Exam 3 Study Guide
Exam 3 Study Guide NROSCI 1000 - Intro to Neuroscience
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This 21 page Study Guide was uploaded by Saranya Govindaraju on Saturday December 5, 2015. The Study Guide belongs to NROSCI 1000 - Intro to Neuroscience at a university taught by Dr. Linda Rinaman in Fall 2015. Since its upload, it has received 20 views.
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Date Created: 12/05/15
NEUROSCIENCE EXAM 3 STUDY GUIDE Homeostasis and Stress Autonomic Nervous System Visceral (Autonomic) Motor System - Motor system that controls the viscera – smooth muscle, glands, cardiac muscle - Sympathetic, parasympathetic, and enteric divisions - Associated visceral sensory feedback pathways, which are not technically part of autonomic nervous system - Central autonomic network “Life depends on the innervation of the viscera…all the rest of biological luxury” – Nauta & Feirtag - Visceral motor system; “autonomic” o Most basic nervous system linkages to body o Can’t control because it is beyond the level of our consciousness (ex. heartbeat) - Homeostasis vs. allostasis o Homeostasis = similar balance, things are constant (implies that heart rate won’t change with regard to the autonomic nervous system – not true!) o Allostasis = stability through change Who are Walter Gaskell and John Langley? - Credited with finding autonomic ganglia and two visceral motor systems with opposite effects (18601890) - Located in the periphery - Came from neural crest Controls smooth muscle - Receive signals from the spinal cord and vagus nerve Who is Walter Cannon? - “The Wisdom of the Body” - Performed an experiment where he damaged the pathways and either: o Treated the animals well animal survived o Treated the animals poorly animal died - Concluded that the autonomic nervous system helps us recover from threats and challenges to life Somatic Motor System - One alpha motor neuron synapses onto individual muscle fibers and releases acetylcholine to move joints by contracting fibers of opposing skeletal muscle groups - Lower motor neurons in CNS (brainstem + spinal cord) - Central integration and control Autonomic Nervous System - Has two divisions: parasympathetic and sympathetic - Diffuse branching to target tissue and local transmitter diffusion to receptor sites - Lower motor neurons in CNS and PNS - Highly varied inhibition or stimulation of target tissue by different transmitters and receptors - Central and peripheral integration and control - Slower and less precise – no motor units - Ganglia can be modulated to respond to hormones and feedback to modulate output o Cholinergic receptors – release acetylcholine o Adrenergic receptors – release norepinephrine and epinephrine Comparison of Autonomic and Somatic Motor Systems Somatic Nervous System Autonomic Nervous System Cell body in CNS Cell body in CNS Single neuron chain from CNS to effector organ Twoneuron chain from CNS to effector organ Heavily myelinated axon Lightly myelinated preganglionic axons Unmyelinated postganglionic axons Stimulatory effect Stimulatory or inhibitory effect depending on neurotransmitters and receptors on effector organs Effector organ = skeletal muscle Effector organs: smooth muscle, cardiac muscle, glands Parasympathetic “rest and digest” Sympathetic “fight or flight” Releases acetylcholine at ganglion and target Releases acetylcholine at ganglion and tissues norepinephrine at target Supports functions related to reproduction and Releases acetylcholine on chromaffin cells in the food intake adrenal medulla which releases norepinephrine or 4 cranial nerves: oculomotor, facial, epinephrine in blood vessels (occurs during a big glossopharyngeal, vagus threat) Vagus nerve provides bulk of parasympathetic outflow to body Sends signals slower Located in thoraciclumbar region Located in cranialsacral region Descending projection leads to changes in flight Assimilates energy to prepare for future and or fight response anabolic functions Energy expenditure and catabolic functions What happens to various organs in response to increased sympathetic nervous system activity? - Also known as response to norepinephrine and adrenergic receptor signaling o Heart: beats faster and stronger o Blood vessels: constrict to move blood away from skin and towards muscles o Eyes: pupils dilate o Respiratory tree: airways dilate o Salivary glands/ GI tract: decreased secretion and motility o Adipose tissue: increased lipolysis o Pancreas: increased glucagon release o Liver: glycogenesis, gluconeogenesis o Sweat glands: increased sweating o Bladder: urine voided - What is Mass Activation? o If all of the above were activated o The “fight or flight” response is achieved via sympathetic inputs to adrenal medulla chromaffin cells What happens to various organs in response to increased parasympathetic activity? o Eyes: pupils constrict o Salivary glands/ GI tract: stimulates salivary production + digestion o Bladder: bladder constricts o Pancreas/ Liver: slight stimulation of glucose uptake and glycogen synthesis o Heart: slows heartbeat o Airways: airways constrict What is one way hormones are different from neurotransmitters? - Hormones get released in the blood and act on a far away target What is the sympathoadrenal system? - It is the sympathetic nerves that terminate in the adrenal cortex - The nerves terminate on chromaffin cells in the adrenal medulla o Chromaffin cells are secretory cells from neural crest origin o No axons and dendrites o Have acetylcholine receptors that will release norepinephrine in blood What occurs during a spider bite? Spider venom is an acetylcholine receptor antagonist. - Toxin blocks acetylcholine receptors so acetylcholine cannot act - Paralyzed – skeletal muscle cannot contract without action potential - Suffocation - Heart rate and blood pressure increase How does the sympathoadrenal response occur? - Hypothalamus is stimulated by stress, physical activity, or low glucose levels - This causes an action potential through sympathetic nervous system to the adrenal medulla - Epinephrine and norepinephrine secretions increase which act on target tissues Anatomy of adrenal cortex - Adrenal cortex sits on top of the kidneys (kidneys not associated with adrenal glands) - Core of adrenal gland = location of chromaffin cells o Adrenal cortex = a true endocrine gland o Adrenal medulla = modified sympathetic ganglion o Chromaffin cells = modified postganglionic sympathetic neuron Central Autonomic Network Descending preautonomic motor control - Starts in the insular cortex + medial prefrontal cortex and goes to cortical areas, amygdala, and hypothalamus (areas that control outflow) - Goes to preganglionic neurons in CNS and to primary motor neurons in ganglia and terminated on the target end organs Ascending viscerosensory - Can ascend to higher levels in brain - Regions that provide descending control will also receive input so their outputs can be modulated - Hypothalamus provides a source of control - Part of visceral sensory network - Begins in the end organs and sends signals to cranial nerves IX and X which go to the nucleus of the solitary tract - The nucleus of solitary tract sends signals to descending control areas and higher brain regions What is the visceral sensory system? - Visceral SDU’s: mechanoreceptors, chemoreceptors, and nociceptors - Spinal nerves from viscera go to the dorsal root ganglion - Visceral sensory input via cranial nerves IX and X - Axon terminals synapse in nucleus of solitary tract (in top of medulla) o Region receives and processes visceral sensory feedback from glossopharyngeal and vagus nerve Medial/ Ventral Forebrain: hormonal/ behavioral responses Viscera Nucleus of Solitary l Tract Sensory Preganglionic neurons: motor Input responses rd What is the enteric nervous system – 3 division of autonomic nervous system? - Digestive tube (esophagus to rectum) and pancreas + gallbladder (associated organs) - Autonomous activity is subject to central control via primary parasympathetic inputs - Collection of neurons: motor, sensory, interneurons - Neurons live in wall of gut (myenteric nerve plexus), which make CCK, secretin, GABA, glutamate, substance P, etc. o Most neurotransmitters were first found in the enteric nervous system and then the brain - Diverse collection of enteric neurons Stress - Physiological stressors can have a biological effect - Many different types of stressors - Stress response is adaptive and helps cope/ perceive threats in environment - Stressors are things that challenge homeostasis – can be real/ anticipated challenges What systems does the stress response include? - Nervous - Musculoskeletal - Respiratory - Cardiovascular - Gastrointestinal - Endocrine Physical Stress Responses - Overall effect: increase catabolic (burn energy and increase sympathetic) and decrease anabolic processes (decrease parasympathetic action) - Hypothalamus organizes stress responses by integrating signals/ asking if it meets threshold - Endocrine, autonomic, and behavioral components are organized by hypothalamus What is the role of the hypothalamus in stress response? - Reading environmental + making a decision “is homeostasis being threatened?” - Recruits neural pathways - Periventricular nucleus in the hypothalamus controls endocrine, behavioral, and autonomic outflow o Special role for PVN in physical stress responses - Sensory inputs and contextual information goes to the PVN in the hypothalamus which compares the inputs to biological set points and accordingly creates visceral motor, somatic motor, neuroendocrine, or behavioral responses - PVN = “decider” and main nucleus in hypothalamus that controls stress - It has information delivered from forebrain, brainstem, circumventricular areas, and other hypothalamic regions to control stress responses Emotions and Limbic System A TwoSystem View of the Physical Stress Response (both systems controlled by the PVN) SlowActing Pathway – Hormonal FastActing Pathway – Sympathoadrenal Signal begins in the PVN Signal begins in the PVN 1) Hypothalamus releases corticotrophin releasing 1) Brain sends a message via the spinal cord to hormone onto the anterior pituitary activate the sympathetic system 2) Anterior pituitary (cells called corticotrophs) 2) The sympathetic system stimulates the adrenal releases adrenocorticotrophic releasing hormone gland onto the adrenal cortex 3) The adrenal medulla releases epinephrine into 3) Adrenal cortex releases cortisol to act on cells, the circulatory system to act on cells, endocrine endocrine glands, and brain gland and the brain What is the role of cortisol? - Carbohydrate metabolism – to increase and maintain circulating glucose levels - Cortisol = glucocorticoid Cognitive Awareness of Emotion (feelings/ affect) - Introceptive: stimulus coming from within body - exteroceptive: stimulus coming from outside of body - An emotional response brings into play a motor system (yelling/ crying) Triggering Stimuli Amygdaladependent associative Immediate conscious (interceptive or learning experience of emotional exteroceptive) Hippocampaldependent explicit feelings Cognitive perception = memory (specific details) where feelings come in Emotion = physiological motor response - It can be measured (ex. polygraph test) - Autonomic, hormonal, and somatic outflow to body - Physiological changes (emotional motor responses) are accompanied by cognitive “feelings” affective state - Two different things occur o Body response controlled at low levels o Higher level of cognitive intellectual response JamesLange Theory - Closer to the truth - Muscle responses first and visceral responses lag behind - “You are sad because you are crying” - Event that produces an emotional reaction goes to the brain which triggers muscles, the autonomic nervous system, and the endocrine system - Endocrine response, behavior, and autonomic response contribute to the feelings of emotion Discussion: A woman with a fear of snakes is on a hike and almost steps on a snack, these are her physical responses in order: - Quick posture change to avoid stepping on snake - Scream (physical somatic response) - Heart rate and increased blood flow to muscles - Epinephrine levels increase in blood - Cortisol levels increase at the same time as feelings of dread - Runs back to car CannonBard Theory - Emotional response precedes emotional expression - “Feeling of fear causes the bodily response” Emotions and “Feelings” – Which comes first? Emotional State = physiological state - Can be measured with appropriate tools - Product of endocrine, autonomic, and somatic output systems which comprise the emotional motor system - Product of innate and learned responses to external stimuli and internal thoughts – most responses occur ‘subconsciously’ o Most things are neutral o Low level emotional responses guide our behavior Feelings are constructed from sensory feedback to the brain about emotional state - Reflect a contextdependent cognitive process - Shaped by exteroceptive cues in environment and experience What is the embodied appraisal theory? - Embodied appraisal means “what is my body during this specific time” - Feelings reflect an embodied appraisal of one’s physiological emotional state within a real (or anticipated) environmental context - The hippocampus and amygdala intervene between emotional state expression (emotional motor system) and cortical/ cognitive processing of “feelings” o Both are important in creating the embodied appraisal o The amygdala mediates dynamic interactions between cortical and subcortical processes o These processes are initiated by sensory input and further modulated by sensory feedback The Limbic Lobe – forms a rim around the corpus callosum and diencephalon - There are other brain regions now known to be part of limbic system o Orbital/ medial prefrontal cortex o Mediadorsal nucleus of the thalamus o Ventral basal ganglia – gets dopamine inputs from a different brain region that boosts reward (pleasure) o Amygdala How do stimuli/events attain emotional significance? - Some emotional responses are automatic (innate) and are part of genetic makeup o Ex. lab rats display fear when exposed to fox scent - Most emotional responses are LEARNED (conditioned) o Conditioning depends on experience o Emotional learning: construction of implicit memories linking a situation or event to an emotional body state o Emotional learning can be conscious, but often is subconscious o Modulated by arousalrelated activity of central glucocorticoid and noradrenergic signaling What is arousal? - Arousal is a major aspect of many learning theories and is closely related to other concepts such as anxiety, attention, agitation, stress, and motivation - Low levels of physical performance leads to low levels of memory o Also linked to low levels or stress or arousal in the body Pavlovian Learning/ Conditioning Question: does the animal learn the association between emotional experience and environmental stimuli? Experiment: - Rat is given electric shock and initial reaction is to jump and try to escape - Rat shows emotional response when it realizes it can’t escape - Electrical shock is given with a sound - Rat associates the shock and sound - Rat shows emotional response when only sound is played Conclusion: rat has learned an association between the tone and shock, which produces a fear response. Circuits that include the amygdala take part in this learning process. - Unconditioned stimulus: shock - Unconditioned response: freeze in fear - Conditioned stimulus: sounds - Conditioned response: freeze in fear Pavlovian Fear Conditioning - Emotional unconditioned responses and conditioned responses are outputs of the central nucleus of the amygdala - Central nucleus of the amygdala o Important in driving all fear responses o Where emotional learning takes place o Characterized by response divergence o Sends command messages to anatomical brain targets o If central nucleus is lesioned, you lose the emotional response What are inputs to the amygdala neurons? - Neutral sensory stimuli – visual or auditory stimuli that’s related to an object o Needs to be coupled with something else to elicit a response o When inputs are paired – the same amygdala neurons are activated which makes paired stimuli stronger - Primary reinforcers – taste, touch, pain What are outputs from the amygdala neurons? - Orbital and medial prefrontal cortex o Implicit motor actions o Explicit conscious processing - Hypothalamus and brainstem (key output area) o Visceral motor effector systems to prepare body for action Pyramidal vs. Extrapyramidal Motor Pathways = 2 major pathways that control facial expressions Pyramidal - Corticobulbar pathway – originates in the motor cortex and brainstem - Voluntary somatic motor control pathway - Descending “pyramidal” and “extrapyramidal” projections from motor cortex and brainstem - “Fake smile” Extrapyramidal - Originates in limbic areas o Amygdala is part of limbic system - Descending “extrapyramidal” projections from medial forebrain and hypothalamus - Duchenne smile – “genuine smile” French neurologist/ physiologist “Duchenne” - Happiness produces a “Duchenne” smile - Cannot be voluntarily products - Some muscle groups are put into play - Actors and actresses fake a “Duchenne” smile by thinking of a time where they were genuinely happy - Electricity can be used to stimulate artificial smile by stimulating muscle What is voluntary facial paresis? - Cannot fully voluntarily control a smile - If you tell a joke, involuntary (Duchenne smile) is fine What is emotional facial paresis? - Able to voluntarily show a smile but not involuntarily - Maybe something wrong in the amygdala or hypothalamus – location of emotional system The Amygdala and Fear Case study: Patient S.M. - Had UrbachWiethe disease - Amygdala was destroyed bilaterally - Calcification and degeneration of tissue What are the effects of no amygdala? - Amygdala primary role is fear - Patient S.M. was asked to keep a diary and record her feelings (sad, angry, surprised, etc) - Lost the ability to be scared or fearful - Lost the ability to recognize fear in others Braindamaged controls vs. Patient S.M. Brain damaged controls Some kind of neurological damage No damage to amygdala Patient S.M. Damaged amygdala Unable to recognize fear How does amygdala damage affect sympathetic nervous system? - In animals the sympathetic responses to emotional stimuli would be halted Affective Disorders Affective (Mood) Disorders - Affective disorder = mood disorder - Psychiatric illnesses characterized by disordered feelings/ mood that are disconnected from reality o Not easy to explain what’s going on What are the three main classes of affective disorders? - MDD = major depressive disorder o AKA clinical depression or unipolar depression - Bipolar disorder o AKA manicdepression - Anxiety disorders o Panic disorder, social anxiety, PTSD, OCD, generalized anxiety What is major depressive disorder? - Most common affective disorder - 23x more common in women than men What are the diagnostic criteria for MDD? - Depressed mood - Loss of interest in daily activities for more than two weeks - Impaired social, educational, and occupational functions Symptoms - Depressed mood or irritable - Decreased interest or pleasure in most activities - Significant weight change (+/) - Change in sleep - Fatigue or loss of energy - Feelings of guilt or worthlessness - Concentration problems - Suicidal thoughts Depression (MDD) - No one knows for sure the cause but there are theories and evidence - Genetic component o Identical twins are 70% likely to share the disorder if one has it (even if they were separated at birth) - Individual does not have enough norepinephrine and serotonin What is the Monoamine theory of depression? - Discovered by accident – researchers were interested in BP regulation o Found a native plant that was also used to calm people down - Reserpine (drug) – derived from snake root plant - 10% of patients became extremely suicidal - Reserpine was successful in lowering blood pressure How does Reserpine work? - Depletes norepinephrine and serotonin content in synaptic vesicles = reduced neurotransmitter release o Less neurotransmitters in brain and periphery o Norepinephrine and serotonin are monoamines o If you reduce norepinephrine and serotonin in some people, they will become depressed o Sympathetic and behavioral agitation system suppressed Monoamine Transmitters (NE, 5HT, DA) - MAO = monoamine oxidase o Breaks down monoamines o Chews up old neurotransmitters and controls the levels of monoamine release - Reserpine interferes with the storage of neurotransmitters in vesicles so they release much less o Blocks the step where neurotransmitters are packaged into vesicles at noradrenergic and serotoninergic nerve terminals Norepinephrine Signaling Pathways - Starts in the locus coeruleus in midbrain/ pons region - Makes norepinephrine - High density noradrenergic neurons with axon terminals that go to entire cortical mantle and hippocampus - Widespread projections o Almost like a sympathetic response in brain o Flooding brain with norepinephrine Serotonin (5HT) Signaling Pathways - Looks similar to norepinephrine and projects to same places - Comes from Raphe nucleus – located in the midbrain and pons region Depression – Treatment Five Treatment Strategies – to increase levels of serotonin and norepinephrine - Talk therapy o Repetitive negative thinking has been associated with increased limbic activity and decreased activity in the prefrontal cortex o Cognitive therapy appears to increase inhibitory executive control – helps interrupt or dampen automatic limbic reactions o Medications appear to target limbic regions directly – rather than relying on inhibition through the prefrontal cortex - Monoamine oxidase inhibitors o Monoamine oxidase is an enzyme that breaks down monoamines (serotonin, dopamine, and norepinephrine) o Monoamine oxidase inhibitor is an enzyme that block MAO which leads to the increased effect of monoamines lingering in the synapse o Norepinephrine and serotonin are never in the same nerve terminal – come from different cell bodies - Tricyclic antidepressants and SSRI’s o Tricyclic = 3 rings o Effective on norepinephrine and serotonin nerve terminals o SSRI’s – specific for serotonin o Reuptake transport channel = where neurotransmitter is taken back up and used again Drugs work by blocking the transporter - Electroconvulsive therapy (ECT) – when above options don’t work o How does this work? Patient is put under and hooked up to electrodes on his scalp that induce seizure activity in his brain Causes muscles in body to contract but muscle relaxers are used Increases 5HT signaling in synaptic cleft Evidence on increased receptorligand binding so the patient’s own serotonin has gone up - Deep brain stimulation (also used in treatment of Parkinson’s) o Major brain surgery where electrodes are placed in the brain targeting Brodmann’s Area 25 (ventral anterior cingulate cortex) - Vagal nerve stimulation o Recently approved by the FDA o Much less invasive but still stimulates the nervous system o Exercise and deep breathing is also effective in activating the vagus nerve Reward and Addiction Emotions and “Motivation” - Emotional processing (by limbic system) guides behavioral choices by signaling and impending reward and punishment - DA signaling in dorsal striatum (caudate, putamen) is important for: initiation and smooth integration and completion of behavioral movements - DA signaling in ventral striatum (nucleus accumbens) is important for reinforcement of behavioral movements o More DA signaling increases motivation to perform these behaviors again in the future o DA inputs to nucleus accumbens emotional reward circuit o Important for natural rewards (enjoying lunch, friends, good exam grade) Dopamine Pathways - Substantia nigra – group of dopamine cells - Ventral tegmental area = another set of dopamine neurons important for reward pathway o Projects to the ventral striatum - Substantia nigra and ventral tegmental area located next to each other - Nigrostratial DA projections: motor - Mesolimbic DA projections: reward o Meso = mesencephalon o Limbic = part of limbic system - Mesocortical DA projections: alertness, executive functions (cognitive state) What is the Mesolimbic DA Pathway? - Ventral tegmental area to nucleus accumbens pathway (dopaminergic) - VTA has neurons that use dopamine as a neurotransmitter - Axons project up towards forebrain and terminate in nucleus accumbens Limbic loop vs. Motor loop - Inputs from a variety of limbic areas have input to the ventral striatum called the nucleus accumbens - Dopamine input to the nucleus accumbens comes from the VTA - The substantia nigra projects to the striatum (caudate and putamen) in the direct motor loop pathway DA neurons in the VTA change their activity patterns during reward learning Experiment: What happens to DA neurons when juice is delivered to a monkey’s mouth? A) VTA neural response to an unexpected juice reward – dopamine neurons start to spike B) After learning (juice and sound), VTA neural response to the cue the predicts the impending juice award C) When juice reward is predicted, but not delivered – VTA neural activity is suppressed Emotional Reinforcement and Addiction - Mesolimbic reward circuit normally directs/ motivates behavior towards pursuit of natural rewards (food, social engagement, pain relief) o Increases DA release in nucleus accumbens and away from nonrewarding behaviors that suppress DA release in nucleus accumbens - Reward circuit is vulnerable to dysregulation by exposure to drugs of abuse o Drugs of abuse activate the natural emotional reward pathway – can cross the blood brain barrier and hijack natural rewards o Prolonged drug use will alter biology and functions of the pathway and lead to addiction o Drugs are brought into body and absorbed through blood stream o All drugs act of different parts of reward pathway Alcohol and opiates act on GABA neurons Nicotine acts in 4 ways – powerfully addictive Cocaine acts directly on the dopamine terminal Rest attach to nucleus accumbens directly or indirectly o Brain won’t respond to natural stimulus in the same way after drug o Drugs of abuse will activate this pathway very effectively (larger than natural stimulus) Rats will work to electrically stimulate the VTAtoNA pathway - Self administer drugs that activate this pathway - Rats will press a button repeatedly to induce deep brain stimulating - Rat will do this and ignore food/ drink (natural rewards) How do we know that dopamine signals to the ventral striatum? - Blocking DA receptor signaling in the NA will eliminate these behaviors - Drugs cause neurons to change their physiology o Neurons try to balance all neural input and drugs try to shift neurons around o Drug causes brain to change and when drug is withdrawn, the brain has to respond to that o Neural circuit changes with prolonged drug use - Many different routes that affect the DA pathway o Alcohol and opiates interact with GABAergic neurons o Nicotine acts directly on the VTA/NA neurons Drugs - Behavioral stimulants (cocaine and amphetamine) = highly rewarding o Block the reuptake transport channel of of dopamine and fosters symptoms of schizophrenia o The “high” effect is because of excess DA - Increased DA signaling in brain (3 pathways: somatic motor, reward, and mesocortical) will: o Increase activity and motor behavior o Elevates mood and alertness o Interferes with executive cognitive control - The three pathways control motivation, behavior and ability to plan that behavior Dopamine Receptor Blockers - Occupies the dopamine site on the receptor which prevents receptor activation by dopamine - Side effects interfere with drug treatment for schizophrenia - Chlorpromazine activates dopamine receptors and can be used to block action of cocaine and amphetamine (usually used to treat schizophrenia) o Decreased pleasure so patients don’t want to take drug o Some motor problems (clumsiness) o Sometimes patients will smoke more to boost reward level (boost dopamine levels) - More DA increased reward - Can be used to suppress a “high” in acute overdoses - When the DA system is disrupted – huge effects with ability to plan and execute behavior Rat Study: effects of drugs on dopamine release - DA inputs are increased to high levels with drugs o Cocaine high parallels levels of cocaine in system - Natural rewards also increase DA levels (but not to the same level as with drugs) o Natural rewards increase right away and don’t wait for digestion Dopamine Pathways Relevant to Schizophrenia Symptoms - Hypothesis: overactive DA signaling in cortex is a hall mark of schizophrenia - Positive symptoms – appearance of new/ abnormal behaviors (ex. hallucinations and feelings that your expertise is needed) - Negative symptoms – suppression of normal behaviors (ex. lack of emotional expression) What is schizophrenia? - Disorganized thought patterns and language - Unusual, repetitive, or odd behaviors - Flat affect/ low emotionality - Rule of thirds: 1/3 have an episode + treated and return to normal life, 1/3 live in institution, 1/3 live with family and have constant care - Antipsychotic drugs are effective on DA D2 receptors Speech, Language, and Consciousness Language is lateralized and localized - One half of brain serves a higher degree of functioning – two halves are always communicating - Language = left side of brain (for 97% of people) o Moreso for men than women - Left frontal and temporal association cortices o Primary motor cortex – generating language o Primary somatic sensory cortex – reading braille o Primary auditory cortex – hearing language o Primary visual cortex – seeing and reading - Wernicke’s Area: merger of parietal and temporal lobe o Important for receiving and understanding language o Ex. reading, listened to, or talking to yourself - Broca’s Area: frontal lobe o Important for producing language - Both Wernicke’s and Broca’s area interact with each other – direct link from Wernicke’s Broca’s Role of the Right Hemisphere - Prosody = coloring of speech (emphasis) - Includes the rhythm, timing, emphasis, volume, tonal (pitch) variations of verbal speech o Conveys emotion and grammatical emphasis - You can convey information with changes in tone Sites where electrical stimulation interferes with speech production (W. Penfield, 1950s) - Individual will stop speaking when certain areas of the brain are electrically stimulated Wernicke’s Area - Location: rear left temporal lobe (Brodmann area 22) - Primary auditory cortex (A1) communicates with Wernicke’s area - Wernicke’s Aphasia (aphasia = abnormal speech) o Sensory/ receptive aphasia o Language is produced and sounds normal, but doesn’t make any sense/ don’t respond to questions o Many patients are unaware of their problem Broca’s Area - Location: left frontal lobe (Brodmann areas 44,45) - Broca’s aphasia o Motor, “expressive” aphasia o Disruption of language production Difficulty finding and expressing the right words Organization of language problem (grammar and syntax) o Problems with written, spoken, and “signed” language o Disruption between what you want to say and what you actually say o Patients are aware of their problem, may become frustrated, won’t talk much Characteristics of Two Aphasias - May not have every symptom - Different scales of severity for each aphasia What is the arcuate fasciculus? - An arching fiber that carries information from Wernicke’s area to Broca’s area What happens if arcuate fasciculus is damaged? - Produces conduction aphasia (similar to Broca’s aphasia) - Information of taking a thought to language production is damaged What is conduction aphasia? - Damage to fibers linking Wernicke’s and Broca’s areas - Problems producing appropriate responses to language even though the language is understood - Poor speech repetition Case Study - If left hemisphere is damaged (in early development), the right hemisphere may be able to show plasticity SplitBrain Subjects - Radical neurological surgery done because of epilepsy that cannot be controlled with drugs - Issues arise when right brain jumps in but can’t communicate because not in charge of language o Ex. left hand trying to close book while reading (right brain is bored) - Corpus callosum is severed o Links two hemispheres together, which are in constant communication - After surgery will say weird things because two halves of brain aren’t communicating o Left hemisphere: language expresses one thing o Right hemisphere: does the opposite of what the person’s original intentions were Normal Individual vs. SplitBrain Individual Normal individual: image in left visual field Image in left visual field goes to right visual cortex and crosses over to Broca’s area because the corpus callosum is in tact Splitbrain individual: image in left visual field - Image goes to right visual cortex and does not go to Broca’s area Splitbrain individual: image in right visual field - Image goes to left visual cortex and can go to Broca’s area Experiment: subject explores objects behind a screen (cannot see what they are) – only works with splitbrain individuals Language and “Consciousness” - Babies o React to sensory stimuli o Do not have ability to represent construct abstract thoughts – can’t store that information because you need language for that o No higher selfconsciousness o This is why you don’t have memories from infancy - “Feral children” o Children raised with no human interaction o Difficult to newly generate language o Seem to have Wernicke’s aphasia - Individuals with Wernicke’s aphasia o No evidence of self awareness of thoughts, abstract thinking, social interactions, ability to understand, not really conscious - Individuals with left hemisphere brain damage (ex. stroke) o Certain things are normal language drawbacks and unable to be human connected - “Normal” individuals under drug influence o if language and memory suppressed the information wont make it into memory storage What is the Wada test? - Sodium amytal = a local anesthetic that is injected into the left or right carotid artery to anesthetize a hemisphere - Used to help determine whether an individual has his or her language function localized in the left or right hemisphere - If right hemisphere is anesthetized: unaware of everything - If left hemisphere is anesthetized: individual is very fuzzy with the details What is the right brain better at doing? - Right brain (left hand) is better at drawing than the left brain Memory Learning and Memory - Learning = acquiring new information, general knowledge, and skills o Learning can be conscious or subconscious o Always requires experience - Memory = encoding, storing, retrieving learned information and skills o Information needs to be stored for it to be learned o Encoding = turning a stimulus into a neural signal o Amnesia: Failure to recall previously learning information (retrograde) Failure to store new information (anterograde) o Retrograde – means going back (past information) o Anterograde – means going forward (new information) Qualitative Categories of Learning and Memory - Declarative and Explicit o Acquisition, storage, retrieval of information that is available to consciousness o Can be expressed using language Includes episodic memory: autobiographical record of things that happened to you Includes semantic memory: learning about things external to yourself (facts/ history) Able to be processed by language systems - Procedural (Nondeclarative)/ Implicit o Skills and associations that are largely subconscious o Difficult or impossible to express though language, but demonstrate though behavior Ex. learning how to ride a bike Easier to show someone than to tell them using words Temporal Categories of Declarative Learning and Memory - Immediate memory (lasts a few seconds) o Ex. looking up a phone number and repeating it to a friend - Working memory/ Shortterm memory (lasts seconds to minutes) o Ex. repeating phone number so it stays in your consciousness - Longterm memory (days to years) o Information is stored so you can recall it at a later time o Requires consolidation (rehearsal) - Consolidation process o Ex. listening to a song repeatedly so you learn the lyrics - Most of the time an event will go from our immediate memory to shortterm, and then to longterm memory after consolidation - Sometimes if you are extremely focused, information can go directly from immediate memory into longterm memory Consolidation of LongTerm Declarative Memories - Consolidation requires the hippocampus and adjacent parahippocampal cortex (rhinal cortex) o Located in the bottom of temporal lobe - Closely associated with limbic areas and communicates with the amygdala Brain areas that are associated with declarative memory disorders - Learned about these brain regions because of damage to these areas: o Thalamus o Hippocampus o Rhinal cortex o Mammillary body o Prefrontal cortex o Basal forebrain o Fornix o Amygdala Case Study: Henry Molaison (Patient H.M.) - Had seizures that could not be controlled so got bilateral medial temporal lobe surgical resection - Portions of amygdala, hippocampus, and underlying cortex (parahippocampal tissue were removed) - Surgery was successful in fixing seizures, no loss of IQ, no personality changes Surgery left Patient H.M. with severe anterograde amnesia - Profound loss of shortterm declarative memory, unable to consolidate new longterm declarative memories o Could not remember what was said a few minutes ago o Feels familiar around certain people (family, doctors) but doesn’t remember them - Episodic and semantic memories (presurgery) remained intact - Recognized that there was a disconnect - Procedural learning and memory remained in tact Conclusion - Hippocampus and rhinal cortex are important areas for consolidating and making memories Case Study: Clive Wearing - Patient suffered from chronic anterograde and retrograde amnesia because of a viral infection that destroyed his hippocampus (encephalitis) - Shortterm memory of a few seconds - Lacks ability to form new memories and cannot recall aspects of his past - No semantic or episodic memory - Feels like he has just woken up – when he looks to the past there is nothing Nondeclarative Procedural Learning and Memory - Cerebellum can be involved - Can learn new motor tasks and demonstrate that they have learned it, but no memory of the task - Applicable to Patient H.M. and Clive Wearing The MirrorDrawing Task Objective: trace object by looking only at its reflection in a mirror - The number of errors decreases over time (3 day period) - Demonstrates that they have learned the task, but have no memory of it Pavlovian Conditioned Learning Procedural Learning – “Priming” - Patient H.M. showed normal priming effects o Priming effects are resistant to hippocampal/ medial temporal lobe damage - Powerful influence of previously presented information – despite a lack of conscious awareness of this influence - Falls into implicit category Brain Regions Involved in Declarative vs. NonDeclarative Learning and Memory - Arousal engages the amygdala signals level of importance of the event to be learned and remembered Explicit Implicit What is the Yerkes Dodson Law? - Memory, performance, and efficiency are related to stress (arousal) - Optimal levels of performance occur during medium levels of stress
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