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Physio > Chapter 14 > Flashcards

Chapter 14 Flashcards

1
Q

dyslexia

A

impairment in learning to read and write; probably the most common learning disability.

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2
Q

learning

A

Relatively permanent change in an organism’s behavior as a result of experience.

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3
Q

memory

A

ability to recall or recognize previous experience.

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4
Q

Pavlovian conditioning

A

Learning procedure whereby a neutral stimulus (such as a tone) comes to elicit a response because of its repeated pairing with some event (such as the delivery of food); also called classical conditioning or respondent conditioning.

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5
Q

memory trace

A

mental representation of the previous experience

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6
Q

eye-blink conditioning

A

commonly used experimental technique in which subjects learn to pair a formerly neutral stimulus with a defensive blinking response.

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7
Q

conditioned stimulus (Cs)

A

in pavlovian conditioning, an originally neutral stimulus that, after association with an unconditioned stimulus (ucs), triggers a conditioned response.

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8
Q

unconditioned stimulus (uCs)

A

a stimulus that unconditionally—naturally and automatically—triggers a response.

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9
Q

unconditioned response (uCR)

A

in classical conditioning, the unlearned, naturally occurring response to the unconditioned stimulus, such as salivation when food is in the mouth.

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10
Q

conditioned response (CR)

A

in pavlovian conditioning, the learned response to a formerly neutral conditioned stimulus (cs).

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11
Q

fear conditioning

A

learned association, a conditioned emotional response, between a neutral stimulus and a noxious event such as a shock.

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12
Q

operant conditioning

A

learning procedure in which the consequences (such as obtaining a reward) of a particular behavior (such as pressing a bar) increase or decrease the probability of the behavior occurring again; also called instrumental conditioning.

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13
Q

cerebellum

A

has circuits designed to pair various motor responses with environmen- tal events

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14
Q

what circuits are involved in fear conditioning?

A

Because the CR is emotional, circuits of the amygdala rather than the cerebellum mediate fear conditioning.

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15
Q

dissociation

A

a disconnect—occurs between the memory of the unconscious (or implicit) learning and explicit memory,

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16
Q

implicit memory

A

unconscious memory: subjects can demonstrate knowledge, such as a skill, conditioned response, or recalling events on prompting, but cannot explicitly retrieve the information.

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17
Q

amnesia

A

partial or total loss of memory.

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18
Q

explicit memory

A

conscious memory: subjects can retrieve an item and indicate that they know that the retrieved item is the correct item.

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19
Q

declarative memory

A

ability to recount what one knows, to detail the time, place, and circumstances of events; often lost in amnesia.

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20
Q

procedural memory

A

ability to recall a movement sequence or how to perform some act or behavior.

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21
Q

learning set

A

the “rules of the game;” implicit understanding of how a problem can be solved with a rule that can be applied in many different situations.

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22
Q

priming

A

using a stimulus to sensitize the nervous system to a later presentation of the same or a similar stimulus.

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23
Q

how in implicit information encoded?

A

data-driven, or bottom-up, processing

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24
Q

how in explicit information encoded?

A

depends on conceptually driven,or top-down,process- ing: the person reorganizes the data.

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25
Q

why is implicit memory difficult to recall spontaneously?

A

bc we have a passive role in encoding it, but will recall it more easily when there is priming

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26
Q

short term memory

A

information is held in memory only briefly, for a few minutes at most, and then discarded

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27
Q

long term memory

A

information is held in memory indefinitely, perhaps for a lifetime.

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28
Q

are implicit and explicit memories processed in the same way?

A

no

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29
Q

Frontal lobes play an important role in what

A

short-term memory

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30
Q

Temporal lobe plays a central role in what

A

long-term storage of verbal info

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31
Q

Where are motion and color processed?

A

carried out in different locations in the temporal lobe, and thus the activity linked with the memories of color and motion also might be dissociated.

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32
Q

what area does recall of color activate?

A

a region in the ventral temporal lobe, just anterior to the area controlling color perception,

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33
Q

what area doe recall of action words activate?

A

a region in the middle temporal gyrus, just anterior to the area controlling motion perception

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34
Q

autobiographical memory

A

personal memory

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35
Q

episodic memory

A

autobiographical memory for events pegged to specific place and time contexts.

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36
Q

what may cause episodic amnesia?

A

frontal lobe injuries

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37
Q

psychogenic amnesia

A

a massive reduction in brain activity in frontal regions that is remarkably similar to that seen in neurological patients with episodic amnesia

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38
Q

what did Lashley find?

A

the severity of the memory disturbance was related to the size of the injury rather than to its location

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39
Q

what does the basal ganglia play a role in?

A

motor control

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40
Q

entorhinal cortex

A

–Receives projections from Parahippocampal and Perirhinal cortices; integrative function — first area to show cell death in Alzheimer’s disease

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41
Q

parahippocampal cortex

A

–Receives connections from parietal cortex; believed to be involved in visuospatial processing

42
Q

perirhinal cortex

A

–Receives connections from the visual regions of the ventral stream; believed to be involved in visual object memory

43
Q

prime structures for explicit memory

A

medial temporal cortex (entorhinal cortex; parahippocampal cortex; perirhinal cortex), and the frontal cortex and structures closely related to them; subcortical hippocampus and amygdala,

44
Q

visual object memory

A

The prominent input from the neocortex to the perirhinal region is from the visual regions of the ventral stream coursing through the temporal lobe

45
Q

visuospatial memory,

A

the parahippocampal cortex has a strong input from regions of the parietal cortex believed to take part in visuospatial processing

46
Q

two principal neuronal changes take place in alzheimer’s disease:

A
  1. Loss of cholinergic cells in the basal forebrain 2. Development of neuritic plaques in the cerebral cortex. a neuritic plaque consists of a central core of homogeneous protein mate- rial (amyloid) surrounded by degenerative cellular fragments.
47
Q

Hippocampus and Spatial Memory

A

probably engaged in visuospatial memory processes required for places, such as recalling the location of an objec

48
Q

visuospatial learning

A

using visual information to recall an object’s location in space.

49
Q

neuritic plaque

A

area of incomplete necrosis (dead tissue) consisting of a central protein core (amyloid) surrounded by degenerative cellular fragments; often seen in the cortex of people with senile dementias such as alzheimer’s disease.

50
Q

reciprocal connections in explicit memory

A

The temporal pathway of explicit memory is reciprocal: connections from the neocortex run to the entorhinal cortex and then back to the neocortex

51
Q

benefits of reciprocal connections in explicit memory

A

1.Signals from the medial temporal regions back to the cortical sensory regions keep the sensory experience alive in the brain: the neural record of an experience outlasts the actual experience. 2. The pathway back to the neocortex means that it is kept apprised of information being processed in the medial temporal regions.

52
Q

what do people with frontal lobe injuries have trouble with?

A

have difficulties with memory for the temporal (time) order of events

53
Q

brain areas implicated in korsakoff’s syndrome

A

medial thalamus and mammillary bodies in the hypothalamus

54
Q

Korsakoff’s syndrome

A

permanent loss of the ability to learn new information (anterograde amnesia) and to retrieve old information (retrograde amnesia) caused by diencephalic damage resulting from chronic alcoholism or malnutrition that produces a vitamin b1 deficiency.

55
Q

retrograde amnesia

A

inability to remember events that took place before the onset of amnesia.

56
Q

anterograde amnesia

A

inability to remember events subsequent to a disturbance of the brain such as head trauma, electroconvulsive shock, or certain neurodegenerative diseases.

57
Q

consolidation

A

process of stabilizing a memory trace after learning.

58
Q

reconsolidation

A

process of restabilizing a memory trace after the memory is revisited.

59
Q

purpose of basal forebrain structures in short term memory?

A

hypothesized to play a role in maintaining appropriate levels of activity in the forebrain structures so that they can process information.

60
Q

purpose of temporal-lobe structures in short term memory?

A

hypothesized to be central to the formation of long-term explicit memories.

61
Q

purpose of the prefrontal cortex structures in short term memory?

A

central to the maintenance of temporary (short-term) explicit memories as well as memory for the recency (chronological order) of explicit events.

62
Q

role of hippocampus in memory?

A

hypothesis that the hippocampus consolidates new memories, a process that makes them permanent. Once they move, hippocampal involvement is no longer needed.

63
Q

Neural circuit for implicit memories

A

the basal ganglia receive input from the neocortex and send projections to the ventral thalamus and then to the premotor cortex. The basal ganglia also receive widely and densely distributed projections from dopamine-producing cells in the substantia nigra.

64
Q

what is necessary for circuits in the basal ganglia to function?

A

dopamine

65
Q

Does the neocortex receive direct information from the basal ganglia?

A

no–neocortex does not know about activities of the basal ganglia

66
Q

why are implicit memories unconscious?

A

this unidirectional flow accounts for the unconscious nature of implicit memories. For memories to be conscious, the neocortical regions involved must receive feedback, as they do in the explicit-memory system

67
Q

emotional memory

A

Memory for the affective properties of stimuli or events.

68
Q

what is involved in emotional memory?

A

amygdala; The amygdala seems to evoke our feelings of anxiety toward stimuli that by themselves would not normally produce fear.

69
Q

Damage to the amygdala

A

Damage to the amygdala abolishes emotional memory but has little effect on implicit or explicit memory.

70
Q

neural circuits for emotional memory

A

amygdala sends projections to the brainstem structures that control autonomic responses such as blood pressure and heart rate, to the hypothalamus that controls hormonal systems, and to the periaqueductal gray matter (PAG) that affects the perception of pain. The amygdala hooks in to the implicit- memory system through its connections with the basal ganglia.

71
Q

activating systems in emotional memory

A

emotionally driven hormonal and neurochemical activating systems (probably cholinergic and noradrenergic) stimulate the amygdala. The amygdala in turn modulates the laying down of emotional memory circuits in the rest of the brain, especially in the medial temporal and prefrontal regions and the basal ganglia.

72
Q

habituation

A

a weakened response to a stimulus

73
Q

sensitization

A

a strengthened response

74
Q

associative learning

A

Linkage of two or more unrelated stimuli to elicit a behavioral response.

75
Q

long-term potentiation (LTP),

A

Long-lasting increase in synaptic effectiveness after high frequency stimulation.

76
Q

long-term depression (LTD)

A

Long-lasting decrease in synaptic effectiveness after low- frequency electrical stimulation. 

77
Q

what is LTP a mechanism for?

A

creating memories

78
Q

what is LTD a mechanism for?

A

clearing out old memories

79
Q

LTP and synaptic change

A
  1. enhanced LTP in recruited pathways 2. LTP produces enduring changes in synaptic morphology
80
Q

What receptors are most active in LTP?

A

glutamate

81
Q

what does glutamate act on?

A

postsynaptic membrane—NMDA and AMPA

82
Q

what do AMPA receptors do?

A

mediate the responses produced when glutamate is released from a presynaptic membrane. They allow Na􏰅 ions to enter, depolarizing and thus excit- ing the postsynaptic membrane.

83
Q

steps of LTP and glutamate

A
  1. Because the NMDA receptor pore is blocked by a magnesium ion, release of glutamate by a weak electrical stimulation activates only the AMPA receptor. 2. A strong electrical stimulation can depolarize the postsynaptic membrane sufficiently that the magnesium ion is removed from the NMDA receptor pore. 3. Now glutamate, released by weak stimulation, can activate the NMDA receptor to allow Ca2+ influx, which, through a second messenger, increases the function or number of AMPA receptors or both.
84
Q

measuring synaptic change

A
  1. Measuring the extent of dendritic changes can infer synaptic change. 2. neurons change their structure in response to changing experiences 3. New synapses can result either from the growth of new axon terminals or from the formation of synapses along axons as they pass by dendrites
85
Q

creating new brain circuits

A

-The reason is not yet clear, but adult neurogenesis may enhance brain plasticity, particularly with respect to processes underlying learning and memory. -Experience appears to increase the generation of these new neurons

86
Q

How does the brain change with enriched experiences?

A

-an increase in brain weight that may be on the order of 10 percent relative to cage-reared animals, even though the enriched rats typically weigh less, in part because they get more exercise. -a coordinated change occurs not only in the extent of dendrites but also in glial, vascular, and metabolic processes in response to differential experiences -implies that experience not only can alter existing circuitry but also can influence the generation of new neurons and thus new circuitry

87
Q

can brain growth be manipulated experimentally?

A

yes–by placing a patch over the eye of a rat. A comparison of the neurons in the two hemispheres revealed that those in the visual cortex of the trained hemisphere had more extensive dendrites. The researchers concluded that some feature associated with the encoding, processing, or storage of visual input from training was responsible for forming new synapses because the hemispheres did not differ in other respects.

88
Q

Is the motor cortex just shaped by motor use?

A

No! the functional topography of the motor cortex is shaped by learning new motor skills, not simply by repetitive motor use.

89
Q

does the cortex vary depending on skills?

A

Yes! Thus, the functional organization of the motor cortex is altered by skilled use in hu- mans

90
Q

focal hand dystonia

A

abnormal finger and hand positions, cramps, and difficulty in coordinating hand and finger movements.

91
Q

Education and brain change

A

a relation between the size of the dendrites in Wernicke’s area and the amount of education. In the brains of deceased people with a college education, the cortical neurons from this language area had more dendritic branches than did those from people with a high-school education, which, in turn, had more dendritic material than did those from people with less education.

92
Q

methylation and memory

A

They showed that fear conditioning is associated with rapid methylation, but if they blocked methylation, there was no memory. The investigators conclude that epigenetic mechanisms mediate synaptic plasticity broadly, but especially in learn- ing and memory.

93
Q

Do gonadal hormones influence the brain?

A

yes, continue to influence cell structure and behavior in adulthood.

94
Q

estrogren and memory

A

women’s performance on various cognitive tasks changes throughout the menstrual cycle as their estrogen levels fluctuate; As the estrogen level rises, the number of synapses rises; as the estrogen level drops, the number of synapses declines.

95
Q

does estrogen influence all of the brain the same way?

A

estrogen’s influence on cell structure may be different in the hip- pocampus and neocortex

96
Q

Testosterone and memory

A

middle-aged men, who show a slow decline in tes- tosteronelevelsthatcorrelateswithadropinspatialability

97
Q

nerve growth factor (NGF)

A

Neurotrophic factor that stimulates neurons to grow dendrites and synapses and, in some cases, promotes the survival of neurons.

98
Q

what does the body produce when stressed?

A

the pituitary gland produces adrenocorticotrophic hormone (ACTH)

99
Q

adrenocorticotrophic hormone (ACTH)

A

which stimulates the adrenal cortex to produce steroid hormones known as glucocorticoids.

100
Q

what are glucocorticoids important for?

A

protein and carbohydrate metabolism, controlling sugar levels in the blood, and the absorption of sugar by cells, glucocorticoids have many actions on the body, including the brain.

101
Q

what do glucocorticoids kill with prolonged stress?

A

cells in the hippocampus

102
Q

Neurotrophic factors

A

chemical compounds that signal stem cells to develop into neurons or glia

Physio (20 decks)

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