Exam 4 Flashcards

(42 cards)

1
Q

What is Retrograded amnesia

A

The inability to remember events prior to impairment.

Caused by damage to the entire hippocampal formation which can extend back 15 years or more.
extensive impairment occurs with broader damage or deterioration (Alzheimer’s, Parkinson’s, Huntington’s disease.

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2
Q

What is Anterograde amnesia

A

An impairment in forming new memories

Damage in CA1 part in both hippocami cause moderate anterograde amnesia but severe is damage include the rest of the hippocampus

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3
Q

Memory consolidation and physiology of this process

A

The process in which the brain forms a more or less permanent physical representation of a memory.
Hippocampus and adjacent cortex seem to be activated during consolidation.

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4
Q

How is the temporal cortex involved in memory function and consolidation?

A

It include the hippocampus which stores new memories temporaily before they are later moved to the prefrontal cortex

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5
Q

How is the prefrontal cortex role involved in memory function and consolidation?

A

It is responsible for encoding new memories and retrieval of old memories

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6
Q

Neurotransmitters involved in memory function and consolidation

A

Increasing dopamine levels by injecting the dopamine precursor levodopa improves memory in humans.

Glutamate receptors being blocked, disables the hippocampi resulting in impaired retrival and consolidation.

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7
Q

The physiology of LTP/learning

A

Long-term potential (LTP) is a persistent strengthening of synapses that result from the stimultaneous activation of presynaptic and postsynapic neurons. Appears to be a characteristic of much of neural tissue in areas likeily involved in learning.
Includes: Hippocampus; visual, auditory and motor cortex.

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8
Q

LTP & the NMDA Receptors

A

Initially, glutamate activates the AMDA receptors but not the NMDA receptors, which are blocked by magnesium ions. However, if the activation is strong enough to partially depolarize the postsynaptic membrane, the magnesium ions are ejcted. The NMDA receptors can then be activated, allowing sodium and calcium ions to enter.

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9
Q

Where are certain types of memories stored in the cortex?

A

Long-term memory= hippocampus
Explicit memories= hippocampus
Short-term memory= prefrontal cortex
Spatial Memory= Hippocampus and medial entorhinal cortex.
Procedural Memory (Motor Skills)= Cerebellum.
Emotional Memory= Amygdala.
Visual Memory= Frontal and occipital lobes.
Auditory Memory= Auditory cortex, including the superior temporal lobe

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10
Q

Iconic Memory

A
  • Holds visual information ~500 ms
  • Neurons in occipital lobe responsible for holding incoming visual input
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11
Q

Echoic Memory

A
  • Holds auditory information ~3 seconds
  • Neurons in temporal lobe responsible for holding incoming auditory input
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12
Q

Haptic Memory

A
  • Holds somatosensory information 150 ms – 10 sec (10,000 ms) depending on
    receptor type
  • Neurons in parietal lobe responsible for holding incoming somatosensory input
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13
Q

Donald Hebb; The Hebb Rule

A

The principle stating that if an axon of a presynaptic neuron is active while the postsynaptic neuron is firing, the synapse between them will be strengthened.

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14
Q

How does sleep/ napping impact consolidation and performance?

A

Hippocampus tranfers info to the cortex during times of rest.
Human EGG and PET studies show the hippocampus repeatedly activating the cortical areas that participated in the daytime learning, and reactivation was accompanied by significant task improvement the next morning w/o further practice.

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15
Q

Reconsolidation and vulnerability

A

The process where a previously formed memory, after being retrieved, becomes temporarily vulnerable to modification or even disruption.
Our brain does this because it helps in responding to a changing enviroment by weakening a now irrelevant memory or strengthening an adaptive one.

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16
Q

Dementia and physiology/causes (e.g neurofibrillary tangles, beta amyloid)

A

Substantial loss of memory and other cognitive abilities.
Most common is Alzheimer’s disease (60-80%), a disorder characterized by progressive brain deterioration and impaired memory and other cogntive abilities.
Clumps of beta amyloid (plaques) cluster among axon terminals and interfere with neural transmission.
The ratio of AB42 to AB40 leads to the accumulation of the protein tau to form neurofibrillary tangles inside neurons; tangles are associated with the death of brain cells.

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17
Q

Brain regions and IQ

A

Overall, larger brain size and volume is associated with better cognitive functioning and higher intelligence. The specific regions that show the most robust correlation between volume and intelligence are the frontal, temporal and parietal lobes of the brain

18
Q

What is the PFIT theory?

A

General intelligence depends on how well parietial and frontal brain networks integrate with each other.

19
Q

What are the gender differences in IQ and brain physiology?

A
  • No major differences in general IQ, but some subtest differences
  • Women tend to show slightly better verbal abilities (gray matter increased in frontal areas)
  • Men tend to show slightly better visuospatial abilities and higher variability in quantitative abilities (gray matter increased in frontal and parietal lobes)
  • differences could be due to social effects or sexual dimorphism in the brain
20
Q

How does IQ impact glucose usage?

A

Brains of people with higher IQ use __less_ glucose
Higher IQ = more efficient brain

Brains of people with lower IQ use __more_ glucose (they have to think harder so use more brain power)

21
Q

What is the heritability of IQ?

A

Averages at 50% but increases with age, from 41% in childhood to 55% in adolescence and 66% in adulthood.

22
Q

What is the importance of myelin for IQ?

A

increased white matter, equals increased myelin, = faster neural conduction and nerve conduction velocity.

Myelination, speed of info processing, and intelligence all follow a curvilinear time path, increasing from childhood to maturnity and then declining in old age.

23
Q

What is the Flynn Effect??

A

A worldwide increase in IQ scores over the last several decades, at a rate of about 3 points per decade, IQ Increase of 5-25 points with every generation

24
Q

What is the heritability of Schizophrenia?

A

Familial disorder, increases with genetic closeness. Identical twin are three times at higher risk if one twin has it compared to faternal twins.

25
What is the heritability of Depression?
children of parents with depression are two to three times more likeily to develop depression themselves.
26
What are the theories of Schizophrenia?
The vulnerability model Dopamine Hypothesis (DA) Glutamate Theory Serotonin Theory
27
The Vulnerability Model
Some threshold of casual forces must be exceeded for the illness to occur; enviromental challenges combine witha person's genetic vulnerability to exceed that threshold
28
The Dopamine Hypothesis
Schizophrenia involves excessive dopamine activity in the brain. 1st Generation antipsychotics, though effective, often produce tardive dyskinesia. Atypical antipsychotics target D2 receptors less; help resistant cases through action on serotonin synapses
29
The Glutamate Theory
Hypofunction of NMDA receptors result in increases in glutamate and downstream increases in dopamine, which together produce positive and negative symptoms. increasing glutamate amounts through direct administration of glycine decreases positive and negative symptoms.
30
Serotonin Theory
It is though serotonin also influences positive symptoms. Drugs that affect 5-HT- hallucinations. Atypicals block 5-HT receptors which could decrease hallucinations.
31
What brain regions differ in patients with Schizophrenia?
Reduced gray matter and limbic area volume, sometimes resulting in increased ventricular size. Hypofrontality due to disrupted communication between the hippocampus and the prefrontal cortex. Neural connections and synchrony are decreased between brain areas including reduced white matter and impaired auditory gating. Hallucination are due to hyper-excitability in sensory areas.
32
SLC6A4 serotonin transport gene
Some studies have indicated that the so-called short allele of the 5-HTTLPR segment of the serotonin transporter gene (SLC6A4) contributes to depression in individuals exposed to high levels of stress. But other results have been negative and, and even meta-analyses disagree.
33
SSRIs
Selective serotonin reuptake inhibitors. Tricyclic antidepressants block reuptake (like SSRIs) ex: Prozac (fluoxetine), an atypical (second generation) antidepressant affects a single neurotransmitter.
34
MAOIs
Monoamine oxidase inhibitors (MAOI) block MAO. Some antidepressantscan increase the activity of norepinephrine or serotonin or both, at the synapses by blocking the destruction of excess monoamine by enymes in the terminals.
35
Impacts of depression on stages of sleep?
Circadian rhythm tends to be phase advanced in patients with affective disorders; so the person feels sleepy early in the evening and then wakes up in the early morning hours, regardless of the previous evening's bedtime. The person also enter rapid eye movement sleep earlier in the night and spends more time in this state than normal.
36
Explain seasonal depression and how regions of the PFC are affected seasonally
Some people's depression rises and falls with the seasons and is known as seasonal affective disorder (SAD). Follows a circannual rhythm, one that follows the changes of seasons. Studies have indicated that reduced sunlight exposure can impact serotonin levels and may lead to underactivity in certain PFC regions in people with SAD
37
List Affective Disorders brain regions that are active/change.
The brain scan picture; The middle rowm shows the sudden increase in activity during a manic episode, just a day after the previous scan during deepression. In the bottom row, the patient had returned to the depressed state. The dark areas in the subgenual prefrontal cortex indicate decreased activity during depression. Comparison of groups show that activity in the subgenual PFC is lower during depression and higher during mania, which suggest that it controls cycling between depression and mania.
38
Theories of sleep and dreaming
39
Brain regions associated with sleep
40
Neurotransmitters associated with sleep
**Acetylcholine and glutamate:** High during wakefulness and REM **Histamine:** High during wakefulness, low during sleep; Lower during REM and NREM **Norepinephrine and serotonin:** High during wakefulness; Lower during NREM; No activity during REM 16 **Adenosine:** Builds up during wakefulness; Gradually drops during sleep; Caffeine blocks adenosine receptors **Melatonin:** Onset of dark cycle; Surge before “opening of sleep gate”
41
Hormones associated with sleep
INcreased secretion of cortisol and adrenocorticotropic hormone during the night causes insomnia.
42
Circadian Rythms
A rythm that is about a day in length; the term circadian comes from the Latin circa meaning "approximately" and dia, meaning "day"