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research methods > Neuro Exam 4 > Flashcards

Neuro Exam 4 Flashcards

1
Q

Neural Tube Development

A

-Ectoderm (top layer) becomes nervous system and skin
-Mesoderm
-Endoderm (lining closest to mom)
-Primitive streak (middle indention that eventually forms neural tube)
-Notocord (cartilage providing structure to embryo and increases gene expression-eventually becomes vertebra)
-neural crest
-neural tube (becomes spinal cord and brain)

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2
Q

Neurogenesis Step

A

-First Step of cellular development
-creation of neurons mostly around center of neural tube

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3
Q

Migration Step

A

-second step of cellular development
-neurons move from site of origin in neuronal plate to where they are supposed to be in the central nervous system.

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4
Q

Differentiation Step

A

-third step of cellular development
-each cell becomes a specific type of neuron or glial cell

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5
Q

Synpatogenesis Step

A

-fourth step of cellular development
-axons and dendrites extend to form many synapses

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6
Q

Apoptosis Step

A

-fifth step of cellular development
-cells that die off early in development

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7
Q

Synapse Rearrangement

A

-sixth step of cellular development
-synapses change and make new connections to other cells

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8
Q

Myelogenesis Step

A

-seventh step of cellular development
-creation of myelin sheaths

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9
Q

Radial Glial Cells

A

-Early glial cells in neural tube
-neurons wrap around glial cells and climb (like climbing a rope)

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10
Q

Gliogenesis

A

development of glial cells

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11
Q

Neurotrophins

A

proteins that support the development of neurons

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12
Q

Chemokines

A

proteins that induce directional movement of leukocytes

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13
Q

Synaptic Plasticity

A

as spine is used, changes in shape allow for stronger connections

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14
Q

Dendritic spine types

A

-Filopodia (squiggle)-least mature
-long thin
-thin
-stubby
-mushroom
-branched (most mature)

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15
Q

Synaptic Pruning

A

brain produces many neurons, then goes back through and selects the ones that works the best (efficient)

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16
Q

Differences in serotonin during development

A

sourced from the placenta

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17
Q

Differences in GABA during development

A

GABA acts as excitatory even though its usually inhibitory (fetus has high Cl and Na which is opposite from adults)

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18
Q

Adult Neurogenesis

A

Neurogenesis declines as we age resulting in less plasticity

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19
Q

myosin

A

Protein that makes up muscles. Myosin heads grab onto actin ropes to pull and shorten muscle (contraction).

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20
Q

actin

A

Protein that makes up muscles. Contributes to muscle contraction.

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21
Q

muscle fiber

A

large cells that make up muscles

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22
Q

myofibril

A

groups of parallel contracting fibers that make up muscle fibers

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23
Q

sarcomere

A

composed of actin and myosin

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24
Q

neuromuscular junctions/acetylcholine

A

-neuron talking to the muscle
-acetylcholine cues actin and myosin to interact
-myosin heads grab onto actin ropes and pull into middle to shorten muscle (contract)

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25
Q

cross-bridge mechanism

A

bridge between actin and myosin

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26
Q

proprioception

A

-sensation which tells the body how it’s positioned/moving
-“what body pose am in in?”

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27
Q

muscle spindles

A

-receptor sensor
-stretch receptors that detect changes in the length of a muscle

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28
Q

golgi tendon organs

A

-receptor sensor
-manage muscle tension
-in tendons

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29
Q

dorsal root

A

transmits sensory info from peripheral to central nervous system

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30
Q

ventral root

A

transmits motor info from spinal cord to rest of the body

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31
Q

efferent

A

-AWAY from brain
-dorsal and sensory

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32
Q

afferent

A

-TO the brain
-ventral and motor

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33
Q

decussation

A

Medulla crossover. Relaying of one side of the brain to the other (sending messages)

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34
Q

Brainstem in relation to motor movement

A

Mediator for sensory and motor messages (cranial nerves)

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35
Q

primary motor cortex

A

-CEO of motor control
-initiates messages from brain to brain stem
-located in dorsal portion of frontal lobe across top of brain

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36
Q

non-primary motor cortex

A

-Sits in front of PMC consisting of the supplementary motor cortex and premotor cortex
-Not much is known other than it’s the first consultant to brain messages
-SMA seems to help posture, temporal coordination, and bimanual movements
-think control and understanding movements of others

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37
Q

basal ganglia functions

A

-second consultant to brain messages
-determines strength of a particular movement and its intensity
-patterns like walking
-balance between opposing muscles
-“Go, no go?” signaling

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38
Q

Basal Ganglia areas

A

1.Dorsal Striatum (caudate nucleus & Putamen)
2. Globus Pallidus (external and internal)
3. Subthalamic Nucleus (STN)
4. Substantia Nigra (reticulata/parscompacta)
-Works as a chain, each modifying a message, then gets sent back to cortex
SNR(reticulata) & GPI(internal) are a team

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39
Q

direct pathways

A

Movement (the “Go”)

40
Q

indirect pathways

A

Inhibition of movement (“no go”)

41
Q

Parkinson’s Disease

A

-degenerative disease caused by loss of dopamine cells in substantia nigra over time
-symptoms= tremors, altered posture, impaired gait, muscle rigidity, slower movement
-treatments= dopaminergic drug(Ldopa), deep brain stimulation(implanted electrodes)

42
Q

deep brain stimulation

A

-treatment for Parkinson’s
-used when drug treatment doesn’t work
-theory that it works by stimulating remaining dopaminergic neurons

43
Q

cerebellum

A

-balance, coordination, posture
-can effect emotions and cognition
cerebellar ataxia= odd walk, difficulty balancing, issues with targeting, eyes don’t move smoothly
peduncles=what connects cerebellum to brainstem

44
Q

Ataxia

A

odd walk, difficulty balancing, issues with targeting, eyes don’t move smoothly

45
Q

Dysarthria

A

trouble speaking due to weak speech muscles

46
Q

Dysmetria

A

unable to control distance, speed, and range of motion to perform a smoothly coordinated movement (over/under reach for an object)

47
Q

Dysdiadochokinesis

A

inability to perform rapid alternating muscle movements (finger tapping)

48
Q

Gait

A

impaired walking

49
Q

postural instability

A

can’t maintain equilibrium standing still or in movement

50
Q

Oculomotor

A

Unable to control eye movement

51
Q

Intentional Tremor

A

intense shaking which worsens as one gets closer to grabbing target

52
Q

Order of messaging within the motor system

A

PMC, NMC, basal ganglia & cerebellum, back to cortex through thalamus, out through brainstem and spinal cord

53
Q

free nerve endings

A

Pain receptors in epidermis (outermost layer)
-detect pain and temperature
-chemoreceptors (chemicals)
-thermoreceptors (temperature)
-cutaneous mechanoreceptors (touch/bruises/cuts)

54
Q

Merkel’s Discs

A

-located in dermis (second layer)
-slow adapting
-accurate with location of touch
-vesicles pop releasing neurotransmitter

55
Q

Meissner’s Corpuscle

A

-located in dermis (second layer)
-touch
-fast adapting
-accurate with location of touch
-discs shift opening ion channels

56
Q

Hair Follicle Receptors

A

-located in dermis (second layer)
-wraps around base of hair follicle
-when hair stretches, it opens ion channels

57
Q

Pacinian Corpuscle

A

-located in hypodermis (third layer)
-gauges how much pressure is received
-detects vibrations
fast adapting, but hard to detect location of vibration
-ion channels open when spring is stretched

58
Q

Ruffini’s Endings

A

-located in hypodermis (third layer)
-detects stretch
-slow adapting and hard to detect where stretch originates

59
Q

Pathway from sensory receptor to primary somatosensory cortex

A

-touch receptors release action potentials
-message is sent to the spinal cord
-sent to medulla
-sent to thalamus
-thalamus sends message to somatosensory cortex

60
Q

seudounipolar sensory cells

A

-very long neurons
-reaches organs in periphery while also reaching spinal cord

61
Q

Decussation motor vs. sensory

A

motor=medulla
sensory=thalamus

62
Q

Primary somatosensory cortex & somatotopic map

A

located in anterior (front) part of the parietal lobe

63
Q

changes in cortex following changes in sensory exposure

A

repeated exposure to something can lead to larger amount of cortex being designated to that given body part (trained).

64
Q

phantom limb pains

A

-neighboring functions to area designated to lost limb can’t always take over
-designated area still sends signals to a limb that’s not there
-pain is response to no confirmation from the area back to the brain
-brain thinks signal wasn’t received!

65
Q

TRP Channels

A

blend/combination of free nerve ending receptors (ex. heat and chemical pain)

66
Q

A- Alpha fibers

A

-largest and fastest (plane)
-info about proprioception
-myelinated

67
Q

A-Beta fibers

A

-second largest and second fastest (race car)
-info about touch
-myelinated

68
Q

A-Delta fibers

A

-less fast and smaller (biking)
-mechanical and thermal pain
-myelinated

69
Q

C fibers

A

-slowest and smallest (walking)
-mechanical, thermal, AND chemical
-non-myelinated

70
Q

“Types” of schizophrenia

A

disorganized, paranoid, catatonic

71
Q

positive schizophrenia symptoms

A

-hallucinations
-delusions
-disorganized thoughts and speech
-movement disorders (catatonic)

72
Q

negative schizophrenia symptoms

A

-flat affect (don’t show emotion)
-lack of pleasure
-lack of motivation
-withdrawal, little dialogue
-lack of self care

73
Q

cognitive schizophrenia symptoms

A

-poor executive functioning
-trouble focusing
-poor working memory

74
Q

Hallucinations

A

false perception of the senses (touch, taste, sight, hearing, seeing, smell)

75
Q

Delusions

A

false beliefs (“someone’s trying to kill me”)

76
Q

Age of onset for schizophrenia

A

around 25 years old

77
Q

Heritability of schizophrenia

A

not always genetic but stronger between twins, siblings, and children

78
Q

Environmental factors effecting schizophrenia

A

-born in urban areas
-maternal viral or parisite infections
-paternal age
-insufficient prenatal nutrition
-stress
-drug use

79
Q

Neurodevelopmental Theory

A

genetic or environmental events during early developmental periods increased risk of schizophrenia
-overlaps with multiple genetic disorders
-male bias
-physical congenital abnormalities predict schizophrenia (ex. low set ears)

80
Q

Neurodegenerative Theory

A

degenerative diseases like Alzheimer’s can put one at risk for schizophrenia

81
Q

Neurotransmitter Theories

A

influenced by pharmacological research and treatments for schizophrenia

82
Q

Dopamine Hypothesis

A

-excess of dopamine/receptors

83
Q

Serotonin Theory

A

-some psychedelic drugs are serotonin agonists and produce hallucinations
-some serotonin antagonists reduce symptoms

84
Q

Glutamate Theory

A

-under-stimulation of receptors
-excessive glutamatergic activity may cause excitotoxisity

85
Q

Neuroinflammation Theory

A

symptoms are due to brain inflammation
-higher levels of microglia in people at risk & with schizophrenia which causes inflammation

86
Q

Unification of schizophrenia theories

A

all theories for onset of schizophrenia play a role together

87
Q

Major Depressive Disorder Criteria and Symptoms

A

-depressed mood
-anhedonia
-weight loss/gain
-oversleep/lack of sleep
-fatigue/loss of energy
-psychomotor agitation or retardation
-feelings of worthlessness/ guilt
-indecisive/lack of concentration
-recurrent thoughts of death

88
Q

Hippocampus changes in stress and depression

A

-shrinks when stressed

89
Q

Functional brain changes in depression

A

-increased activity in prefrontal cortex and amygdala (amygdala won’t stfu so cortex tries to overcompensate)
-decreased activity in parietal, temporal, and anterior cingulate (brain fog, sad, memory)

90
Q

Sleep disturbances in depression

A

-difficulty falling and staying asleep
-enter REM early
-REM pattern disturbed

91
Q

Drugs used to treat depression

A

MAOIs, tricyclics, SSRIs

92
Q

Significance of the delayed effectiveness of antidepressant drugs

A

don’t notice the impact until person taking the antidepressant falls into depressive episode (when serotonin drops)

93
Q

ECT for depression

A

electroconvulsive therapy
-“shocks”
-used when other treatments don’t work
-side effect=memory impairment

94
Q

TMS for depression

A

Transcranial Magnetic Stimulation
-magnetic wand
-noninvasive
-used when other treatments didn’t work

95
Q

DBS for depression

A

Deep-brain Tissue Stimulation
-invasive surgery
-electrodes implanted into brain (similar to Parkinson’s treatment)

96
Q

Learned helplessness

A

giving up on a behavior when it continues to get you nowhere

97
Q

behavioral measures of depression in mice

A

-can genetically manipulate genes in mice to express similarities to depression (learned helplessness) and use an SSRI to treat it
-mouse tail suspension and mouse forced swim test (SSRI makes the subject try to escape again)

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