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Cognitive Neuroscience > Brain Structure Slides > Flashcards

Brain Structure Slides Flashcards

1
Q

Thomas Willis

A
  • coined term neurology
  • known for circle of willis
  • first anatomist to link brain structure with behaviour
  • started the field of cog neuro
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2
Q

Franz Gall

A
  • known for phrenology
  • localization of function
  • not a scientist
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3
Q

marie jean pierre flourens

A
  • best known for whole brain theory
  • first to show localization of function through animal brain lesion studies
  • no area responsible for higher functions
  • coined “aggregate field theory” - faculties of perception and volition are one faculty
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4
Q

john hughlings jackson

A
  • best known for human neuropsychology
  • observed behaviour of patients with brain damage
  • noticed that seizure progressed in a stereotypical manner form one body part to another
  • led to the idea of topographic organization
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5
Q

paul broca

A
  • best known for broca’s area
  • patient tan - large left hemisphere lesion
  • speech production
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6
Q

carl wernicke

A
  • best known for Wernicke’s area
  • speech comprehension
  • damage to posterior left hemisphere at temporal-parietal junction
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7
Q

wilder penfield

A
  • best known for mapping humonculus
  • how biology shapes behaviour
  • used electrical stimulation to map sensorimotor cortices
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8
Q

Donald hebb

A
  • psych and bio cannot be separated
  • best known for hebbian synapse
  • “cells that fire together wire together”
  • brain is always active even without external input
  • beginnings of neural networks
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9
Q

cajal’s neuron doctrine

A

refer to connectional specificity and dynamic polarization

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10
Q

connectional specificity

A

cells are separate and connections among neurons are not random. circuits pass information through specific pathways

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11
Q

dynamic polarization

A

portions of neurons are for different purposes: some for gathering information, some for outputting information

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12
Q

difference between dendrites and axons

A

dendrites receive - axons send information

in between is the synapse

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13
Q

glial cells make up how much of the brain’s volume

A

half

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14
Q

astrocytes

A
  • surround neurons and connect to blood vessels
  • transport substances from blood to neuron
  • gating - lets in some substances, keeps out others
  • barrier is called Blood Brain Barrier (BBB) which protects the CNS from dangerous agents in blood
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15
Q

microglial cells

A

remove damaged cells

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16
Q

oligodendrocytes

A

form myelin to wrap around axons in the CNS: can cover several axons

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17
Q

Schwann cells

A

form myelin to surround axons in PNS, can only cover one axon

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18
Q

multiple sclerosis

A

damage to myelin sheath in PNS or CNS or both

  • cause unknown, probably auto-immune
  • symptoms depend on which neurons are being de-myelinated
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19
Q

first stage of neuronal signaling

A

neurons receive information through chemicals (neurotransmitters, environmental, or physical)

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20
Q

second stage of neuronal signaling

A

signals from chemicals initiate changes in the membrane of the neuron that allow electrical current to flow

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21
Q

third stage of neuronal signaling

A

electrical currents, if strong enough, spike during transmission and create an action potential

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22
Q

4th stage of neuronal signaling

A

action potentials transmit signal down axon to terminal buttons

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23
Q

5th stage of neuronal signaling

A

terminal buttons release neurotransmitters to next neuron

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24
Q

depolarization

A

makes the neuron LESS negatively charged - this gain can reach threshold for an action potential.

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25
Q

action potential

A

rapid depolarization and repolarization of membrane

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26
Q

hyperpolarization leads to..

A

refractory period

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27
Q

saltatory conduction

A

nodes between myelin sheath allows the action potential to travel down the axon more quickly

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28
Q

large diameter axons conduct signals slower or faster? why?

A

faster due to decreased axon resistance

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29
Q

what can cause an action potential signal to flow faster?

A

increase in membrane resistance or decrease of axon resistance

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30
Q

nodes

A

breaks among the myelin sheath where action potentials can occur

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31
Q

first step of chemical transmission

A

action potential arrives at axon terminals which leads to depolarization

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32
Q

second step of chemical transmission

A

vesicles containing neurotransmitters fuse with membrane and release into synaptic cleft

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33
Q

third step of chemical transmission

A

transmitter diffuses across cleft and binds with receptors on postsynaptic dendrite

34
Q

4th step of chemical transmission

A

initiates changes in dendrite membrane of postsynaptic neuron - either depolarization (leads to AP) or hyperpolarization (away from AP)

35
Q

5th step of chemical transmission

A

if depolarization – EPSP –> Action Potential

36
Q

EPSP

A

excitatory post synaptic potential - leads to action potential

37
Q

IPSP

A

inhibitory post synaptic potential - less likely to generate action potential

38
Q

5 common excitatory neurotransmitters

A 
acetylcholine
glutamate
histamine
serotonin
some neuropeptides
39
Q

3 common inhibitory neurotransmitters

A

GABA
glycine
some neuropeptides

40
Q

3 methods of neurotransmitter inactivation

A
  1. active reuptake back into presynaptic terminal (dopamine, serotonin)
  2. enzymatic breakdown (Ach)
  3. diffusion away from cleft.
41
Q

autoreceptor function

A
  • located on presynaptic cleft

- monitor amount of NT in cleft

42
Q

3 ways that drugs can change NT transmission

A
  1. mimicking the action of the NT on the postsynaptic receptor
  2. blocking the receptor
  3. manipulate reuptake
43
Q

agonists

A

agents that mimic NT or increase levels of NT

44
Q

antagonist

A

agents that prevent normal action of NT by binding to receptors and blocking

45
Q

gray matter

A

capillary beds and neurons

46
Q

white matter

A

axons

47
Q

nucleus or layers

A

groups of cell bodies

48
Q

tract

A

collection of axons from a nucleus

49
Q

gyri

A

bumps

50
Q

sulci

A

grooves

51
Q

cortex

A

outer layer of brain

made up of dendrites and some axons

52
Q

anatomical divisions of cerebral cortex (4 lobes)

A

frontal lobe
parietal lobe
temporal lobe
occipital lobe

53
Q

functional localization

A

idea that there are specific locations in the brain of given functions (mostly debunked)

54
Q

caveats to functional localization (3)

A
  1. functions are localized via brain damage and neuroimaging (imperfect methods)
    - functions are predominantly in one area, but are parts of systems which can recruit several areas
    - functions are often localized through specific tasks, and may be involved in many other tasks, not exhaustive
55
Q

occipital lobe

A

contains visual pathways

56
Q

pathways from V1

A

primary visual cortex
association cortices
projections to entire brain
-more in visual processing slides

57
Q

deficits caused by damage to occipital lobe

A

visual field deficits

color identification deficits

58
Q

pathway into V1 (occipital lobe)

A

optic nerve - LGN - v1

extra striate cortex

59
Q

hippocampal formation is in which lobe?

A

temporal

60
Q

auditory cortex is in which lobe?

A

temporal

61
Q

fusiform gyrus (function and lobe location)

A

Function: important visual association cortex
location: temporal lobe

62
Q

superior temporal gyrus (function and lobe)

A

function: important for language system
location: temporal lobe

63
Q

3 functions of temporal lobe

A
  1. superior portion
  2. inferior portion
  3. medial portion
64
Q

function of superior portion of temporal lobe

A

sound processing and analysis - highly connected to language system

65
Q

function of inferior portion of temporal lobe

A

visual processing: highly connected to occipital lobe and frontal areas.

66
Q

function of medial portions of temporal lobe

A

hippocampal formation for memory and spatial processing

67
Q

major structures of parietal lobe

A

primary somatosensory cortex
posterior parietal cortex
angular gyrus

68
Q

function of posterior parietal cortex

A

integration of visual, motor, auditory

divided into supramarginal and angular

69
Q

function of angular gyrus (of parietal cortex)

A

reading, writing

70
Q

4 functions of parietal lobe

A

mathematical processing
spatial processing
writing and reading systems
attention

71
Q

damage to parietal lobes causes…(6)

A 
tactile processing problem
academic skill deficits
left right confusion
body orientation problems
optic ataxia
neglect
72
Q

3 motor function structures of frontal lobe

A

primary motor cortex
pre-motor cortex
supplementary motor cortex

73
Q

function of primary motor cortex

A

effector movement control

74
Q

function of pre-motor cortex

A

lateral surface, motor programs initiated by external stimuli

75
Q

supplementary motor cortex function

A

programs initiated by internal control

76
Q

other structures of the frontal lobe (4)

A

prefrontal cortex
dorsal-lateral prefrontal
ventromedial prefrontal
orbitofrontal

77
Q

function of the prefrontal cortex

A

planning movement, integration of info over time

EXECUTIVE FUNCTION

78
Q

function of dorsal-lateral prefrontal

A

motor association cortices

79
Q

ventromedial prefrontal

A

speech, motor control, sequencing

80
Q

orbitofrontal

A

smell, taste

81
Q

issues caused by damage to frontal lobe (8)

A 
sequencing
decision making
attention
personality
problem solving
verbal expression
spontaneity
emotional control
movement initiation
82
Q

brain protection

A

cerebral spinal fluid (CSF) protects from shock and changes in pressure
made by glial cells in ventricles

Cognitive Neuroscience (4 decks)

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