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Neuroscience 2016 > Test 3 Review Powerpoint > Flashcards

Test 3 Review Powerpoint Flashcards

1
Q

Isotonic contraction

A

agonist contracts, antagonist releases basis of movement

pulling up, like with a weight weight

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2
Q

isometric contraction

A

agonist/antagonist contract across joint, stabilizing joint

no movement

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3
Q

structure of skeletal muscle

A

axons from CNS innervate muscle fibers

actin in sarcomeres

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4
Q

alpha motor neuron

A

innervates extrafusal muscle fibers

contraction

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5
Q

motor unit

A

alpha motor neuron and all muscle fibers it innervates

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6
Q

innervation ration

A

number of muscle fibers innervated by a motor unit
higher is less fine control
lower is more fine control (1:1)

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7
Q

Lower motor neurons (LMN)

A

-Ventral horn
-Motor neurons that innervate SKELETAL muscle
directly command muscle contraction
-Ventral horn size differs along length of spine, # of motor neurons differ by how many muscles innervated (arms vs stomach)
-

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8
Q

CNS Control of Contraction

A

Increasing firing rate of alpha
motor neurons
Recruiting more alpha motor neurons from motor neuron pool

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9
Q

Fast motor units

A

rapidly fatiguing white fibers

low mitochondrial content

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10
Q

slow motor units

A

slowly fatiguing
red muscle
high mitochondrial content

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11
Q

Excitation of Muscle

A

-Alpha motor neuron fires AP
-Ach released from alpha motor neuron at NMJ
-Nicotinic channels open
-Na+ rushes through sarcolemma, causing type of EPSP called EPP (end plate potential)
-one EPP depolarizes sarcolemma enough to cause AP
-AP sweeps down sarcolemma through T tubules
-Voltage gated Ca2+ channels in T tubules open
-Ca 2+ spills out of sarcoplasmic reticulum
Releases calcium all over, amplified, bigger response

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12
Q

Contraction of muscle

A
  • Ca2+ binds troponin
  • Myosin-binding sites on actin exposed
  • Myosin head binds to actin
  • Myosin heads rotate
  • Myosin heads use ATP to disengage
  • Cycle continues as long as Ca2+ and ATP are present
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13
Q

Sarcomere

A

basic contracting unit of muscle

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14
Q

Relaxation of muscle

A

-As EPP (end plate potential)s end, sarcolemma and T tubules return to resting membrane potential
-Ca2+ returns to sarcoplasmic reticulum via ATP-driven pumps
-Myosin-binding sites on actin are covered by troponin
Fast process because we can contract fast

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15
Q

Reflexive movement

A
  • controlled by spinal cord and brainstem circuitry
  • cannot improve with practice
  • initiated by sensory stimulation
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16
Q

Voluntary movement

A
  • controlled by cerebral corex
  • can be improved with practice
  • initiated by thoughts
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17
Q

Gamma motor neuron

A
  • innervate intrafusal muscle fibers
  • adjust tension in muscle spindle
  • extrafusal muscle fibers to shorten
  • if spinals are slack, can’t report length of muscle so GMN contracts poles of spindle to align and gage stretch
  • contraction of two poles pulls on equatorial region, keeping 1a axons active
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18
Q

Myotatic reflex

A
  • stretch reflex
  • muscle spindle stretched –> mechanosensitive ion channels, depolarize, 1a afferent activated –> increased AP –> alpha motor neuron activated –> muscle contracts
  • monosynaptic arch: one synapse separates primary input from motor output
  • muscle length info
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19
Q

golgi tendon organ

A
  • sensor in skeletal muscle, monitors muscle tension/force of contraction
  • 1b axons
  • muscle tension info
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20
Q

reverse myotatic reflex

A
  • muscle tension increases
  • 1b axons synapse on interneurons in ventral horn
  • interneurons are inhibitory, protects muscle from being overloaded
  • for example, if muscle tension increaes and almost snaps, inhibits motor neurons so that muscle neurons stop contracting
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21
Q

1a

A

muscle length info

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22
Q

1b

A

muscle tension info

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23
Q

corticospinal tract

A
  • LATERAL PATHWAY (voluntary movement)
  • voluntary movement in humans
  • if cut, lose muscle control, rubrospinal can take over and help rebuild general control but lose fine muscle
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24
Q

rubrospinal tract

A 
LATERAL PATHWAY (voluntary movement)
important in non primates
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25
Q

tectospinal tract

A

VENTROMEDIAL (involun movement of proximal and axial muscles)
-orienting response, esp with eyes

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26
Q

vestibulospinal tract

A

VENTROMEDIAL (invol move of proximal and axial muscles)

-stability of head and back area to keep head

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27
Q

Pontine reticulospinal tract

A

VENTROMEDIAL (invol movement of prox and axial muscles)
enhances antigravity reflexes
balance

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28
Q

Medullary reticulospinal

A

VENTROMEDIAL (invol movement of prox and axial muscles)
liberates antigravity muscles
balance

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29
Q

motor area 6: what projects heavily into it?

A

basal ganglia and cerebellum

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30
Q

motor area 6: where does it project heavily?

A

area 4

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31
Q

roland’s tapping experiment

A

motor areas of brain

  • M1=simple movement
  • SMA + M1 complex movement
  • SMA thinking about complex movement
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32
Q

premotor area

A

planning movement

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33
Q

function of motor cortex

A

M1 neurons code for force and direction of movement

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34
Q

Force

A

frequency of action potentials

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35
Q

direction

A

population coding of action potentials

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36
Q

Basal ganglia

A

willed movement

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37
Q

parts of basal ganglia

A 
caudate nucleus
putamen
globus pallidus
subthalamic nucleus
substantia nigra
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38
Q

caudate nucleus

A 
motor processes
learning processes (associative, etc)
executive functioning
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39
Q

globus pallidus

A

movement

pacemaker

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40
Q

putamen

A

regulate movements

learning

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41
Q

subthalamic nucleus

A

action selection

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42
Q

substantia nigra

A

rewards, eye movement, motor planning, addiction

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43
Q

Parkinson’s disease

A
  • degradation of neurons in substantia nigra
  • depleletion of dopamine, prevents normal motor activity to basal ganglia
  • bradykinesia: slowness in movement
  • difficulty initiating willed movements
  • increased muscle tone and rigidness
  • tremors of hand and jaw
44
Q

process behind parkinson’s (chem)

A
  • depletion of dopamine
  • closes funnel that goes through Ventral Lateral Nucleus to SMA (cortex)
  • DA inhibits neurons that send inhibitory output
  • over excitation in subthalamic nucleus, can’t fire
45
Q

treatments of parkinson’s

A
  • L-DOPA treatment: activates neuron in putamen, replaces lost DA in striatum
  • DBS: stimulates subthalamic nucleus, less excitatory on global pallidus, less inhibition on VL, more excitatory on SMA
46
Q

Huntington’s disease

A
  • loss of neurons in caudate, putamen, and globus pallidas
  • hereditary, progressive, fatal
  • hyperkinesia and dskenesia: abnormal movements
  • dementia; cognitive, personality
  • autosomal dominant
  • *chorea: spontaneous, uncontrollable, purposeless movements
  • losing inhibitory input, opening funnel to SMA
47
Q

Cerebellum

A
  • sequence/timing of muscle contractions
  • planned, voluntary movement
  • multi joint movement
  • M1 through VL
48
Q

Cerebellar disease

A

DIDAD

  • dysmetria: loss of coordination
  • Dysdiadochokinesia: inmpaired ability for rapid alternative movements
  • Ataxia: loss of full control of body movements
  • Intention tremor
49
Q

hyperreflexia

A

motor cortex lesions

increased reflexes

50
Q

hypertonia

A

motor cortex lesions

increased muscle tone

51
Q

babinsky reflex

A

motor cortex lesion (if exists after 12 months

upward flexion of big toe

52
Q

clonus

A

motor cortex lesion

rhythmic cycles of contraction and relation after stretch of limb muscle

53
Q

point to point communication

A

most neurons

Glu, GABA, peptide NTs

54
Q

secretory hypothalamus communication

A

going to various neurons
ANS: sympathetic, parasympathetic
through blood system

55
Q

diffuse modulary communication

A

diffuse like secretory
going to various neurons
but doesnt go through blood system

56
Q

lateral and medial hypothalamus

A

functions to control homeostasis

57
Q

periventricular hypothalamus

A
  • functions in circadian rhythms and endocrine system
  • superchiasmatic nucleus
  • circadian rhythm
  • endocrine system
  • pituitary
  • more innervated with blod vessels: secretory hypothalamus communication
58
Q

hypothalamic magnocellular cells

A
  • posterior pituitary
  • true neural tissue
  • oxytocin, vasoprecin (love hormone for prairie voles, in humans, kidneys for water concentration
59
Q

hypothalmic parvocellular cells

A
  • anterior pituitary
  • true gland
  • endocrine system
  • hormones for puberty: growth, follical stimulating, glutenizing, prolactin (testes, gonads)
  • certain mass (obese people=earlier) –> glutenizing –> testosterone and estrogen
60
Q

sympathetic nervous system

A

fight or flight

increases heartrate, blood pressure, eyes dilate, rapid breathing

61
Q

parasympathetic nervous system

A

calm
rest and digest
digestion, lowers heartrate, lowers blood pressure, return to normal breathing

62
Q

outputs of CNS from somatic motor fibers

A

to skeletal muscle

63
Q

outputs of CNS from ANS (sympathetic and parasymp systems)

A

to smooth muscle, cardiac muscle, gland cells

64
Q

sequence of events ins tress response

A

Amygdala feels stress, increases reaction, signals to hypothalamus
Release corticaltropin
Goes to anterior pituitary (highly innervated with blood vessels)
ACTH has to be released into blood to get to adrenal glands
Cortisal

65
Q

increased cardiovascular tone in chronic stress

A

hypertension, atherosclerosis

66
Q

mobilization of energy in chronic stress

A

fatigue, diabetes, obesity

67
Q

suppression of digestion in chronic stress

A

ulcers

68
Q

suppression of growth in chronic stress

A

decrease growth + muscle mass, dwarfism

69
Q

suppression of reproduction in chronic stress

A

decreased libido, no ovulation

70
Q

suppression of immune system in chronic stress

A

infections

71
Q

sharpening of cognition in chronic stress

A

memory impairment

72
Q

stimulants

A
  • cocaine, amphetamines, etc block NE and DA receptors
  • if you take too quickly, NE causes increased heartrate and die
  • addiction
73
Q

ADHD

A
  • DAT transporter works in reverse, increases DA in cleft
  • symptoms: inattention, hyperactivity, impulsivity
  • knockdown DAT transporters in mice –> hyperactive
  • knockout DAT transporters in mice –> extremely hyperactive
74
Q

Ecstasy (MDMA)

A
  • higher affinity for SERT than 5HT itself
  • reverses SERT activity
  • long term=loss of serotonin axons
  • depression, anxiety, disturbed sleep, substance abuse disorders, mood
75
Q

sexual differentiation

A 
mullarian ducts (f) preset for humankind
TDF
mullarian ducts dev into oviducts
wolffian ducts into vas deferens
76
Q

male sexual dev

A 
XY chromosomes
TDF
testes
AMH means no mullarian ducts, instead wollfian (seminal vesicles, prostate glands, etc)
male brain, and male external genitalia
77
Q

female sexual dev

A

no tdf, ovaries, no AMH, mullarian ducts (inner vagina, uterus, fallopian tubes), outer genitalia, female brain

78
Q

gonadal intersexuality

A
  • “true hermaphroditism”
  • gonads have both ovarian and testicular tissue
  • majority are infertile
  • external genitalia variable
  • female structure usually predominate
  • most identify as women
79
Q

turner’s syndrome

A
  • XO female
  • neck webbing
  • short, barrel chest
  • no ovaries
  • no gonadal hormones
  • infertile
  • no testosterone
  • problems with visual/spatial/mathematical tasks
80
Q

kleinfelter’s syndrome

A
  • XXY male
  • intersexuality
  • “pseudo hermaphroditism”
  • tall, small testes, gynecomastia
  • feminine body contours
  • low testosterone leves
  • language skills impaired
81
Q

Complete AIS (androgen insensitivity syndrome)

A
  • XY male
  • intersexuality
  • “pseudo hermaphroditism”
  • normal prenatal testosterone levels
  • mutation in androgen receptor
  • shallow vagina, undescended testes
  • no male or female internal genitalia
  • taller than most females
  • caused by absent or non functional androgen receptors
82
Q

Partial AIS

A

XY Male
Mutation in androgen receptor
Semenya olympics

83
Q

Congenital Adrenal Hyperplasia (CAH)

A
  • XX Female
  • intersexuality
  • “pseudo hermaphroditism”
  • defect in production of enzyme cortisol
  • hyperplasia of adrenal cortex
  • increased cortisol precursor steroids that get converted to androgens
  • masculinize female genitalia
  • behaviorally masculinized, likely to be sexually attracted to women
  • if untreated, infertility
84
Q

Second wave of hormones

A
  • puberty
  • hypothalamus: GnRH (gonadotrpin-releasing hormone)
  • activates anterior pituitary (LH and FSH)
  • Females: ovaries, estrogen, breasts
  • Males: testes, teststerone, male genitalia
85
Q

Estrodiol

A

estrogen
monthly on period
increase in synthetic spines in hippocampus
to choose mate, increased cognition

86
Q

right hemisphere 2% larger

A

straight men

lesbians

87
Q

hemispheres are nearly same size

A

straight women

gay men

88
Q

sexually dimorphic nucleus (SDN)

A

inah 3 INH 3 in humans
sexual orientation
women have more widespread of cells, diffuse

89
Q

Dimorphisms

A
  1. ) differences in density, size of cells, # of axons and synapses (amygdala, symmetry of hemispheres, cerebral cortex etc)
  2. ) microscopic/molecular differences (size and number of nerve cells, synapses, brain circuits, hormone receptors, neurotransmitters)
90
Q

Male cognition

A
  • navigate with compass direction
  • mental rotation
  • judgment of line orientation
  • more aggressive, competitive
91
Q

female cognition

A
  • navigate with landmarks
  • verbal fluency
  • reading facial expression
  • memory of object location
92
Q

same sex attraction

A
  • early play patterns predict sexuality
  • women exposed to high androgens more likely to be gay
  • prenatal hormones, so conversion therapy doesn’t work
93
Q

otoacoustic emissions

A
  • men roughly equal
  • straight women have most
  • bi and gay women less than straight
94
Q

Glascow coma scale

A

content: cerebral cortex
VS
arousal (RAS): brainstem modulatory systems

95
Q

EEG

A

measures voltages generated by excitation of many neurons in cerebral cortex
depends on
1. number of neurons
2. synchronous activity

96
Q

Synchronous activity of neurons

A

pacemaker (thalamus)
high freq
high amplitude
sleep

97
Q

seizure activity

A

runaway excitation of brain circuitry
-> pathologically synchronous activity (high freq high amp)
very synchronous
-upset in balance of synaptic excitation and inhibition

98
Q

treatment for seizures

A

-GABA agonist
promote inhibition mediated by GABA
-in seizures, sodium channels try to stay open for longer, more sodium enter, hyperexcitable
–> block Na+ channels

99
Q

Stage 1 of sleep

A
  • transitional sleep (eyes make slow rolling movements, drowsy)
  • lightest
  • only few minutes
100
Q

Stage 2 of sleep

A
  • EEG is irregular, short bursts
  • sleep spindles diminish brain’s sensitivity to sensory stimuli (thalamic pacemaker)
  • k complex keeps person asleep
101
Q

stage 3 of sleep

A
  • 20-25% delta waves
  • delta wave
  • high amplitude, low freq
102
Q

stage 4 of sleep

A
  • increase in delta waves
  • deepst stage of sleep
  • changes most during life
  • decreases with age, ending after 60 years
103
Q

REM sleep

A
  • sympathetic system
  • no muscle tone, paralyzed body
  • beta rhythms
  • brain incredibly active (dreaming is random activation of circuits that are easily accessible)
  • newborn has mostly REM, decreases with age
  • paradoxical sleep (waking EEG, but not easily aroused)
104
Q

Bottlenose dolphin

A
  • microsleeps

- sleeping with one brain hemisphere

105
Q

Neurotrans in response to sleep (increase or decrease in firing rate?)

A

Increase: NE, 5-HT, Ach
decrease: dopamine

106
Q

sleep in brain processing, memory, creativity

A
  • novel solutions to complex problems
  • 3x creativity
  • synaptic connections are linked and strengthened
107
Q

Hypocretin

A

dog falling asleep
arousal
mutation in receptor, narcolepsy, blocked

Neuroscience 2016 (7 decks)

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