Exam 2 Master Study Guide PDF

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Psych 381 Study Guide for Exam #2 The exam will consist of 75 questions (multiple choice, T/F, and matching). Each question is worth 2 points for a total of 150 points possible. There will be several case examples. Focus on the information from the study guide and you will do well. If it is not on the study guide, it will not be on the exam. Chapter 5/Neuro Methods 1. What is the rational of the experimental ablation? What is the major problem with this technique? During experimental ablation, part of the brain is damaged and then subsequent behaviors are observed to try and isolate the function of that specific area of the brain. The problem: it can be difficult to tell if it is just that area controls a specific function and damaging the brain may ruin other connections (the radio analogy). 2. Understand the following terms: stereotaxic apparatus, sham lesion, excitotoxic lesion, CT, MRI, single-unit recording. Stereotaxic apparatus: device the permits a surgeon to position an electrode into a specific part of the brain. Sham lesion: placebo procedure that duplicates all the steps of producing a brain lesion except for the one that actually causes brain damage (this is how they produce controls). Excitotoxic lesion: brain lesion produced by intracerebral injection of an excitatory amino acid. It can target specific cells and can kill the neuron without killing nearby axons. CT: computerized tomography; it is 2D and x-ray. Blood is white, CSF is black. MRI: Measures the amount of time it takes proteins that are aligned after frequency is sent through to return to their original position. It is good for soft tissue and examining white matter, and it is more accurate and can identify finer details. 2-DG: sugar that enters cells when glucose isn’t metabolized. It is injected in subjects so that the most active areas of the brain can be seen when a brain slice is later removed. Single unit recording: using an electrode to record the activity from a single neuron. PET: device that reveals localization of a radioactive tracer in the brain. 3. Understand broadly table 5.3 (page 141) from the book. You don’t have to memorize the whole thing, just understand the general goals of the different types of measurements. 4. What is temporal and spatial resolution? Which brain imaging technologies are best for each resolution? Does fMRI have better temporal or spatial resolution then event-related potentials? Temporal resolution: speed of activity, spatial resolution: location of activity. fMRI=better spatial, EEG=better temporal 5. What are the major differences between fMRI and PET scanning? fMRI is examining oxygenated blood and does not involve radiation. 6. How do neuroscientist trace the efferent and afferent connections of a brain region? Efferent: anterograde method using PHA-L or immunocyto chemical method (dye) Afferent: retrograde method using a dye called Fluorogold 7. Define the following vocabulary terms from chapter 5: TMS, monozygotic twins, dizygotic twins. TMS: stimulation of the cerebral cortex using magnetic fields produced by passing pulses of electricity through a coil of wire placed next to the skull—interferes with functions of the stimulated brain region Monozygotic: identical twins, have identical genotypes. One egg that was split apart. Dizygotic: fraternal twins. Come from two different eggs. Target mutations: mutated gene (knockout gene) is produced in the lab and inserted in chromosomes of mice— fails to produce a functional protein. 8. What is gene knockout? How is it used in research? What are the advantages of the technique? (you will get this information from the book) Gene knockout is used to make an animal analogue of a disease, then apply it to humans.

9. Compare the twin method with the adoption method for the purpose of assessing the contribution of genes versus environment. Be clear on how you can tell from these methods if a trait has genetic or environmental aspects. Twin studies on monozygotic twins allow you to examine the environment because genetic information is shared, so variation is likely due to environmental influences. Adoption studies allow you to study the biological aspects influencing monozygotic twins because they are raised in different environments, so their similarities are likely due to genetics. Chapter 12/Learning and Memory 10. What are the 3 major brain regions that induce amnesia in humans? What are the types of information processing problems associated with each of these areas? Medial temporal lobe: basis of consolidation. Have anterograde amnesia (intact procedural memory), some retrograde amnesia. Diencephalon (medial thalamus): Korsakoff’s Disease and bilateral thalamic strokes. Mostly anterograde amnesia but a little retrograde. Here you cut off the ability to send information to the rest of the brain. Basal forebrain: Anterior communicating artery aneurysms (ACoA), confabulation, frontal extension of lesions. Prominent anterograde, variable retrograde. 11. What are the differences between encoding, storage and retrieval? How can disturbances in each of these processes be distinguished? Be prepared for some case examples in this regard. Encoding= registering info, Storage= organize and retain info, Retrieval= recall or recognize info- where strengthening of the synapse occurs. Never register info=encoding errors Recognize NOT recall=disorder is at level of retrieval Long delay occurs, don’t recognize or remember=encoding problem 20 min delay and the person can’t recall as many, problem could be storage or retrieval. So, administer recognition test. If they are unable to recognize the items the problem is storage. 12. What is anterograde amnesia? What is a retrograde amnesia? What is a remote memory disturbance? How can you differentiate between the three? Anterograde: defect in new learning Retrograde amnesia/remote memory disturbance: defect in retrieving old memories Remote memory disturbance: loss of old memories The direction of memory loss: Remote memories are the oldest, retrograde are “newer” old memories Remote memories > retrograde > *INJURY* > anterograde 13. What is Hebb’s rule? How does it apply to learning and memory? Hebb’s rule: the cellular basis of learning involves strengthening of a synapse that is repeatedly active when the postsynaptic neuron fires. The synapse itself changes! 14. Using the pictures below (and on the lecture slides), be able to identify the entorhinal cortex, subiculum, dentate gyrus, CA3, and CA1. Also, know the order of transmission of information in the hippocampus between these areas.

Entorhinal Cortex>Perforant Path>Dentate Gyrus (think mossy fibers)>CA3>CA1>Output via Subiculum>Fornix>Mamillary bodies and out to the frontal cortex Information into entorhinal cortex>dentate gyrus>CA3>CA1>subiculum 15. Describe long-term potentiation. Why is long-term potentiation important for learning and memory? Relate longterm potentiation to Hebb’s law. Long-term potentiation: Long-term increase in the excitability of a neuron to a particular synaptic input caused by repeated high-frequency activity of that input. In other words, when a pathway is potentiated, it is more likely to fire in the future under the same conditions. This supports Hebb’s law because as the activity is repeated, the synapse is strengthened, making future firing easier and more likely. This is important for learning and memory because memory is based on the synaptic connections—the stronger they are, the more we excite those neurons, the more we will remember those things! 16. How does long-term potentiation differ from long-term depression? Again, relate to Hebb’s law. Long-term depression: a long term decrease in the excitability of a neuron to a particular synaptic input caused by stimulation of the terminal button while the post-synaptic membrane is hyperpolarized—INHIBITORY. Neural circuits that contain memories are established by strengthening some synapses and weakening others. So, according to Hebb’s law, it is not just about strengthening. It involves the combo of strengthening and weakening! 17. What is an NMDA receptor? What is an AMPA receptor? Know the role of each in learning and memory. NMDA: specialized ionotrophic glutamate receptor that controls a calcium channel that is normally blocked by magnesium ions. Involved in long-term potentiation. Calcium channels act as second messenger to activate various enzymes and biochemical processes. AMPA: an ionotrophic non-NMDA glutamate (excitatory) receptor that controls a sodium channel; when it is open it produces EPSP’s (depolarization). They sit idle at the base of the dendritic spines then flood the spines during EPSP. Normally, when a glutamate binds with NMDA receptor, the calcium channel can’t open because the magnesium is blocking it. Depolarization of the membrane evicts the magnesium ion and unblocks the channel. Now glutamate can open the channel and permit the entry of calcium ions. 18. Are NMDA receptors neurotransmitter or voltage dependent? Describe why. BOTH! Calcium only enters the cell when glutamate is present AND the postsynaptic membrane is depolarized. 19. What is a perforated synapse? How does this relate to AMPA and NMDA receptors? A perforated synapse occurs when the influx of calcium (which occurs when the membrane is depolarized and NMDA receptors bind and allow calcium ions to enter) changes the membrane to increase glutamate channel

AMPA receptors which insert into the post-synaptic membrane=perforated membrane. Calcium is responsible for fusing of vesicle to membrane (allows binding to occur!), which allows things to insert and remove from the postsynaptic and presynaptic membranes. So, increased calcium increases the ability of AMPA receptors to bind with the postsynaptic membrane. Perforated means there are lots of receptors on the membrane. Because there are more receptors, it is more likely to depolarize (because these receptors control sodium channels)= Hebb’s Law! Memory strengthens when you use the area—“use it or lose it”. 20. How much information can we hold in “short term memory”? What is the primary difference between short-term memory and working memory? STM: Duration: seconds, unless info is rehearsed or otherwise held Capacity: 7 +- 2 bits of info Working memory is defined by the objective, NOT by duration! Working memory is an “executive function”. Know the figure below, including the definitions of each of the parts.

Declarative: accessible to conscious awareness, usually intentional recollection. Function is to process info in such a way as to consolidate it for storage in the brain. Episodic: Memory for individual episodes that have a contextual tag Semantic: Memory for info (general knowledge) w/ no conceptual tag Procedural: Usually not accessible to conscious awareness, demonstrated through performance. Ex: skill learning and perceptual motor adaptation, habit memory, conditioning. 21. Referencing the figure above, what parts are spared in amnesia? What parts are impaired? Procedural is spared, declarative is not (think of Clive). 22. Know what are considered “normal” losses/declines in memory. Infantile amnesia: inability to recall events from first 1-3 years of life. Mild decline in memory function with age (hugely different from dementia!) Forgetting with the passage of time Loss of memory immediately after awakening from sleep. 23. Know what happens to IQ and attention in individuals with amnesia. Usually left intact. AKA nothing. 24. What is confabulation? Damage to which parts of the brain is most often associated with confabulation? Confabulation=make up memories or events to fill void in memory. Usually associated with basal forebrain damage. Basal forebrain

25. What do the entorhinal cortex and parahippocampal cortex do in memory? Is a lesion of the hippocampus without damage to these areas as detrimental as a lesion that includes these areas? Entorhinal cortex=neurons here have axons that terminate in dentate gyrus, CA3, and CA1. It receives input from several areas. Basically, it is an important relay station between areas of the brain for output and input of info. Parahippocampal cortex=relays info between entorhinal cortex and other brain regions. Not just the hippocampus is important in recalling memory! Greatest memory impairment comes from combined lesions of all three of these areas because memory involves communication between all of these areas. 26. What is Korsakoff’s disease? Why does it occur? Know the symptom profile. -Bilateral damage to diencephalic structures (mammillary bodies of hypothalamus). -Korsakoff’s disease typically occurs due to alcoholism—When people drink excessively they don’t eat. This lack of nutrition causes deficiency of vitamin B, yet alcohol also increases body’s requirements for B vitamins. Dysregulation of glucose then causes damage to medial thalamic areas. -Leads to anterograde amnesia. 27. What happened to cases H.M., N.A., and Clive? How are the cases similar and how are they different? -H.M.= medial temporal lobe damage. Lost declarative memory but not procedural (mirror tracing task he learned and improved over time, showing he still had skill learning) -N.A.= thalamic lesion due to fencing incident. He had a little retrograde amnesia but marked anterograde. -Clive= bilateral medial temporal lobe damage due to encephalitis. He still had some degree of declarative memory but those memories could not be consciously recalled (e.g., he knew his wife didn’t live with him anymore—that she had to go away, and he could still play piano=motor memory). 28. Be able to differentiate between Alzheimer’s disease, Vascular dementia, and Fronto-temporal dementia. What would the case presentation look like for each of these types of dementia? Understand the differences in age of onset, symptom profile (example: stepwise versus gradual memory decline versus behavioral difficulties), and etiology (may need to refer to the neurological disorders lectures as well for this part). Alzheimer’s disease: Gradual cognitive decline. Can recall old memories, procedural memories are intact. Onset ~60. Symptom chart: early diagnosis=cognitive symptoms, loss of ADL. Mid-moderate= behavioral problems, nursing home placement, death (on border with severe, usually occurs after about 6 years). Hippocampus is degenerating so unable to encode information. Vascular dementia: Series of strokes. Can be large, involving much of the cerebral hemisphere. Blockage of extracranial arteries and main intracranial arteries can lead to large vessel disease. Stepwise decline, as decline occurs with each successive stroke. Cognitive abilities that are impaired typically result in frontal symptoms but can also include other things depending on stroke location. Typically results in etrieval problems. MRI shows focal small strokes within subcortical and cortical regions. Cardio risk factors: hypertension, cholesterol, smoking, obesity, diabetes. Fronto-temporal dementia: Starts in the frontal lobes>temporal lobes. Present with behavioral problems but intact memory, over time start forgetting. Occurs usually after age 40 and usually before age 65. Equal in men and women, in ~50% of patients, history of this exists in first degree relative. Can look like late stage Alzheimer’s. Decline in social interpersonal conduct, impairment in regulation of personal conduct, emotional blunting, loss of insight. Behavioral disorder, impaired speech and language, physical signs, investigations such as imaging, etc. Symmetrical or asymmetrical frontal atrophy in dorsolateral or ventrofrontal regions. Prevalence= 1) Alzheimer’s 2) Vascular dementia 3) fronto temporal

Chapter 13/Language and Communication 29. Know the following anatomical structures, locations, and role in language: Broca’s area, Wernicke’s area, arcuate fasciculus, supramarginal gyrus, angular gyrus, Heschl’s gyrus (there may be a figure on the test for you to label) Wernicke’s area: posterior aspect of superior temporal gyrus, secondary auditory cortex, comprehension Just posterior to Heschl’s gyrus. So dorsal posterior temporal and inferior parietal. It is a THIRD area. Primary auditoryAuditory associationWernickeArcuate fasciculusBroca Broca’s area: 3rd frontal convolution of the left inferior frontal gyrus, production Arcuate fasciculus: Connective fibers between Wernicke’s and Broca’s, damage to this disrupts repetition of speech sounds, causes conduction aphasia They don’t really have issues except for REPEATING phrases. Supramarginal gyrus: Integrate visual and spatial info from occipital and parietal lobes with auditory info Reading of words, visual (seeing angry face, etc) Angular gyrus: Integrates other info, plays a role in reading comprehension by matching phenomes to graphemes (sounds to words), reading and writing Vocabulary. Heschl’s gyrus: Primary auditory cortex. Left hemisphere (bilateral correct??), at top of superior temporal lobe, inferior parietal, tonotopic=organized by frequency 30. Understand what is meant by “tonotopic organization” of the primary auditory cortex Heschl’s gyrus divided into different areas associated with different tones Posterior= 15000 Hz, Anterior =500 Hz 31. Differentiate between speech and language; differentiate between dysarthria and aphasia Language: intent, concepts, grammar, semantics, phonology Speech: motor articulation system, bilateral Dysarthia: disorder of motor apparatus of speech. Thus, they have language representations in their head but they cannot actually say the words. Problem with the MUSCLES in vocal cord (different than language). Aphasia: acquired disorder of language due to brain damage—articulators are intact but they do not have the representation in their head. Don’t affect IQ, attention, etc. Broca homolog: porosity production Wernicke homolog: understanding porosity 32. What is the most common cause of aphasia? Stroke 33. How to the angular and supramarginal gyri (the posterior language areas) contribute to reading? What are the main roles in reading? Simply, it doesn’t allow them comprehend meaning. They still can repeat meaning but CANNOT understand what is going on

34. Be able to differentiate between Broca’s aphasia, Wernicke’s aphasia, Conduction aphasia, transcortical motor, transcortical sensory, and global aphasias. Particularly understand deficits in fluency, comprehension, naming, and repetition between each of these types of aphasia. There are several questions about the aphasias on the exam. Perisylvian (around sylvian fissure) Brocas, Wernickes, Conduction Aphasia Transcortical Aphasia Motor, Sensory, Mixed, Global

Broca: impaired production,

Fluency

Comprehension

Naming

No

Good: some degree of deficit The deficit appears when they need to tell the meaning from GRAMMAR Most Broca’s cannot write Poor

Poor

Sensory deficits Few

Poor

Some

Poor

Telegraphic effortful speech (leave out “and, but”, etc)(have the most important pieces, they leave out the verbs) agrammatism, writing and reading deficits, weakness in right hemi thing

Repetition Poor: drops function words

Wernicke: grammar better preserved than BA, reading impairment often present, may be aware or unaware of deficit, finger agnosia, acalculia (problems doing math), alexia withough agraphia (can’t read but can write)

Yes: fluent

Conduction: Hesitations and

Yes

Good

Good

Some

Poor

No

Poor

Poor

Yes

Poor

No

Good

Poor

No

Good: because

word-finding pauses, sometimes intact reading abilities, damage to arcuate fasiculus Often you cannot TELL that they have an issue until you say “Repeat after me” Global: overall decrease in function in multiple domains, most widespread deficits of all the aphasias, due to damage in multiple perisylvian regions Worst of all. Giagantic lesions.

Transcortical motor:

but nonsensical Don’t use a lot of MEANING words just a lot of connectors

disturbed spontane...