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Intro to neuroscience > Lecture 8: Bridging human and animal neuroscience > Flashcards

Lecture 8: Bridging human and animal neuroscience Flashcards

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1
Q

Why do psychologists learn about animal neuroscience?

A

learning about functions from evolution
practical reasons
ethics
interesting
to understand human behavior via animal models

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2
Q

What are major similarities between humans and animals?

A

neurons and glia cells

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3
Q

What are major differences between humans and animals?

A

number of neurons and glia cells, structures

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4
Q

Why studying invertebrates is easier?

A

no ethical permission needed
genetic manipulations easier and faster
cheap
famous research: giant axon of squid

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5
Q

Why most labolatory animals are rats and mice?

A

there is already a lot of data; especially about mice genome; easy to keep and breed, pretty cheap, brain fairly similar to humans, genetic approaches possible

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6
Q

What are characteristics of human brain?

A

convoluted with bulges (gyri) and spaces (sulci)
neurons + glia cells
1300-1400 grams
mess in comparison to rodent brain

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7
Q

astrocytes

A

control the microenvironment around neurons, provide strutural integrity, important for maintaining blood-brain barrier

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8
Q

Why brains post-mortem are smaller?

A

because people who died are usually old and brain is affected by different diseases
major difference in rodent research: rodents are healthy!

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9
Q

Rodent brain

A

smooth, no gyrification
neurons and glia present
better organized than human brain

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10
Q

microglia

A

phagocytic -> they eat and clean staff, part of immune system
changes its shapes when deals with pathogens

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11
Q

oligodendrocytes

A

myelination of neurons in CNS

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12
Q

when myelination occurs in human CNS?

A

at 4 month of gestation (lasts until 2nd decade of life)

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13
Q

How can we study development of human brain?

A

studying children with EEG
sometimes, children may be placed in MRI scanner - due to disease
very rarely, studying children brains post-mortem

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14
Q

How does development of rodent brain relates to human brain?

A

humans are born after 9 months of pregnancy, rodents after 21 days of pregnancy - they look like half embryos

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15
Q

What happens when myelin sheeth fails?

A

multiple sclerosis (can be seen on the brain scan as white spots)

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16
Q

ependymal cells

A

line ventricular cavities and central canal of spinal cord
they sense what is going on in CSF via cilia

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17
Q

Schwann cells

A

responsible for myelination in PNS

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18
Q

What happens when your brain gets bigger evolutionary?

A

neuronal density gets smaller - fewer neurons per brain because they increase in size
however, glia density gets bigger - because they don’t grow over evolution as neurons

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19
Q

What happens if you damage primary motor cortex?

A

contralateral spastic paresis - weakening of voluntary movement contralateraly

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20
Q

What happens if you damage premotor cortex?

A

apraxias - inability to perform purposeful movement

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21
Q

prefrontal cortex

A

rostral to premotor area
1/4 of human cerebral cortex
organizing and planning of intellectual and emotional aspects of behavior

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22
Q

What happens if you lesion prefrontal cortex?

A

loss of concentration, distraction, lack of initiative, foresight and perspective, apathy, suckling and grasp reflexes evident; similar to what happens at the very end of Alzheimer’s disease

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23
Q

expressive aphasia

A

are in left or dominant hemisphere affected -> Broca’s area damage = difficulty in speech production

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24
Q

parietal lobe

A

place of sensory homunculus - postcentral gyrus
holds primary somatosensory cortex

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25
What happens if you lesion posterior parietal association cortex?
lesions in dominant hemisphere result in apraxia (difficulty with motor planning to perform tasks or movements) astereognosia may be present no loss of tactile sensations
26
What is astereognosia?
inability to recognize objects by touch
27
receptive aphasia
inability to comprehend spoken language, possible inability to read (alexia), there may be fluent verbalization BUT lacking meaning
28
Why is occipital lobe best studied in MRI?
because it lays closest to the coil
29
occipital lobe
primary visual cortex, homunuculus of an eye (retinal surface orderly represented)
30
what happens if you damage occipital lobe?
scotoma = black spots in vision hemianopsia = damage to right visual cortex causes lose of image from left eye and vice versa
31
temporal lobe
auditory cortex
32
what happens if you unilaterally lesion temporal lobe?
difficulties in locating sound in contralateral field
33
hippocampus
located in medial temporal lobe - important for learning, formation, organization, memory retrieval, mood, alertness, attention, spatial navigation
34
cerebellum
derived from metencephalon dorsal to pons and medulla fine tuning of movement and muscle coordination
35
what type of task would be difficult to perform for a person with lesion to cerebellum?
walking a line and then turning
36
what are other symptoms associated with cerebellar lesions?
tremour with intended movement without paralysis; ipsilateral symptoms, posture, gait
37
how can you differentiate tremour caused by cerebellar lesion from Parkinson's disease?
cerebellar lesion -> tremor with intended movement Parkinson's disease -> tremor at rest
38
thalamus
major relay for ascending tactile, visual, auditory, gustatory information to the neocortex
39
hypothalamus
essential for survival water balance adenohypophysis - anterior pituitary -> releasing factors neurohypophysis - posterior of pituitary gland -> hormones hunger autonomic regulation thermoregulation sexual urges
40
What is characteristic for people with tumor in hypothalamus?
they can easily get hypothermia or fever (environmentally dependent), often obese (no sense of hunger or satisfaction)
41
CSF
cerebrospinal fluid - creates buffor - so brain doesn't turn into pudding, produced by choroid plexus
42
4th ventricles
-> 2 lateral ventricles deep in each hemisphere -> 3rd ventricle midline diencephalon -> 4th ventricle dorsal surface of pons and upper medulla
43
hydrocephalus
water brain - neurological disorder caused by an abnormal buildup of cerebrospinal fluid in the ventricles (cavities) deep within the brain remedy - excess fluid is either drained to abdominal cavity or heart
44
capillary (general)
smallest blood vessel, surrounded by endothelial cells with small holes in-between - molecules can travel through them
45
How capillaries in the brain differ from general ones?
In the brain, there are no holes between surrounding enthothelial cells. Instead, there are tight junctions (astrocytes important for maintenance)
46
What are symptoms of Alzheimer's disease?
Alzheimer's patients show reverved development -> half of brain weigh post-mortum -> memory loss -> difficulty performing familiar tass -> problems with language -> disorienting time and place -> poor judgement -> problems with abstract thinking -> misplacing things -> mood/behavioral changes -> loss of initiative
47
what is neurological pathology in Alzheimer's disease?
brain filled with extracellular amyloid beta plaques (form in old brains) and neurofibrillary tangles (formed by hyper-phosphory-lated tau) synapse loss cell death
48
describe first (mild) stage of Alzheimer's disease
2-4 years; less energetic and spontaneous; getting lost, repetitive questions and conversations, losing things or misplacing them, noticable mood or personality changes
49
describe second (moderate) stage of Alzheimer's disease
2-10 years; clearly disabled, foregtting recent events and their personal history, disoriented, speech problems arise, reading and writing more difficult
50
describe third = last (severe) stage of Alzheimer's disease
1-3 years, loss of ability to feed oneself, speak, recognize other people, control bodily functions; memory worsens and may be almost non-existant, sleeping, grunting, moaning
51
what are Braak stages?
focus on brain pathology
52
are Braak stages corresponding to clinical progression of disease?
not really - often they don't match
53
Braak stage 0-II
cognition intact; AD pathology absent in areas involved in memory and cognition; PFC has no tangles, but might have plaques; hippocampus may have few tangles
54
Braak stage III-IV
mild cognitive impairment; in PFC plaque density increases dramatically; in hippocampus there is significant tangle pathology
55
Braak stage V-VI
full blown Alzheimer's; overt dementia, plaques and tangles can be observed throughout most brain areas
56
What is amyloid hypothesis in Alzheimer's disease?
theory states that due to accumulation of amyloid beta, neurons become more and more active until system breaks however, nowadays this hypothesis is questioned as accumulation of tau in hippocampus may be better explanatory factor
57
risk factors for Alzheimer's disease
after age 65 (rises sharply after age 75); genetics, women bias, Down syndrome, ApoE4 (gene)
58
mouse models of Alzheimer's disease
mouse don't develop amyloid plaques - but you can always inject them
59
What behavioral changes can be found in Alzheimer's mouse models?
in hidden platform paradigm, mouse keeps swimming and cannot remember location of the platform; model mouse is interested in both novel and old objects, whereas control is interested in novel objects solely
60
What other animal models can be used to study Alzheimer's disease?
fruit flies, worms
61
What are causes of Parkinson's disease?
idiopathic (unknown causes), may be related to environmental toxins (pesticides), viral infections and genetics
62
What is incidence of Parkinson's disease?
annually: 0.2/1000 prevalence: 1.5/1000 similar across the world (although lower in China and West-Africa) 1% of population above 55 y.o. 1.5% of population aged 70-79 y.o. sex incidence equal early onset correlated with genetic mutations
63
what is a difference between incidence and prevalence?
Incidence is a measure of the number of new cases of a characteristic that develop in a population in a specified time period; whereas prevalence is the proportion of a population who have a specific characteristic in a given time period.
64
What is neuropathology in Parkinson's disease?
depletion of pigmented dopamine neurons in substantia nigra; atrophic changes in substantia nigra and depletion of neurons in the locus coeruleus clinical features evident when 60-80% of dopamine neurons lost there are compensatory changes -> hyperactivity in remaining neurons, increase in dopamine receptors, receptor supersensitivity also other iron rich/pigmented nuclei affected (locus coeruleus and raphe) Lewy bodies
65
what are Lewy bodies?
abnormal aggregations of alpha synuclein protein
66
How to study Parkinson's disease?
SPECT, PET - how much dopamine binding occurs staining for Lewy bodies
67
How are animals models for Parkinson's disease made?
MTPT - chemical causing Parkinson
68
How in the old-days people dealt with Parkinson's disease?
lesion surgery (thalamus)
69
How nowadays Parkinson's disease is treated?
deep brain stimulation to subthalamic nucleus - modulating activity

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