Post Midterm 2 Flashcards

1
Q

What are the different types of learning?

A

Motor, perceptual, relational, stimulus-response

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2
Q

How stable is sensory memory

A

(perceptual memory) lasts only a couple seconds, Allows an individual to retain the experience of the sensation slightly longer than original stimulus

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3
Q

How stable is short term memory

A

lasts for seconds to minutes, can be extended through rehearsal

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4
Q

What parts of the brain are involved in motor learning?

A

Cerebellum, thalamus, basal ganglia and motor cortex

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5
Q

What does perceptual learning involve?

A

Changes in strength of connections between neurons in primary and association sensory cortices

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6
Q

How does visual agnosia connect to memory?

A

Disrupts people’s memory of visual properties
Not only ability to recognize visual stimuli

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7
Q

What brain pathways are involved in instrumental conditioning?

A

Direct transcortical connections, basal ganglia

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8
Q

How are direct transcortical connections involved in instrumental conditioning?

A

Involved in creation of new complex motor sequences that involve deliberation or instruction

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9
Q

Direct transcortical connections:

A

connections from one area of the cerebral cortex to another

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10
Q

How are the basal ganglia involved in instrumental conditioning?

A

regulate habit learning… integrate sensory and motor info from throughout the brain, initially acting as a passive observer… When successful behaviors are repeated, basal ganglia starts to automate stimulus-response process… Creates habitual ways of responding, leaving transcortical circuits free

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11
Q

How is dopamine involved in instrumental conditioning?

A

signaling drives habit learning by controlling synaptic plasticity in the basal ganglia

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12
Q

Nearly every area of the cerebral cortex projects to the

A

basal ganglia

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13
Q

Inputs to the basal ganglia synapse in the

A

striatum

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14
Q

the striatum consists of 3 parts:

A

caudate, putamen, and nucleus accumbens

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15
Q

How do dopamine neurons contribute to learning?

A

Dopamine neurons in the midbrain (substantia nigra and ventral tegmental area) signal reinforcement and punishment by releasing more or less dopamine in the striatum

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16
Q

What kind of information is processed in the striatum?

A

Different areas process different information … Nucleus accumbens in the ventral striatum: receives input from limbic areas such as the hippocampus, amygdala and parts of PFC… Seems to regulate priorities and cravings

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17
Q

What is the role of the basal ganglia?

A

Reinforcement learning, different circuits within the basal ganglia become involved in the action selection and execution process across this transition

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18
Q

Lesions of the basal ganglia disrupt

A

reinforcement learning and habit learning, but do not strongly affect perceptual learning or stimulus-stimulus learning

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19
Q

What is Korsakoff’s syndrome?

A

permanent anterograde amnesia caused by brain damage, usually resulting from chronic alcoholism, often coupled with confabulation

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20
Q

What is anterograde amnesia?

A

Unable to form new memories but can still remember old ones before the damage

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21
Q

What is confabulation?

A

reporting of memories of events that didn’t take place (no intention to deceive)

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22
Q

Afferent neurons carry information from

A

sensory receptors to the CNS (OUT TO IN)

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23
Q

Efferent neurons carry information from

A

CNS to the muscles (IN TO OUT)

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24
Q

Anterograde movement

A

Soma to distal axon (IN TO OUT)

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25
Q

Retrograde movement

A

Axon to soma (OUT TO IN)

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26
Q

What is the role of the hippocampus in relational learning?

A

Forming new episodic and semantic memories

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27
Q

Hippocampus is NOT the location of

A

short or long term memories

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28
Q

Hippocampus is critical for

A

consolidation of short term into explicit long term memories

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29
Q

What is memory encoding?

A

Consolidation, making memories ‘permanent’

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30
Q

During any given moment, unique pattern of neural activity in the ___ reflects sensory input, thought processes, emotions, etc

A

cerebral cortex

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31
Q

Where are spatial memories stored?

A

Consolidated and stored in the cerebral cortex after 30 days
need functional hippo. to remember newly learned

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32
Q

Retrograde amnesia

A

inability to remember events that occurred ‘before’ brain injury

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33
Q

When amnesic patients are tested, found that they still have ___, ____, and ____ learning

A

perceptual, motor and stimulus-response

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34
Q

What is the directionality of verbal behavior in the brain?

A

Lateral

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35
Q

Most language disturbances occur after damage to the ___ side of brain

A

left

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36
Q

What is prosody and what part of the brain is it understood in?

A

Pitch/tone, right hemisphere

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37
Q

What is phonagnosia?

A

Difficulty recognizing voices

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38
Q

What does phonagnosia result from?

A

localized brain damage to the right superior temporal cortex

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39
Q

What is aphasia?

A

Disturbance in understanding, repeating or producing meaningful sound, Isolated deficit, patient is capable of recognizing when others are attempting to communicate

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40
Q

Where does language comprehension take place?

A

Posterior language area

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41
Q

Where is the posterior language area?

A

located at the junction of the temporal, occipital and parietal lobes, around the posterior end of the lateral fissure

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42
Q

Neurons in the posterior language area activate the ensemble of neurons throughout sensory association cortices that store…

A

representations of words

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43
Q

Damage to the posterior language area causes

A

transcortical sensory aphasia:

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44
Q

transcortical sensory aphasia:

A

failure to comprehend the meaning of words and an inability to express thoughts with meaningful speech, Word perception and speaking might be fine (without any comprehension of what is heard or spoken)

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45
Q

What is conduction aphasia?

A

Inability to repeat exact words, other than that, speech is meaningful, fluid and with good comprehension, can’t repeat nonsense words

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46
Q

What causes conduction aphasia?

A

damage to the connection between Wernicke’s area and Broca’s area known as the arcuate fasciculus: bundle of axons that connects the two areas

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47
Q

What is Wernicke’s Area?

A

Involved in analysis of speech sounds and in recognition of spoken words

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48
Q

Where is Wernicke’s Area?

A

Region of auditory association cortex on left temporal lobe of humans

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49
Q

Being able to hear is one thing (___) and recognizing words (____) amd comprehending them (____)

A

primary auditory cortex, Wernicke’s area, Posterior Language Area

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50
Q

Pure word deafness: result of damage to

A

a small part of Wernicke’s area

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51
Q

Pure word deafness

A

Disorder of auditory word recognition, an inability to comprehend or repeat spoken words

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52
Q

Wernicke’s aphasia

A

features of transcortical sensory aphasia and pure word deafness, poor language comprehension, fluent speech production, but what they say is meaningless and typically filled with function words (not nouns, verbs, adjectives)

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53
Q

Wernicke’s aphasia results from

A

damage to both Wernicke’s area and PLA which means you have features of transcortical sensory aphasia and pure word deafness

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54
Q

What is pure alexia?

A

Disrupts ability to perceive written words, Cannot read, but writing skills are fine

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55
Q

Pure Alexia results from

A

damage to visual word-form area (VWFA)

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56
Q

visual word-form area VWFA is in the

A

fusiform gyrus of left hemisphere

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57
Q

What is surface dyslexia?

A

Inability to recognize whole-words, can only read phonetically, Irregularly spelled words are difficult to perceive

58
Q

What is phonological dyslexia?

A

can read familiar words but difficult to read unfamiliar or non-words

59
Q

What area controls speech production?

A

Broca’s area

60
Q

What is Broca’s aphasia

A

difficult for patients to express themselves verbally, slow non-fluent speech

61
Q

What is anomic aphasia?

A

hard time thinking of the word they want to say

62
Q

What is Anomia?

A

difficult in remembering appropriate word to describe object

63
Q

What is Circumlocution?

A

strategy by which people with anomia find alternative ways to say something when they are unable to think of the most appropriate word

64
Q

What can increase the risk of a stroke?

A

Atherosclerosis: process in which linings of arteries develop a layer of plaque, deposits of cholesterol, fats, calcium and cellular waste products

65
Q

What is an hemorrhagic stroke?

A

rupture of a cerebral blood vessel

66
Q

What is an ischemic stroke?

A

occlusion of a blood vessel

67
Q

Thrombus:

A

blood clot that forms within a blood vessel, which may block it and reduce blood flow to the affected area

68
Q

Embolus:

A

piece of matter (such as a blood clot, fat, or bacterial debris) that dislodges from its site or origin and occludes an artery

69
Q

In the brain an ___ can lead to a stroke

A

embolus

70
Q

To treat a stroke you can administer

A

drugs that dissolve blood clots in an attempt to reestablish circulation to an ischemic brain region

71
Q

Malignant tumor:

A

cancerous, lacks distinct border and may metastasize

72
Q

Non-malignant tumor:

A

non-cancerous, “benign” tumor, has distinct border and cannot metastasize

73
Q

How does a tumor affect the brain?

A

Compression: directly destroys brain tissue, or indirectly by blocking flow of CSF and causing hydrocephalus & Infiltration: occupying space and pushes against brain

74
Q

Example of malignant tumour

A

Glioma, Tumor initiating cells originate from the neural stem cells that make glia

75
Q

Example of Non-malignant tumour

A

meningioma, Composed of cells that constitute the meninges, often right between the two cerebral hemispheres

76
Q

What are the common causes of seizures?

A

Injury, stroke, tumor, developmental abnormality, high fevers, and withdrawal from GABA agonists, such as alcohol and barbiturates

77
Q

Neural network instability and increased risk of seizures can be because of genetic reasons, involving mutations that affect

A

Amount or function of different ion channels in the brain
The reciprocal wiring of excitatory and inhibitory neurons
Rules that govern synaptic plasticity

78
Q

Do all seizures cause convulsions?

A

No, in fact most do not
If neurons that make up motor system are involved, a seizure can cause a convulsion

79
Q

What are the different types of seizures?

A

Partial (focal) and generalized

80
Q

Partial seizure:

A

begins at a focus and remains localized, not generalizing to rest of brain

81
Q

A simple partial seizure:

A

does not produce loss of consciousness

82
Q

A complex partial seizure:

A

produces a loss of consciousness

83
Q

A Generalized seizure:

A

involves most of the brain

84
Q

What are the different types of generalized seizures?

A

Grand mal, atonic, absence

85
Q

Tonic-clonic:

A

grand mal that typically starts with an aura followed by a tonic phase and clonic phases, involves convulsion

86
Q

Aura:

A

sensation that precedes a seizure, exact nature depends on location of the seizure focus

87
Q

Tonic phase:

A

first phase, all skeletal muscles are contracted

88
Q

Clonic phase:

A

second phase, rhythmic jerking movements

89
Q

Absence (petite mal):

A

common in children, very brief seizures
Generalized complex seizures
People stop and stare into the distance, often blinking eye repeatedly

90
Q

Can seizure disorders be treated?

A

Yes, effectively with meds, usually benzos

91
Q

What is MS (multiple sclerosis)?

A

Autoimmune demyelinating disease
Usually occurs late 20s/30s
Certain genes can increases one’s susceptibility for getting MS, but generally a sporadic disease

92
Q

In MS, at scattered locations within the central nervous system, ___ are attacked by the ____

A

myelin sheaths, immune system

93
Q

In MS, normal transmission of ___ is interrupted because of ___

A

neural messages, demyelinated axons

94
Q

In MS, wide variety of neurological disorders are seen because

A

damage occurs in white matter located throughout brain and spinal cord

95
Q

Neurodegen. disease typically results from

A

large scale apoptosis

96
Q

Neurodegen. disease is triggered by

A

aggregates of misfolded proteins that disrupt normal cellular function, some conditions injure particular kinds of cells, others are more widespread

97
Q

What is prion protein disease?

A

Contagious brain disease whose degenerative process gives the brain a sponge-like appearance, eg. mad cow

98
Q

Accumulation of misfolded prion protein is responsible for

A

transmissible spongiform encephalopathies

99
Q

Prion:

A

misfolded proteins with the ability to transmit their misfolded shape onto normal variants of the same protein

100
Q

When a misfolded prion protein interacts with correctly folded prion proteins, it will…

A

cause them to misfold as wel

101
Q

What is Huntington’s disease caused by?

A

Caused by one dominant mutation in Huntingtin gene, Mutated protein tends to aggregate and over time this cause degeneration of neurons in these regions

102
Q

In Huntington’s the protein produced from the bad gene causes aggregates in the

A

basal ganglia, protein is heavily expressed in the input nuclei of the basal ganglia (the striatum - caudate nucleus and putamen)

103
Q

Huntington’s disease is characterized by

A

severe lack of coordination, uncontrollable jerky limb movements, and eventually dementia followed by death

104
Q

What is Parkinson’s disease associated with?

A

Associated with degeneration of dopamine neurons in the midbrain, specifically in the substantia nigra

105
Q

Parkinson’s disease is characterized by

A

Shaking, muscular rigidity, slowness of movement, eventually dementia

106
Q

Causes of Parkinson’s are largely unknown (genetic, environmental), however the death of midbrain ____ neurons seems to relate to aggregation to the protein ____

A

dopamine, alpha synculein

107
Q

Alpha-synuclein:

A

protein that is heavily expressed in dopamine neurons, tends to aggregate at some rate

108
Q

Lewy body:

A

aggregate of misfolded alpha-synuclein protein; found in the cytoplasm of midbrain dopamine neurons in Parkinson’s patients

109
Q

Reduced dopamine signaling in the ___ disrupts movement

A

basal ganglia

110
Q

L-dopa (as a treatment drug) has to be taken instead of dopamine because

A

Dopamine cannot cross the blood-brain barrier

111
Q

What other cellular components are involved in Parkinson’s disease?

A

Ubiquitin, parkin and proteasome

112
Q

Ubiquitin:

A

protein that is put on faulty/old/misfolded proteins, which targets them for degradation
Ubiquitinated proteins get brought to proteasomes, which breaks them into their constituent amino acids for recycling

113
Q

Parkin:

A

protein that plays a critical role ubiquitination
Mutated parkin is a cause of familial Parkinson’s disease
If parkin is defective, misfolded proteins accumulate, aggregate, and eventually kill the cell

114
Q

Proteasome:

A

organelle responsible for destroying ubiquitinated proteins within a cell
Dopaminergic neurons are especially sensitive to loss of parkin function and alpha-synuclein aggregation

115
Q

What is toxic gain of function?

A

Genetic disorder caused by a dominant gene mutation that produces a protein with toxic effects

116
Q

Mutations in alpha-synuclein gene cause

A

Parkinson’s

117
Q

Mutation in in huntingtin gene cause

A

Huntington’s

118
Q

What is loss of function?

A

Genetic disorder caused by recessive gene mutation that fails to produce a protein that is necessary to avoid problem

119
Q

example of loss of function

A

Loss of or mutations in the parkin gene can cause misfolded alpha-synuclein protein to not be degraded/discarded

120
Q

What is dementia?

A

Progressive impairments to memory, thinking and behavior as a result of a neurological disorder

121
Q

What is Alzhemier’s disease?

A

Neurodegenerative disorder that causes progressive memory loss, motor deficits and eventual death

122
Q

Alzheimer’s is associated with aggregates of misfolded ____ protein and severe degeneration within and around the ____ and ____

A

B-amyloid, hippocampus, neocortex

123
Q

B-amyloid precursor protein (APP):

A

gene for this protein is located on chromosome 21

124
Q

Secretase:

A

class of enzymes that cut the B-amyloid precursor protein into smaller fragments, including B-amyloid

125
Q

Presenilin:

A

protein that forms part of the secretases that cut APP

126
Q

Mutations in ___ can cause it to preferentially generate the abnormal long form B-amyloid, which causes early onset Alzheimer’s disease

A

Presenilin

127
Q

Apolipoprotein E (ApoE)

A

glycoprotein that transports cholesterol in the blood and plays a role in cellular repair

128
Q

Presence of the E4 allele of the ____ increases risk of late-onset Alzheimer’s disease

A

apoE gene

129
Q

What is ALS (amyotrophic lateral sclerosis)?

A

Motor neuron disease that attacks spinal cord and cranial nerve motor neurons

130
Q

ALS is characterized by

A

spasticity, exaggerated stretch reflexes, progressive weakness and muscular atrophy

131
Q

Is ALS genetic?

A

90% of cases are sporadic
Mutations in 2 or more genes are usually required to cause the disease
10% are inherited, 10-20% of these cases caused by mutation in the gene that produces the enzyme superoxide dismutase 1, found on chromosome 21

132
Q

(ALS) mutation in the gene that produces the enzyme superoxide dismutase 1 causes

A

toxic gain of function that leads to protein misfolding and aggregation, impaired axonal transport, and mitochondrial dysfunction

133
Q

What is schizophrenia?

A

Social withdrawal, disorganized thinking, abnormal speech and inability to understand reality
Affects ~1% of world’s population
Symptoms typically come on gradually, beginning in young adulthood
About 30-50% of patients do not believe they have an illness

134
Q

What are the symptoms of schizophrenia? 3 categories

A

Negative: absence of behaviors
Social withdrawal, reduced emotional expression, poverty of speech, reduced motivation
Typically emerge first
Cognitive: disorganized/irrational thinking
Deficits in learning and memory, poor abstract thinking and problem solving
Positive: presence of delusions
Of persecution, grandeur, control: beliefs that contradict reality
Hallucinations: perception of stimuli that are not actually present
Typically emerge last

135
Q

How can schizophrenia be treated?

A

Main treatment is medication, often in combination with psychological and social supports
Antipsychotics: target the positive symptoms of schizo: typically block the dopamine D2 receptors
But not negative

136
Q

What is the Dopamine Hypothesis?

A

Excessive D2 receptor activity underlies positive symptoms of schizo

137
Q

___ tend to elicit certain aspects of psychosis in people

A

Dopamine receptor agonists, like meth

138
Q

Possible that schizos have too little dopamine in the _____, and too much elsewhere

A

prefrontal cortex

139
Q
A
140
Q
A