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NSC 201 > Unit 4: Brain and Behavior > Flashcards

Unit 4: Brain and Behavior Flashcards

1
Q

EEG

A

Measurement of electrical activity from surface of scalp to measure activity of cerebral cortex

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2
Q

Synchronous

A

EEG signal is large, same timing

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3
Q

Asynchronous

A

EEG signal is small, timing is off

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4
Q

MEG

A

Detects tiny magnetic signals produced by synchronously active neurons, better at localizing sources of neural activity in brain

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5
Q

4 EEG rhythms

A
  1. Beta-awake and alert
  2. Alpha-awake and resting
  3. Theta-sleeping
  4. Delta-deep sleep
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6
Q

Synchronous activity led by one of two things

A
  1. Central pacemaker (thalamus)

2. Collective behavior among cortical cells

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7
Q

Zeitgebers

A

Environmental cues that entrain circadian cycles (primary cue: sunlight)

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8
Q

Internal Circadian Clock

A

SCN in hypothalamus

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9
Q

Where are higher frequency (beta) waves mainly located?

A

Cortex

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10
Q

Where are lower frequency (delta) waves mainly located?

A

Thalamus

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11
Q

Transcriptional-translational feedback loop

A
  1. BMAl1 and CLOCK promote transcription of per and cry genes
  2. Bind together and inhibit transcription of own genes
  3. Degrade
  4. Allows BMAL1 and CLOCk to promote per and cry transcription again
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12
Q

EOG

A

Records eye movements during REM

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13
Q

EMG

A

Detects muscles activity

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14
Q

4 stages of sleep

A
  1. Theta waves
  2. Spindles and K complexes
  3. Occasional delta waves
  4. Predominantly delta waves
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15
Q

Recuperation

A

Sleep is needed to restore homeostatic balance lost during the day

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16
Q

Adaption

A

Sleep is the result of an internal timing mechanism, evolved to conserve energy and to protect us from dangers of the night

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17
Q

Effects of sleep deprivation: in support of theory

A
  • Bad mood, reduced cognitive abilities, and sleepiness

- Reduced immune function, increased BP, lower body temp

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18
Q

Effects of sleep deprivation: inconsistent with theory

A
  • Unimpaired logical and critical thinking
  • Retained physical strength and motor performance
  • Recovery sleep is relatively short
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19
Q

Anterior hypothalamus

A

Sleep

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20
Q

Posterior hypothalamus

A

Wake

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21
Q

Rostral reticular formation

A

Wakeful

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22
Q

Caudal reticular formation

A

Sleep

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23
Q

Anterior sleep area in hypothalamus (VLPO)

A

Inhibits targets using GABA as its NT

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24
Q

Posterior awake center (lateral hypothalamic area)

A

Excited targets using orexin

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25
Q

Rostral RF areas

A

LC, 5-HT, Ach, HA

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26
Q

Human sleep regulated by 2 basic neural processes

A
  1. Sleep need-homeostatic process

2. Sleep urge-circadian process

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27
Q

3 types of drugs that affect sleep

A
  1. Hypnotic-increases sleep
  2. Anti-hypnotic-decreases sleep
  3. Chronotbiotic-alters circadian rhythm
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28
Q

2 types of sleep disorders

A
  1. Insomnia

2. Hypersomnia

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29
Q

Process of homeostasis

A

Sensory transduction of variable, detecting changes from optimal range, integrated response (humoral visceromotor & somatic) to restore parameter back to optimal (negative feedback)

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30
Q

3 zones of hypothalamus

A
  1. Periventricular
  2. Medial
  3. Lateral
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31
Q

4 regions of hypothalamus

A
  1. Mammillary region
  2. Tuberal region
  3. Supraoptic region
  4. Preoptic region
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32
Q

3 components of response from hypothalamus to maintain homeostasis

A
  1. Humeral
  2. Visceromotor
  3. Somatic motor
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33
Q

Humeral

A

Releasing hormones

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34
Q

Visceromotor

A

Adjusting the balance of sympathetic and parasympathetic outputs of the ANS

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35
Q

Somatic motor

A

Motivating appropriate behaviors by the somatic motor system

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36
Q

Paraventricular nucleus

A

Initiates humoral and visceromotor responses

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37
Q

Lateral hypothalamus

A

Motivates the somatic motor response, contains 2 main types of outputs (uses MCH and other uses orexin)

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38
Q

2 lobes in pituitary gland

A
  1. Anterior-synthesizes and secretes hormones in response to hormones released by hypothalamus
  2. Posterior-stores and secretes hormones
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39
Q

What does the ANS do?

A

Influences function of internal organs

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40
Q

Physiological mechanisms if hot or cold

A
  • Decrease or increase metabolism
  • Sweat or shiver
  • Increase or decrease blood flow to skin
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41
Q

Behavioral mechanisms if hot or cold

A
  • Find a cool or hot place
  • Become less or more active
  • Sleep or fluff fur (more or less clothes)
  • Stand alone or together
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42
Q

2 advantages of high body temperature

A
  1. Mobile all year long

2. Protection from fungal infections

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43
Q

Where are the most important neurons for temp homeostasis found?

A

Clustered in preoptic and anterior hypothalamic nuclei (receive input from anterolateral tract and respond to changes in blood temp)

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44
Q

Where are neurons for the 3 responses to temperature changes produced?

A

Humoral and visceromotor: neurons in paraventriclar nucleus

Somatic motor: initiated by neurons of lateral hypothalamus

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45
Q

2 types of thirst

A
  1. Osmotic-eating salty foods

2. Hypovolemic-losing fluid volume

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46
Q

Nuclei that conserve water (2)

A
  1. Supraoptic

2. Paraventricular

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47
Q

What generates desire to drink? (2)

A
  1. Preoptic nuclei

2. Lateral hypothalamic area

48
Q

What is water conservation controlled by?

A

Release of ADH from paraventricular and supraoptic neurons via posterior pituitary

49
Q

What does ADH enable?

A

Enables kidneys to reabsorb water and thus excrete a concentrated urine

50
Q

Baroreceptors

A

Type of mechanoreceptor sensory neuron that is excited by stretch and inhibited by relaxation of blood vessel

51
Q

What does renin do?

A

Hypovolemia causes kidneys to release it, which leads to synthesis of angiotensin II, which causes constriction of blood vessels to increase BP

52
Q

Lateral lesions of hypothalamus cause…

A

Anorexia

53
Q

Lesions of ventromedial hypothalamus cause…

A

Obesity

54
Q

Arcuate nucleus

A

“Master area” for control of appetite

55
Q

2 sets of neurons in arculate nucleus

A
  1. Sensitive to hunger signals (low leptin)-release AgRP and NPY onto PVN and lateral hypothalamic area
  2. Sensitive to satiety signals (high leptin)-release alphaMSH and CART into same targets
56
Q

High orexigenic signals, low satiety signals

A

Food consumption happens

57
Q

Low orexigenic signals, high satiety signals

A

Food consumption is inhibited

58
Q

Hormone in stomach

A

Ghrelin (hunger)

59
Q

Hormone in intestines

A

CCK (satiety), stimulates vagus nerve and closes exit of stomach

60
Q

Hormone in blood

A

Insulin, low=hunger, high=satiety

61
Q

High ghrelin

Low CCK, insulin, & gastirc tension

A

Activates NPY/AgRP (hunger) containing neurons

62
Q

High CCK, insulin, & gastric tension

A

Activates alphaMSH and CART (satiety) containing neurons

63
Q

Hedonic effects modulated by…

A

Dopamine (ventral tegmental area) & serotonin (Raphe nucleus)

64
Q

Mesocorticolimbic pathway

A

(ventral tegmental area and nucleus accumbens) is major “reward” pathway for ICSS and natural rewards

65
Q

7 main areas of cortex for language

A
  1. Primary visual cortex
  2. Primary auditory cortex
  3. Angular gyrus
  4. Wernicke’s area
  5. Arcuate fasciculus
  6. Broca’s area- like secondary motor cortex
  7. Primary motor cortex
66
Q

Wernicke-Geschwind Model: spoken language

A

Auditory cortex –> Wernicke’s area

67
Q

Wernicke-Geschwind Model: words written

A

Visual cortex –> angular gyrus –> Wernicke’s area –> arcuate fasciculus –> Broca’s area –> motor cortex

68
Q

Broca’s (nonfluent) Aphasia

A

Expressive aphasia, normal comprehension but poorly articulated speech, writing difficulties

69
Q

Wernicke’s (fluent) Aphasia

A

Receptive aphasia, poor comprehension and meaningless, fluent speech, writing difficulties

70
Q

Dejerine

A

Reading aphasia, damage to left angular gyrus, inability to read (alexia) and write (agraphia), but no difficulty speaking or understanding speech, damage in pathways from visual coretx

71
Q

Conduction Aphasia

A

Damage to arcuate fasciculus, fluent speech (Broca’s area is working) but there is error awareness with attempts to correct them (Wernicke’s area working), poor repetition of unfamiliar words

72
Q

Effects of cortical damage: anterior lesions

A

Expressive aphasia

73
Q

Effects of cortical damage: posterior lesions

A

Receptive aphasia

74
Q

Sign language: damage to frontal cortex

A

Can impair making of gestures (nonfluent)

75
Q

Sign language: damage to temporal cortex

A

Can impair understanding of gestures (fluent)

76
Q

Bilingual brains

A

Thicker language areas in temporal and frontal cortex, shifting languages activates frontal, temporal, and basal ganglia (helps secondary motor cortex aka Broca)

77
Q

Mutations in FOXP2 gene

A

Verbal dyspraxia- inability to produce the coordinated muscle movements needed for speech

78
Q

What does the FOXP2 gene encode?

A

Transcription factor that affects development of Broca’s area, motor cortex, basal ganglia, and cerebellum

79
Q

KIAA0319

A

Gene associated with dyslexia, chromosome 6 and 18

80
Q

Dyslexia patients have lower activation in…

A

Angular gyrus, but over-active Broca’s area

81
Q

LTM: Declarative memory

A

Explicit-what: broken into semantic and episodic, medial temporal lobe

82
Q

LTM: Procedural memory

A

Implicit-how: includes motor skills, basal ganglia & cerebellum

83
Q

Retrograde amnesia

A

Memory loss for events before trauma

84
Q

Anterograde amnesia

A

Inability to form new memories after trauma

85
Q

Semantic memory

A

General world knowledge, anterior pole of medial temporal lobe

86
Q

Episodic memory

A

Life events, hippocampus and (mostly ) rhinal cortex

87
Q

3 major structures in part of medial temporal lobe caudal anterior pole

A
  1. Amygdala
  2. Hippocampus- spatial
  3. Rhinal cortex
88
Q

Where is short term memory held?

A

Telencephalon- including prefrontal and parietal cortex

89
Q

Lateral intraparietal cortex (LIP)

A

Guides eye movement to locations of objects of interest

90
Q

Cell assembly

A

Internal representation of an object consists of all the cortical cells activated by the external stimulus (Hebb)

91
Q

Learning and memory is a 2 stage process

A
  1. Acquisition of ST memory

2. Consolidation of LT memory

92
Q

How is memory stored in the network?

A

Through a unique pattern or ration of activity across the neuronal assembly

93
Q

Advantages of distributed network (2)

A
  1. No single neuron represents specific memory (population type coding)
  2. Graceful degradation of memories with gradual neuron loss
94
Q

What transmitter is most often at modifiable synapses?

A

Glutamate

95
Q

LTP

A

Strengthening of synaptic connections

96
Q

Hippocampus consists of 2 thin sheets of neurons

A
  1. Dentate gyrus

2. Ammon’s horn (CA3 & CA1)

97
Q

Input specificity

A

When one pathway into synapse is stimulated weakly, it produces insufficient postsynaptic depolarization to induce LTP

98
Q

Cooperatively in LTPs

A

In order to achieve necessary depolarization to elicit LTP, one input must fire fast enough to produce temporal summation of its EPSPs or a set of weak inputs must cooperate to produce spatial summation

99
Q

Associativity in LTPs

A

LTP can be elicited at synapses that are
activated by weak, low-frequency, stimuli if their
activation is temporally concurrent with an LTP inducing stimulus at another set of synapses on the same cell

100
Q

3 phases of LTP

A
  1. Induction
  2. Expression (“early LTP”)
  3. Stabilization (“late LTP”)
101
Q

Rise in postsynaptic Calcium activates what 2 protein kinases?

A
  1. Protein kinase C

2. CaMKII

102
Q

LTD is site specific

A

Homo-synaptic LTD, only on spines getting glutamate (and Calcium)

103
Q

Glutamate receptor trafficking

A

Egg carton model, AMPA receptors are replaced maintaining same number

104
Q

Protein PSD-95

A

Comprises slot protein

105
Q

Where is bidirectional synaptic plasticity found?

A

Area IT (inferotemporal cortex)- stores visual info including familiar faces

106
Q

Blocking NMDA receptors with antagonists

A

No learning in inhibitory avoidance expts & prevented learning of location of escape platform (for rats)

107
Q

Knockout CaMKII or NMDA receptors

A

No learning/ reduced learning

108
Q

Metaplasticity

A

Rules of synaptic plasticity change depending on the history of synaptic or cellular activity (modification threshold slides up or down)

109
Q

NR2A

A

Admits less Calcium

110
Q

NR2B

A

Admits more Calcium

111
Q

Synaptic scaling

A

Adjustment of absolute synaptic effectiveness that preserves the relative distribution of synaptic weights

112
Q

Why is phosphorylation not a viable LT consolidation mechanism? (2)

A
  1. Phosphorylation is not permanent

2. Protein molecules are not routinely replaced

113
Q

ST and LT phases of memory depend on different molecular mechanisms (2)

A
  1. ST (early LTP): kinases

2. LT (late LTP): protein synthesis

114
Q

Molecular Switch Hypothesis

A

Kinases that can auto-phosphorylate could stay “on” all the time (ex: CaMKII)

115
Q

Protein kinase M zeta

A

Involved in regulating AMPA receptor number, involved in mRNA translation and promotes its own synthesis for a time

116
Q

Protein ZIP

A

Temporarily inhibits function of PKMzeta and can erase memories

117
Q

CREB-1

A

LT memory consolidation, gene transcription activator, phosphorylated by protein kinase A (which is activated by cAMP)

NSC 201 (5 decks)

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