>

<p>How does the brain influence the gut (neurophysiologically)</p>

A

<ul> <li>Gut microbiota impacts brain via modulating<strong>immune, circulatory and neural </strong>pathways, ensuring homeostasis and development</li> <li>CNS impacts the gut via <strong>neural and endocrine</strong> response</li></ul>

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12
Q

<p>What is Gut Microbiota Dysbiosis and What are the risk factors?</p>

A

<p>Gut Microbiota Dysbiosis:</p>

<ul> <li>Imbalance of gut microbiota, leading to potential for disease</li></ul>

<p>Risks:</p>

<ul> <li>Genetic</li> <li>Low Sunslight/Vitamin D</li> <li>Tobacco Smoke</li> <li>Obesity</li> <li>Shift-Work (Sleep)</li> <li>Epstein-Barr Virus <ul> <li>Not everyone develops diseases from these risk factors</li> </ul> </li></ul>

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13
Q

<p>What is the link between sickness behaviour and brain</p>

A

<p>Bidirectional link between brain to immune system and immune system to brain</p>

<p>Activation of the immune system due to illness triggers a series of temporary behavioural, cognitive and emotional changes including:</p>

<ul> <li>Fever</li> <li>Increased sleep &amp; general lethargy</li> <li>Depressed mood</li> <li>Hyperalgesia (increased pain sensations)</li> <li>Loss of interest in usual activities</li> <li>Anorexia (reduced appetite)</li> <li>Decreased social interaction</li> <li>Impaired concentration</li></ul>

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14
Q

<p>How does cytokines affect the brain?</p>

A

<p>Too big to pass through BBB.</p>

<p>Enter brain indirectly or trigger new cytokines to be released in the brain</p>

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15
Q

<p>What is an example of our integrated brains</p>

A

<p>Kissing</p>

<ul> <li>Increases risk of transmitting illness</li> <li>Allows transfer of hormones like testosterone to passed on to directly increase arousal</li> <li>Others suggest it is a show of trust and close bond (either between the individuals or to the public)</li></ul>

<p></p>

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16
Q

<p>What is sickness behaviour thought to be</p>

A

<p>Strategy to conserve energy and improve fight against infection</p>

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17
Q

<p>Define "Stress"?</p>

<p>What feelings is it associated with?<br></br></p>

A

<ul> <li>Stress is a response to a <u>perceived</u> aversive or threatening situation</li> <li>Feelings of being overloaded, wound-up tight, tense and worried.</li></ul>

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18
Q

<p>Is stress positive or negative?</p>

A

<p>Both</p>

<p><u>Positive</u>:</p>

<ul> <li>Exciting, motivating, improving alertness &amp; performance</li></ul>

<p><u>Negative</u>:</p>

<ul> <li>Harmful for health and function</li></ul>

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19
Q

<p>What is a critical component of a stress experience?</p>

<p>What are thrill seekers attracted to?</p>

A

<p>Critical Component</p>

<ul> <li><u>Real</u> or <u>perceived</u> lack of control over the stressor (Threat of bad events without control is sufficient)</li> <li><strong>Thrill seekers</strong> are often attracted to “calculate risks,”<strong> with some<em>but not total</em> </strong>control of the risk (Complete lack of control is generally negative)</li></ul>

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20
Q

<p>What are the 3 types of stress. What are the differences.</p>

A

<p><u>1.) Acute Stress</u></p>

<ul> <li>Single eventthat leads to increased “flight or fight” response, raising arousals</li></ul>

<p><u>2.) Episodic Acute Stress</u></p>

<ul> <li>Repeated (but <strong>independent</strong>) acute stress events <ul> <li>e.g. life chaos, excessive worry about normal events.</li> </ul> </li></ul>

<p><u>3.) Chronic Stress</u></p>

<ul> <li>Seemingless endless and uncontrollable</li></ul>

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21
Q

<p>What is the advantage of animal models of stress</p>

A

<p>Human studies are correlational or observational (ethics)</p>

<p>Animal studies provide direct measures of effects of different types of stress on biology</p>

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22
Q

<p>What is the key brain region in stress?</p>

<p>Whatare the 2brain systems mediating stress?</p>

<p>Explan the process briefly.</p>

A

<p><u>Acute stress response:Fight or Flight</u></p>

<ul> <li>Rapid detection of threat in the amygdala</li> <li>Activates hypothalamus (<u><strong>Key coordination centre</strong></u>)</li> <li>Activate the HPA axis and sympathetico-adrenal-medullary pathway <ul> <li>HPA system (Hypothalamus > Putiliary Gland > Adrenal Gland) <ul> <li><strong>Cortisol</strong></li> </ul> </li> <li>Sympathetic Nervous System <ul> <li><strong>Epinephrine/Norepinephrine</strong></li> </ul> </li> </ul> </li></ul>

<p>Coritsol &amp; NA facilitates the fight or flight</p>

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23
Q

<p>Explain the HPA Axis Process</p>

A

<ol> <li><strong>H</strong>ypothalamus activated (Triggers emotional responses)</li> <li><strong>P</strong>ituitary Gland activated</li> <li><strong>A</strong>drenal Cortex activated (Adrenal Gland)</li> <li>Releases cortisol (detected in blood)and adrenaline</li> <li>Increases metabolism, blood flow, HR</li></ol>

<p></p>

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24
Q

<p>Explain the different process in acute moderate vs high stress</p>

A

<p><u>Moderate</u></p>

<ul> <li>Aroused &amp; optimal functioning ofPFC</li> <li>Allow top-down regulation of thought, actions &amp; emotions</li></ul>

<p><u>High</u></p>

<ul> <li>Impaired optimal PFC function</li> <li>Since PFC has inhibitory inputs into subcortical arousal structures (e.g., basil ganglia, amygdala), this increases the influence of emotional responses, habitual action and bodies arousal response</li></ul>

<p></p>

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25
Q

<p>What are the 3 effects of acute stress on the brain</p>

A

<p><u>PFC Impaired</u></p>

<ul> <li>Weakened Inhibitory Control (Substance Abuse)</li></ul>

<p><u>Amygdala Strengthened</u></p>

<ul> <li>Increased memory consolidation of stressful events</li> <li>Increased fear conditioning</li></ul>

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26
Q

<p>What are the 3 effects of chronic stress on the brain (Brain parts)</p>

A

<p>Hippocampus:</p>

<ul> <li>Episodic Memory</li> <li>Declarative Memory</li></ul>

<p>PFC:</p>

<ul> <li>Working Memory</li> <li>Fear Extinction</li></ul>

<p>Amygdala:</p>

<ul> <li>Aggression</li> <li>Emotional Memory</li></ul>

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27
Q

<p>Why does stress increase sensitivity to stress?</p>

A

<p><u>Hippocampus:</u>Contextual Learning</p>

<ul> <li>Impaired emotional and memory function reduces flexible emotional processing and reduce separation between memories</li> <li>Causesovergeneralization and less capacity cope with new real or potential stressful events.</li></ul>

<p></p>

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28
Q

<p>What are theeffects of a.) acute (1) and b.) chronic stress (3) on the body?</p>

A

<p>Release of glucocorticoids (e.g. cortisol) triggers</p>

<p><u>Acute effects</u></p>

<ul> <li>Increased energy availability in muscles and breaking down fats &amp; proteins to glucose.</li></ul>

<p><u>Chronic effects</u></p>

<ul> <li>Suppressimmune system <ul> <li>i.e, train drivers that injure or kill people are more likely to suffer illness months later</li> </ul> </li> <li>High blood pressure <ul> <li>Increasing stroke &amp; heart attacks</li> </ul> </li> <li>Reduced fertility</li></ul>

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29
Q

<p>Why we evolved to get acute and chronic stress?</p>

A

<p>Acute Stress:</p>

<ul> <li>Helps animals to respond to threats to their survival “flight or flight”</li> <li>A reactive/reflexive brain might improve survival in immediate danger.</li></ul>

<p>Chronic Stress:</p>

<ul> <li>Effects of early stress on an individual are clearly negative – leading to increased antisocial behaviour, aggression and/or social isolation.</li> <li>In an evolutionary context, some have suggested that these sustained changes could prepare an animal/human for <strong>similar adversity </strong>later in life (enhance fighting readiness)</li></ul>

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30
Q

<p>What other factors (other than control) influence the stress response</p>

A

<ul> <li>Genetics</li> <li>Environment</li></ul>

<p>Examples:</p>

<p>Hot environmental temperatures linked to higher crime and violence (“hot under the collar”)</p>

<p>Financial crises leads to high levels of violence against women and children.</p>

31
Q

<p>What is PTSD caused by?</p>

<p>What are otherfactors?</p>

<p>What is it associated with?</p>

<p></p>

A

<p><u>Cause</u></p>

<ul> <li>Experiencing or witnessing death/serious harm (actual or threatened) or learning of trauma to loved one</li></ul>

<p><u>Factors</u></p>

<ul> <li>Both environmental and genetic factors</li></ul>

<p><u>Associated with</u></p>

<ul> <li>Recurrent dreams, panic attacks &amp;“flash backs”.</li> <li>Poor mental and physical health</li></ul>

<p></p>

32
Q

<p>What are the brain areas associated with PTSD?</p>

A

<ul> <li>Smaller hippocampus (Twin war veteran)</li> <li>Increased amygdala and insula activity to threat</li> <li>Reduced vmPFC to threat <ul> <li>Similar pattern to chornic stress: Less PFC, more Amygdala</li> </ul> </li></ul>

33
Q

<p>Stress and Psychiatric Disorders - Depression, SZ/Bipolar, AD</p>

A

<p><u>Depression</u></p>

<ul> <li>Similar brain areas are implicated in chronic stress and depression and while depression is different it is often considered a stress-related disorder</li></ul>

<p><u>SZ/Bipolar</u></p>

<ul> <li>Triggers increased severity of symptoms</li></ul>

<p><u>AD</u></p>

<ul> <li>Women with serious stressors in middle age more likely to develop memory impairments</li></ul>

34
Q

<p>How does stress affect emotional memory neurologically</p>

A

<ul> <li>Glucocorticoid (e.g. cortisol) stimulates NA response in the basolateral nucleus of the amygdala (BLA), enhancing retention of emotional stimuli</li> <li>Stress hormones (Cortisol and NA) have been associated with greater memory consolidation in animal and humans</li></ul>

35
Q

<p>How does propranolol work?</p>

A

<p><u>Propranolol</u></p>

<ul> <li>NA enhances emotional memory</li> <li>Propanolol blockactivation ofβ-adrenergic receptors by NAand adrenal stress hormones, inhibiting NA action</li> <li>Triggering memory + propanolol = Memories can be "relearened" without fear response, with original memory intact (Implications for PTSD and anxiety-related conditions)</li></ul>

36
Q

<p>What is MBSR. How does it help?</p>

A

<p><u>MBSR: Mindfulness-Based Stress Reduction</u></p>

<ul> <li>MBSR found to moderately (compared to controls/placebo) improved depression, anxiety, distress, stress, quiality of life</li></ul>

<p><u>​How?</u></p>

<ul> <li>Increasing cognitive flexibility and tolerance for uncomfortable physical stress/anxious sensations</li> <li>Reduce perception of threat</li></ul>

37
Q

<p>Explain the brain-behaviour cycle of stress</p>

A

<ul> <li>Early life stress (Life circumstances) ></li> <li>"Epigenetic changes' ></li> <li>Lasting biologicalchanges ></li> <li>Impair decision making and health</li> <li>More negative behaviour and life circumstances</li></ul>

38
Q

<p>What is fear conditioning a form of and what does it involve?</p>

A

<ul> <li>Classical conditioning <ul> <li>Pairing aversive stimulus (US; Shock) with neutral stimulus (CS; Light)</li> <li>Original neutral stimulus(CS; Light) leads to fear response (CR)</li> </ul> </li></ul>

39
Q

<p>What is classical and operant condiioning. Similarity/Differences</p>

A

<p><u>Classical:</u></p>

<ul> <li>Associating automatic involuntary behaviour and stimulus</li> <li>Neutral stimulus before reflex</li></ul>

<p><u>Operant:</u></p>

<ul> <li>Associating voluntary behaviour and consequence</li> <li>Apply reinforcement or punishment to strengthen or weaken behaviour</li></ul>

40
Q

<p>What is fear extinction?</p>

A

<p>Gradual reduction of fear response when the conditioned stimulus is repeatedly presented without aversive outcome</p>

41
Q

<p>What are threeproperties of fear extinction?</p>

A

<ul> <li>Fear extinction requires <strong>extensive traning</strong> and <strong>fragile</strong>, unlike fear conditioning (rapid and robust) <ul> <li><u>Spontaneous Recovery</u>: Time</li> <li><u>Renewal</u>: Context</li> <li><u>Reinstatement</u>: Re-exposed to original US</li> </ul> </li> <li>Fear extinction is<strong> context-dependent</strong> <ul> <li>Learning to reduce fear in one context may not translate to another</li> </ul> </li> <li>Fear extinction produces <strong>new memory trace</strong> (CS without aversive outcome), inhibiting original CS-US fear association <ul> <li>Not erase, but inhibit</li> </ul> </li></ul>

42
Q

<p>What are typical procedures in animal studies of fear conditioning/extinction</p>

A

<p>1.) Conditiong acquisiton phase</p>

<ul> <li>Light/tone is paired with shock</li></ul>

<p>2.) Extinction phase (Different chamber for context)</p>

<ul> <li>Presented with repeated trials of light without shock</li></ul>

<p>3.) Test Phase</p>

<ul> <li>Subsequent day to assess retention of extinction</li></ul>

43
Q

<p>From Rodent Studies, How is fear conditioned in the brain (Neurologically)?</p>

A

<ol> <li><strong>Sensory input (CS) </strong>from<strong> auditory/visual </strong>cortex<strong></strong>pairs with <strong>pain signals (US)</strong> from <strong>somatosensory </strong>cortex in <u>basolateral nucleus</u> of amygdala (BLA)</li> <li>Conditioned association from BLA activates <u>central nucleus</u> of amygdala</li> <li>Central nucelus of amydala sends <u>afferent to hypothalamic and midbrain regions</u> controlling arousal, freezing, hormonal response.</li></ol>

44
Q

<p>Difference between low and high road</p>

A

<p>Low Road:</p>

<ul> <li>Autonmatic, rapid, reflexive fear response</li> <li>Senory input >thalamus > amygdala</li></ul>

<p>High Road:</p>

<ul> <li>Slower cortical inhibitory response</li> <li>If determined not threatening, PFC in high road inhibits fear response</li></ul>

45
Q

<p>What are the key areas in fearin RODENTS</p>

A

<p><u>Prelimbic Cortex (PL)</u></p>

<ul> <li>Stimulation increase fearand inactivation reduces fear</li> <li>Activity predicts poor extinction <ul> <li>dACC equivalent</li> <li>Fear conditioning</li> </ul> </li></ul>

<p><u>Infralimbic Cortex (IL)</u></p>

<ul> <li>Stimulation reduces fear and inactivation impairs extinction</li> <li>Activity predicts good extinction <ul> <li>vmPFC equivalent</li> <li>Fear extinction</li> </ul> </li></ul>

<p><u>Hippocampus</u></p>

<ul> <li>Contextual information</li> <li>Work with vmPFC to inhibit amygdala</li></ul>

46
Q

<p>What does human neuroimaging found in regions for fear conditioning, extinction and extinction recall studies?</p>

A

<p><u>Conditioning</u></p>

<ul> <li>dACC: Threat appraisal</li> <li>Insula: Introspective awareness of fear</li></ul>

<p><u>Extinction</u></p>

<ul> <li>dACC &amp; Insula (note: there is activity but they are being inhibited)</li> <li>vmPFC (but less roboust)</li></ul>

<p><u>Extinction Recall</u></p>

<ul> <li>dACC &amp; Insula (note: there is activity but they are being inhibited)</li> <li>vmPFC and hippocampus if compare CS+ (extinguished)to CS+ (never extinguished)</li></ul>

<p>fMRI did not see Amygdala</p>

<p>SIMILAR REGIONS</p>

47
Q

<p>Why do we see similar activations in conditionding and extinction in fMRI?</p>

A

<ul> <li>Dorsal ACC and anterior insula are involved in threat appraisal and experience of anxiety. These same networks might be activated in conditioning and extinction but perform different functions</li> <li>Alternatively, these networks might still be activated but no behavioural experience/evidence of conditioning – a dissociation in fear measures</li> <li>Role of vmPFC in extinction still debated – contextual processing rather than fear inhibition?</li> <li>Maybe due to level of threat in healthy controls?</li></ul>

48
Q

<p>According to meta-analysis of fear extinction studies, what is the difference between humans and rodents neurologically</p>

A

<p>Compared to rodents, humans have</p>

<ul> <li>Less robust vmPFC activation</li> <li>More robust dACC and anterior insula (similar to fear conditioning)</li></ul>

49
Q

<p>What are 3 explanations as to a lack of amygdala activity in human fear conditioning studies?</p>

A

<ul> <li>Resolution of fMRI <ul> <li>Can't image subnucleii of amygdala</li> </ul> </li> <li>Amygdala only recruited with intense threat as part of defence-circuitry response (mild anxiety in human studies)</li> <li>Amygdala response habitutate after repeated trials</li></ul>

50
Q

<p>Why are three explanations fear conditioning and extinction involved in etiology of anxiety disorders</p>

A

<ul> <li>Greater conditionability of CS + of anxetiy disorders (<em>Note this is wrong)</em></li> <li>Greater stimulus generalization <ul> <li>Greater Reactivity to CS+ and Generalization to CS-</li> </ul> </li> <li>Impaired capacity to inhibt fear to CS+</li></ul>

51
Q

<p>When compared healthy and anxious participants in fear conditioning and extinction task, what were the results</p>

A

<ul> <li>Greater conditionability of CS + of anxiety disorders <ul> <li><strong><em>No Difference</em></strong></li> </ul> </li> <li>Greater stimulus generalization <ul> <li>Greater Reactivity to CS+ and Generalization to CS-</li> <li>Overgeneralization in anxious patients</li> </ul> </li> <li>Impaired capacity to inhibt fear to CS+ <ul> <li>Reduced vmPPFC activity during extinction recall (another study) as well</li> </ul> </li></ul>

52
Q

<p>What are results of fear conditoning/extinction task with Trauma-exposed vs PTSD</p>

A

<p>Compared to Trauma-exposed controls,</p>

<ul> <li>No greater conditionability in PTSD</li> <li>Impaired fear extinction in PTSD <ul> <li>Increased amygdala activity during extinction recall</li> <li>Reduced vmPFC activity during extinction recall <ul> <li>Note: Extinction recall is stronger than extinction learning</li> </ul> </li> </ul> </li></ul>

53
Q

<p>What is the link between PTSD symptoms and extinction? What is an evidence?</p>

A

<ul> <li>10-15% who develop long-term PTSD have impaired extinction post-trauma (and pre-trauma)</li> <li>Deficits in extinction networks (reduced vmPFC) and increase amygdala activity to threat is normalized after exposure therapy for PTSD (i.e. increase vmPFC; decrease amygdala activity)</li></ul>

54
Q

<p>Why study sex hormones? (4)</p>

A

<ul> <li>Sex hormones have a profound effect on development in the brain and body with important changes across the lifespan (neonatal, puberty, pregnancy in women, older age)</li> <li>They play a critical role in glial and neuronal development, brain structure and function</li> <li>They affect the quality of cognition and mood</li> <li>Thereplay a role in psychopathology and mental health disorders</li></ul>

55
Q

<p>Anxiety disorders rates and gender</p>

A

<ul> <li>Women develop <strong>anxiety/stress-related disorders</strong> 2x the rate of men (<u>not substance use disorder)</u></li> <li>Prevalance rates equal in boys and girls, increased prevalence develops at puberty with sex hormones increase, gender difference reduces post-menopause <ul> <li>Suggest sex hormones' role in psychopathology</li> </ul> </li></ul>

56
Q

<p>Even though it's important to study sex hormones, why are there so few studies?</p>

A

<ul> <li>More expensive having male and female samples</li> <li>More expensive to control menstrual phase</li></ul>

57
Q

<p>What are the main sex hormones</p>

A

<p>1+2.) Estrogen and Progestrone "Female"</p>

<ul> <li>Released from ovaries</li> <li>Flucuates across menstrual cycle</li> <li>Increases in pregnancy</li> <li>Drop post-pregnancy and post-menopause</li> <li>Females have testosterone (at low levels) from ovaries</li></ul>

<p>3.) Testosterone "Male"</p>

<ul> <li>Released from testes</li> <li>Males have estrogen (at lower levels) converted from testosterone</li></ul>

<p>Both men and women have "male" and "female" sex hormones (with individual differences)</p>

58
Q

<p>What explains gender differences?</p>

A

<ul> <li>Exposure to sex hormones both before and after birth (some coded by non-sex chromosomes) required for sexual dimorphism (different characteristics)</li> <li>Importance of <ul> <li>gender roles</li> <li>environmental influences</li> <li>culture</li> </ul> </li></ul>

59
Q

<p>How doessex hormones impact the brain. Elaborate more on estrogen and progesterone</p>

A

<ul> <li>Interacts directly with nervous system</li> <li>Estrogen and progesterone <ul> <li>Brain development and synaptic plasticity</li> <li>Influence activity of main NT systems and can directly affect NT receptor function</li> </ul> </li></ul>

60
Q

<p>What is the trend of sex hormones across the lifespan</p>

A

<p><u>Males</u></p>

<p>Puberty: Marked increase in testosterone, slight increase in estrodial</p>

<p><u>Females</u></p>

<p>Puberty: Marked increase in estrodial, no increase in testosterone</p>

<p>Menopause: Marked reduction in estrodial</p>

<p></p>

<p></p>

61
Q

<p>What happens to hormones at puberty.</p>

<p>Explain the neurological process.</p>

A

<ul> <li><u>Hypothalamus</u> and<u>pituitary gland</u> involved in release of sex hormones</li> <li>GNRH (gonadal-releasing hormone) in the <u>pituitary gland </u>stimulate luteinizing hormone (LH) and follicle-stimulating hormone (FSH) to stimulate the respective reproductive organs (testes and ovaries) <ul> <li>>>> Male testes and female ovaries release testosterone (sperm) and estrogen (egg) respectively</li> </ul> </li></ul>

62
Q

<p>Sex hormones and the menstrual cycle</p>

A

<p><u>Start Cycle</u> (day 1-7)</p>

<ul> <li>Estrogen and progesterone are low.</li></ul>

<p><u>Mid Cycle</u>(day 14)</p>

<ul> <li>Progesterone stay low.</li> <li>Increases estrogen to peak stimulating LH and FSH</li> <li>LH and FSH spikes at midcycle (day 14) in preparation for ovulation <ul> <li>After that, estrogen, LH, FSH drops</li> </ul> </li></ul>

<p><u>Luteal</u>(day 18-24)</p>

<ul> <li>Increase in progesterone and a small increasein estrogen <ul> <li>Progesterone levels remain low until now</li> <li>Causes breakout phase</li> </ul> </li></ul>

<p>Goes down during menstration</p>

<p></p>

63
Q

<p>Gender differences and behavior in children.</p>

A

<p>Girls: likes toys that allow nurturance and social play</p>

<p>Boys: likes toys that are more active</p>

<ul> <li>Unclear how much is nature / nurture <ul> <li>But at 1 day old, boyslook at mobile while female look at faces</li> <li>Male monkeys play with cars/balls while female monkeys play with dolls</li> </ul> </li></ul>

64
Q

<p>What is testosterone associated with, and what should it be conceptualised as?</p>

A

<ul> <li>T is associated with social aggression and response to social challenges <ul> <li>E.g., Male chimps release T and are more aggressivewhen female chimps in reproductive phase</li> </ul> </li> <li>T should not be conceptualized in terms of gender but instead in terms of <u>Competition (high T) &amp; Nurturance (low T)</u></li></ul>

65
Q

<p>What are gender differences in relation to violence?</p>

A

<ul> <li>Offending rates consistently higher for men, butdivergence in offending rates between genders (where male increase substantially) coincides with puberty.</li> <li>Role of Testosterone in violence</li></ul>

<p>Depending on the offence, men often over-represent victims of <strong>violence</strong> (male vs male fighting) but are also frequently impacted by domestic violenc. But the predominant victims of <strong>domestic violence</strong> are women.</p>

66
Q

<p>What is estrogen involved in?</p>

A

<ul> <li>Social Behaviour</li> <li>Higher levels of estrogen linked to better mood, improved memory and executive function</li> <li>Administration of estrogen can bias decision-making toward smaller, more accessible goals</li></ul>

67
Q

<p>What is the difference betweeen hormones and pheromones</p>

A

<ul> <li>Hormones transmit messages from one part of the body (the secreting gland) to another (the target tissue).</li> <li>Pheromones are chemicals that carry messages from one animal to another.Released from one animal that directly affect the physiology or behaviour of another (normally detected by smelling)</li></ul>

68
Q

<p>When exposed to a chemical found in men’s sweat, what do women report?</p>

A

<p>Women reported</p>

<ul> <li>Alertness</li> <li>Psitive mood</li> <li>Icreased sexual arousal</li> <li>Timing of their menstrual cycle was altered</li> <li>When participating in a speed dating experiment women rated men to be more attractive.</li></ul>

<p>Men reported less positive mood.</p>

69
Q

<p>Depression and Sex Hormones (3)</p>

A

<ul> <li>Depression is 1.5 – 3 times more prevalent in women (prior to puberty thenumbers are equal)</li> <li>Periods of hormonal transitions and elevated or fluctuating sex hormones are associated with increased mood-disturbances</li> <li>Correlation between suicide attempts and periods of low estrogen</li></ul>

70
Q

<p>What is the link betwenenhormonal contraception and depression (3)</p>

A

<ul> <li>Compared with non-users, contraceptive users had greater risk of requiring anti depressants and receiving depression diagnosis</li> <li>Contraceptives withgreater progesterone showed greatest risk increase.</li> <li>Greatest impacts were seen in adolescents (15-19yrs) with use of the pill increasing anti-depressant use by 80%</li></ul>

<p></p>

71
Q

<p>What is post-partum depression and how are sex hormones related?</p>

A

<p>Post-partum depression: Onset of depressive symptoms after the birth of a baby.</p>

<ul> <li>Genetic vulnerability</li> <li>Change in hormone levels (<strong>dramatic drop</strong>)</li> <li>High stress (lack of sleep etc.)</li> <li>Lack of support</li></ul>

<p>May contribute</p>

<p>3 levels: Blues, Depression, Psychosis</p>

72
Q

<p>What is the link between anxiety disorders and sex hormones, and PTSD</p>

A

<ul> <li>Anxiety disorders are also 1.5 to 2x greater prevalence in women than men (Only after puberty)</li> <li>Low estradiol associated withimpaired fear extinction recall and PTSD</li></ul>

73
Q

<p>What is the link between schizophrenia and sex hormones</p>

A

<ul> <li>Generally emerge during late adolescence and early adulthood for males and females</li> <li>Low levels of Testosterone also linked to reduced mood, depression and impaired concentration, reduced confidence.</li></ul>