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Fundamentals of Neuroscience > Final Exam > Flashcards

Final Exam Flashcards

1
Q

what does somatic sensation enable?

A

enables us to feel, ache, and sense temp and pressure

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2
Q

how is the somatic sensory system different from other systems?

A

broadly distributed receptors and responds to multiple different stimuli

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3
Q

types of skin

A

hairy and glabrous

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4
Q

layers of skin

A

epidermis (outer) and dermis (inner)

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5
Q

what are the functions of skin?

A

protects, prevents evaporation of bodily fluids, and provides direct contact with the world

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6
Q

what are most somatosensory receptors? what are they sensitive to?

A

mechanoreceptors; physical distortion

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7
Q

what are the difference mechanoreceptors?

A

pacinian corpuscles, ruffini’s endings, meissner’s corpuscles, and merkel’s disks

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8
Q

pacinian corpuscles

A

highest densities in the fingers, lies deep, mm size

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9
Q

meissner’s corpuscles

A

in the ridges of glabrous skin, 1/10 size of p.c.

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10
Q

what are merkel’s disks made up of?

A

a nerve terminal and a flattened non-neural epithelial cell

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11
Q

how do mechanoreceptors vary?

A

stimulus frequencies, pressures, receptive fields, and responses to long-lasting stimuli

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12
Q

what are Pacinian corpuscles sensitive to?

A

vibrations of ~ 200-300 Hz

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13
Q

what are Meissner’s corpuscles sensitive to the best?

A

vibrations around 50 Hz

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14
Q

how do mechanoreceptors convert mechanical force to a change in ion current?

A

they have unmyelinated axon terminals with ion channels that are connected to proteins. when mechanical stimuli is present, a release of second messengers is tiggered

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15
Q

two-point discrimination

A

ability to discriminate the detailed features of a stimulus (between two points) varies throughout the body

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16
Q

how much does two-point discrimination vary across the body?

A

20-fold

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17
Q

why are fingertips good for Braille reading?

A

higher density of mechanoreceptors, enriched in receptor types with small receptive fields, more brain tissue, and there may be special neural mech.s for high-res discriminations

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18
Q

where are primary afferent axons primarily located?

A

dorsal root of spinal cord; enter cord through there.

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19
Q

characteristics of C fibers (primary afferent axons)

A
  • mediate pain, temp, and itch
  • no myelin & ~1 um in diameter
  • slowest (0.5-1 m/sec)
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20
Q

what do Abeta primary afferent axons mediate?

A

touch sensations

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21
Q

4 divisions of the spine and their vertebral adjacents

A

cervical (1-8)
thoracic (1-12)
lumbar (1-5)
sacral(1-5)

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22
Q

total spinal segments?

A

30

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23
Q

dermatones

A

area of skin innervated by right and left dorsal roost of spinal segment; one-to-one correspondence with spinal segments (vertebrae)

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24
Q

what is shingles and what is it’s connection to sensation?

A

herpes virus (chickenpox) that remains in primary sensory neurons and revives; restricted to skin innervated by axons of affected dorsal root

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25
Q

how many branches do the Abeta axons have and what do they do?

A

2 branches. one is on second-order sensory neurons & does rapid unconscious reflexes. other is responsible for perception

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26
Q

where do the Abeta axons enter the spinal cord?

A

in the ipsilateral dorsal column

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27
Q

where do the axons of the dorsal column go in the brain?

A

dorsal column nuclei @ junction of spinal cord and medulla

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28
Q

what is special about dorsal column axons?

A

some of the longest axons

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29
Q

where do the axons of the dorsal column decussate to?

A

VP nucleus of thalamus and primary somatosensory cortex (S1)

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30
Q

what are the sections of the somatosensory areas?

A
  • postcentral gyrus of somatos. cortex (1, 2, 3a)
  • Brodmann’s area of somatos. cortex (3b)
  • posterior parietal cortex (5 and 7)
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31
Q

what is considered the primary somatic sensory cortex and why?

A

area 3b (Brodmann’s)
- receives dense inputs from VP nucleus
- very responsive
- lesions impair somatic sensation
- evokes somatic sensory experiences when electrically stimmied

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32
Q

what info does area 3b send to area 1?

A

texture info

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33
Q

what info does area 3b send to area 2?

A

emphasizes shape and size

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34
Q

where do thalamic inputs to 3b (S1) terminate

A

mainly in layer IV

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35
Q

how are S1 (3b) neurons organized?

A

alternating layers stacked vertically into 6 columns

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36
Q

what is the main difference between the two types of cortical layers in S1?

A

one has rapidly adapting sensory responses and one has slowly adapting sensory responses

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37
Q

what did Wilder Penfield discover?

A

electrical stimulation of S1 surface can map somatic sensations localized across the body

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38
Q

somatotopy

A

mapping of the body’s surface sensations onto the brain (think that really weird cartoon about the different regions of sensation on the brain)

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39
Q

barrel cortex

A

sensory signals from each vibrissa follicle go to one clearly defined cluster of S1 neurons

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40
Q

how many maps of the body does the somatic sensory system have? what are some examples?

A

many maps; some are mirrored (owls monkey hand area)

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41
Q

what happens when someone looses a digit (in owl monkey)?

A
  • neurons devoted to amputated digit will respond to others
  • rep of remaining digits expand to compensate in map
  • phantom limb possible
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42
Q

red muscle fibers

A

large # of mitochondria and enzymes, slow to contract, can sustain contraction; antigravity muscles of leg and torso

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43
Q

white muscle fibers / fast fibers

A

fewer mitochondria, anaerobic metabolism, contract and fatigue rapidly; human arm muscles

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44
Q

fatigue-resistant fast fibers

A

white fibers with moderate strength and fast contractions

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45
Q

fast fatigue fibers

A

fastest, strongest white fibers but rapidly fatiguing

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46
Q

motor unit

A

motor neuron + the muscle fibers it innervates

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47
Q

how many types of muscle fibers can a motor unit have?

A

only one

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48
Q

how many muscle fiber types do most muscles have?

A

all three (red, fatigue-resistant, and fast fatigable)

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49
Q

two types of motor units

A

slow and fast

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50
Q

repeated trains of APs lead to different….

A

rates of fatigue

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51
Q

what did the crossed-innervation experiment discover?

A

switched nerve input -> switch in muscle phenotype

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52
Q

how can you switch muscle phenotype?

A

switching the activity of the motor neuron

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53
Q

can a switch in neuron phenotype happen irl?

A

yes, with changes in synaptic activity with experience

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54
Q

when are muscle fibers formed?

A

early in fetal development by fusion of muscle precursor cells

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55
Q

basic anatomy of muscle fiber

A
  • each cell has >1 nucleus
  • fibers enclosed in sarcolemma (excitable membrane)
  • layers of contractable myofibrils inside
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56
Q

excitation-contraction coupling

A

alpha motor neurons release ACh -> ACh induce EPSP -> EPSP invoke AP -> AP release Ca+2 -> fiber contracts -> calcium reuptake -> fiber relaxes

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57
Q

sarcomere anatomy

A

alternating I and A bands, I contains Z line, A contains H zone. sarcomere extends from one Z line to another

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58
Q

how does muscle contraction occur in regards to the filaments?

A

thin filaments slide along thick filaments, bringing Z lines together and shortening the sarcomere

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59
Q

muscle spindles

A

deep in skeletal muscles; contain stretch receptor; example of proprioceptors

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60
Q

proprioceptors

A

“body sense”

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61
Q

how do stretch receptors cause the muscle to shorten/contract?

A

stretching leads to depolarization of Ia axon -> opening of mechanosensitive ion channels -> AP discharge from Ia depolarizes alpha motor neurons -> contraction

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62
Q

stretch reflex

A

muscle wants to pull back when it’s being pulled

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63
Q

discharge of Ia sensory axons is closely related to …

A

length of the muscle

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64
Q

example of stretch relfex?

A

knee-jerk

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65
Q

many inputs to motor neurons are mediated by…

A

spinal interneurons

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66
Q

reciprocal inhibition

A

contraction of one muscle set is accompanied by relaxation of anatgonist muscle

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67
Q

reciprocal inhibition is done because…

A

inhibitory spinal interneurons are between the Ia axon from the contracting muscle and the alpha motor neuron going to the antagonist muscle

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68
Q

flexor reflect

A

withdraw a limb from an aversive stimulus; excitatory interneurons

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69
Q

crossed-extensor reflex

A

activation of extensor muscles and inhibition of flexors on opposite side during flexor reflex

70
Q

when would crossed-extensor reflex be used?

A

to brace the other leg when you step on something sharp

71
Q

central pattern generators

A

circuits that give rise to rhythmic motor activity

72
Q

examples of central pattern generators

A

spinal motor programs for walking (circuitry in the spinal cord and rhythmic activity in interneurons)

73
Q

how does rhythmic activity in spinal interneurons occur?

A

glutamate activates NMDA channels to open, allowing Ca+2 influx. calcium then activates K+ channels to open, causing K+ efflux. Mg+2 comes in to clog the NMDA channel, and less calcium causes K+ channel to close. reset!

74
Q

what is a possible circuit for alternating rhythmic activity?

A

continuous input from brain goes into two excitatory interneurons that are connected by an inhibitory interneuron. because they can inhibit each other, the activity alternates

75
Q

example of when alternating rhythmic activity would occur?

A

flexion in one limb is accompanied by extension in the other

76
Q

electrical rhythms of the cerebral cortex

A

sleeping, walking, hibernation, and breathing

77
Q

classical method of recording brain rhythms

A

EEG

78
Q

circadian rhythms

A

changes in physiological functions according to brain clock

79
Q

when was first EEG?

A

1929

80
Q

are walking and sleeping EEGs the same?

A

no! distinctly different

81
Q

unit of measurement used in EEG

A

microvolts (uV), usually in tens

82
Q

amplitude of EEG signal measures…

A

synchronous activity of underlying neurons

83
Q

what generates the electrical fields detected by EEG?

A

currents that flow during synaptic excitation of dendrites of many pyramidal neurons; thousands have to activate together to generate signal strong enough to be detected

84
Q

how do we describe EEGs?

A

relative amplitude (suggests how synchronous underlying activity is)

85
Q

how are EEG rhythms categorized?

A

based on their frequency range; 7 catagories

86
Q

what are the 7 categories of EEG rhythms?

A

alpha, beta, gamma, delta, theta, spindles, and ripples

87
Q

alpha EEG

A

8-13 Hz; quiet, walking state

88
Q

beta EEG

A

15-30 Hz; an activated or attentive cortex

89
Q

gamma EEG

A

30-90 Hz; an activated or attentive cortex

90
Q

delta EEG

A

< 4 Hz; deep sleep

91
Q

theta EEG

A

4-7 Hz; some sleep and walking states

92
Q

spindles EEG

A

brief 8-14 Hz waves associated with sleep

93
Q

ripples EEG

A

brief bouts of 80-200 Hz oscillations; in hippocampus, sleep

94
Q

are EEGs specific to species?

A

no, they’re similar across mammalian brains

95
Q

what are high-frequency, low-amplitude EEGs associated with?

A

alertness and walking, or dreaming stages of sleep

96
Q

what are low-frequency, high-amplitude EEGs associated with?

A

non-dreaming sleep states, certain drugged states, or pathological condition of coma

97
Q

what are high synchrony, high amplitude EEGs associated with?

A

deep sleep

98
Q

what is a pacemaker in regards to rhythms?

A

the collective behavior of all participants (in this case neurons)

99
Q

how does pacemaker work in leading a synchronous rhythm?

A
  • take cues from a central clock
  • share or distribute timing function among themselves by mutually exciting or inhibiting one another
100
Q

basic features of a neural oscillator

A
  • source of constant excitatory drive
  • feedback connections
  • synaptic excitation and inhibition (usually one excitatory and one inhibitory neuron)
101
Q

what are some causes of seizures?

A

tumor, trauma, genetics, infection, vascular disease, and other unknown causes

102
Q

seizures can be defined as…

A

the most extreme form of synchronous brain activity (accompanied by very large EEG)

103
Q

generalized seizure

A

entire cerebral cortex, complete behavior disruption, loss of consciousness

104
Q

partial seizure

A

circumscribed cortex area, abnormal sensation/aura (odd smell, sparking lights)

105
Q

absence seizure

A

> 30 sec of generalized 3 Hz EEG waves, characterize a childhood form of epilepsy, motor signs strangely subtle

106
Q

what are the characteristics of the EEG of a generalized seizure?

A
  • beings abruptly
  • synch. across entire head
  • ends abruptly
107
Q

whats the purpose of sleep?

A

dunno

108
Q

sleep is defined as

A

a readily reversible state of reduced responsiveness to, and interaction with, the environment

109
Q

how long do we spend sleeping?

A

1/3 of lifespan

110
Q

what are the three functional brain states?

A

awake, REM sleep, and non-REM sleep

111
Q

rem sleep

A

EEG looks like awake, body immobilized, dreams

112
Q

non-rem sleep

A

no dreams usually, slow large/high voltage EEG

113
Q

we know we go through all 5 stages of sleep, but what happens as we repeat them?

A

non-rem stages get shorter and shallower and rem stage periods get longer

114
Q

what are some physiological changes during REM periods?

A

increases in heart rate, respiration rate, and erections (lmao)

115
Q

non-REM sleep stage 1

A
  • transitional sleep
  • relaxed EEG
  • slow, rolling eye movements
116
Q

non-REM sleep stage 2

A
  • slightly deeper
  • occasional 8-14 Hz EEG oscillation called sleep spindle
  • high-amp sharp K complex
  • almost no eye movement
117
Q

non-REM sleep stage 3

A
  • EEG begins large-amp, slow delta rhythms
  • few eye and body movements
118
Q

non-REM sleep stage 4

A
  • deepest stage
  • large EEG rhythms of 2 Hz or less
119
Q

do we go straight from stage 4 non-REM sleep into REM sleep?

A

no, we go back to stages 3 and 2 before suddenly entering REM

120
Q

what is special about the way dolphins sleep?

A

they sleep with one cerebral hemisphere at a time

121
Q

what are the two main theories of sleep function?

A

restoration and adaptation

122
Q

restoration sleep function theory

A

sleep to rest, recover, and prepare to be awake again; possible some brain regions achieve form of essential rest only during sleep

123
Q

adaptation sleep function theory

A

sleep to keep out of trouble, hide from predators

124
Q

Sigmund Freud dream theory

A

dream functions - wish fulfillment, conquer anxieties

125
Q

Hobson and McCarley dream theory

A

activation-synthesis hypothesis; dreams are seen as associations and memories of the cerebral cortexthat are elicited by the random discharges of the pons during REM

126
Q

Karni dream theory

A

certain memories require strengthening time period, that period being REM. sleep learning

127
Q

neurons most critical to control of sleeping and waking are part of the…

A

diffuse modulatory neurotransmitter systems

128
Q

what do the diffuse modulatory neurotransmitter systems control?

A

rhythmic behaviors of the thalamus -> EEG rhythms of cerebral cortex

129
Q

how are sleep and the branches of diffuse modulatory systems connected?

A

sleep involves activity in the branches, i.e. inhibition of motor neurons during dreaming

130
Q

what did Cirelli and Tononi discover about sleep?

A
  • in rats
  • 0.5% of genes showed differences of expression levels when awake or asleep
  • awake increased intermediate early and mitochondrial genes
  • sleep increased genes that contribute to protein synth and plasticity
  • changes specific to brain, no other tissues
131
Q

what is the hallmark of an anxiety disorder / anxiety?

A

the occurrence of an inappropriate stress response either when a stressor is not present or when it is not immediately threatening

132
Q

characteristics of a stress response

A
  • avoidance behavior
  • increased vigilance and arousal
  • activation of symp. ANS
  • release of cortisol from adrenal gland
133
Q

HPA axis

A

hypothalamus secretes CRH -> anterior pituitary secretes ACTH -> adrenal gland secretes cortisol

134
Q

what activates the HPA axis?

A

amygdala

135
Q

what deactivates the HPA axis?

A

hippocampus via negative feedback; inhibits CRH release

136
Q

what kind of receptors are sensitive to cortisol?

A

glucocorticoid receptors

137
Q

what are available treatments for anxiety disorders?

A

psychotherapy and anxiolytic medications

138
Q

how do anxiolytic medications treat anxiety disorders?

A

alter chemical synaptic transmission

139
Q

types of anxiolytic medications?

A

GABA, benzoids, SSRIs (new drugs targeting CRH receptors)

140
Q

affective disorders are defined as…

A

disorders of mood

141
Q

major depression and dysthymia are part of ___ depression

A

recurrent

142
Q

symptoms of major depression

A
  • lowered mood, interest, pleasure, and appetite
  • insomnia or hypersomnia
  • fatigue
  • feelings of worthlessness or guilt
  • cant concentrate
  • suicidal thoughts
143
Q

dysthymia

A

milder than major depression, seldom disappears spontaneously

144
Q

bipolar disorder

A

repeated episodes of mania, or mixed episodes of mania and depression

145
Q

symptoms of mania

A
  • inflated self-esteem or grandiosity
  • decreased need for sleep
  • increased talkativeness
  • flight of ideas, subjective experience that thoughts are racing
  • distractability
  • increased goal-directed activity
146
Q

type 1 bipolar

A

manic episodes with no depression

147
Q

type 2 bipolar

A

hypomania; mild mania and hella depression

148
Q

what is the monoamine hypothesis of affective disorders?

A

deficit in central diffuse modulatory systems; depression is a consequence of a deficit in one of these d.m.s.; treatments focus on central serotonergic and/or noradrenergic synapses

149
Q

available treatments for affective disorders

A

psychotherapy, electroconvulsive therapy (ECT), and antidepressants

150
Q

characteristics of electroconvulsive therapy

A
  • unknown mechanism in relieving depression
  • affects temporal lobe
  • advantage: quick relief of depression and mania
  • adverse affect: loss of prior memories, impaired storage of new information
151
Q

what are the types of antidepressants?

A

MAO inhibitors, tricyclics, SSRIs, and NE-selective reuptake inhibitors

152
Q

MAO inhibitors

A

reduce enzymatic degradation of serotonin and norepinephrine

153
Q

tricyclics

A

block reuptake of norepinephrine and serotonin

154
Q

SSRIs

A

act only on serotonin terminals (ex: fluoxetine)

155
Q

adaptation of antidepressants

A

therapeutic actions take weeks to develop

156
Q

what common drug is used to treat affective disorders (mainly major depressive disorder)?

A

ketamine

157
Q

how does deep brain stimulation (DBS) help neurologic and psychological disorders?

A

in depression: stimmies anterior cingulate cortex to decrease brain activity in circuits that are chronically overactive

158
Q

what is the first step in wiring the nervous system?

A

neurogenesis

159
Q

when are the majority of neurons made? at what rate?

A

before birth. 250,000 cell/min

160
Q

when will the neuron never divide again?

A

when neuronal fate is reached

161
Q

what are the three stages of neuronal structure development?

A

cell proliferation, cell migration, and cell differentiation

162
Q

subventricular zone (SVZ)

A

in the lining of the lateral ventricles; site where neuroblasts are formed

163
Q

where do neuroblasts migrate to once formed?

A

to the olfactory bulb via the rostral migratory system (RMS)

164
Q

subgranular zone (SGZ)

A

in the dentate gyrus of the hippocampus area

165
Q

are radial glial cells only a scaffold?

A

no, they also give rise to neurons and astrocytes (aka neuro progenators)

166
Q

how many rounds of division will a neuron go through?

A

2 - one symmetrical and one asymmetrical

167
Q

how do pyramidal cells and astrocytes migrate out of the SVZ?

A

vertically by moving along thin radial glial fibers

168
Q

how are inhibitory interneurons and oligodendroglia different in generation and migration?

A

they generate in a different place and migrate laterally

169
Q

when does a cell look like a neuron? when is it programmed to be a neuron?

A

takes on characteristics of neuron once it reaches destination, but is programmed way before that

170
Q

put the following in order from first to differentiate to last: astrocytes, oligodendrocytes, and neurons

A

neurons, astrocytes (peak @ time of birth), oligodendrocytes

171
Q

chemoaffinity hypothesis

A

chemical markers on growing axons are matched with complementary chemical markers on their targets to establish precise connections

172
Q

what are some growth guidance cues?

A

chemoattractant (ex: netrin) and chemorepellent (ex: slit)

Fundamentals of Neuroscience (1 decks)

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