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PSYCH 2220 B Midterm > Lecture 4: Sensorimotor System & Hearing, Balance, Taste, Smell > Flashcards

Lecture 4: Sensorimotor System & Hearing, Balance, Taste, Smell Flashcards

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1
Q

all animals have sensory organs containing

A

receptor cells that sense some forms of energy - called stimuli

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2
Q

the concept of labeled lines:

A

we can distinguish different types of touch because our skin contains a variety of receptors and uses some lines to signal light touch, others to signal vibration, and yet other lines to signal stretching of the skin

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3
Q

sensory transduction

A

Energy transformation from the external to internal world - converting the signal from environmental stimuli into action potentials that our brain can understand

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4
Q

free nerve endings

A

pain, itch, and temp

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5
Q

merkels disc

A

touch responsive to edges and to isolated points on a surface

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6
Q

Meissner corpuscle

A

touch responsive to perceive the forms of objects we touch

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7
Q

hair follicle receptor

A

touch

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8
Q

Pacinian corpuscle

A

vibration and pressure

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9
Q

ruffini corpuscle

A

stretch

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10
Q

The structure and function of the Pacinian Corpuscle

A

each corpuscle surronds an afferent nerve ending

vibration applied to the corpuscle stretches part of the neuronal membrane, opening the ion channels and permitting the entry of Na+, which initiates an action potential

as stimulus intensity increases, so does the neurons response until it reaches threshold, triggering an action potential which makes us aware of the stimulus

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11
Q

intensity of a stimulus can be represented by:

A

the number and thresholds of activated cells

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12
Q

somatosensory system

A

body sensation system

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13
Q

receptive field

A

consists of a region of space in which a stimulus will alter that neuron’s firing range

example: which patch of skin must we stimulate to change the activity of one particular touch receptor

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14
Q

sensory adaptation

A

progressive decrease in a receptor response to a sustained stimulation

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15
Q

phasic receptors

A

display adaptation to stimuli

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16
Q

tonic receptors

A

show little or no adaptation and thus can signal the duration of a stimulus

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17
Q

sensory systems often shift

A

away from an accurate portrayal of the external world

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18
Q

central modulation of sensory information

A

the brain actively controls the information it receives and helps the brain attend to some stimuli more than others

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19
Q

somatosensory projections ascend as part of the spinal cords:

A

dorsal column system, a large wedge of white matter in the dorsal spinal cord

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20
Q

dermatome

A

the strip of skin that is innervated by a particular spinal nerve

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21
Q

describe the pathway of sensory inputs to the CNS

A

touch receptors detect stimulation and send action potentials along axons that enter dorsal roots of the spinal cord. This axon is part of a unipolar neuron, the cell body of which resides in the dorsal root ganglion

once the axon enters the spinal dorsal horn, it joins the dorsal column of white matter and ascends to the brain

in the medulla, the axon from the periphery makes its first synapse, innervating a neuron of the dorsal column nuclei. this medullary neuron in turn sends its axon across the midline and up to the thalamus

at this point, the left thalamus will be receiving information about the right side of the body, this thalamus will in turn send this information to the somatosensory cortex

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22
Q

for most senses, information reaches the ________ before being relayed to the cortex

A

thalamus

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23
Q

Levels of sensory processing:

A

sensory information enters the CNS through brainstem or spinal cord and travels to the thalamus

the thalamus shares the information with the cerebral cortex, the cortex directs the thalamus to suppress some sensations

primary sensory cortex swaps information with the nonprimary sensory cortex

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24
Q

primary sensory cortex

A

generally the initial destination of sensory inputs to the cortex

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25
Q

nonprimary sensory cortex

A

may receive and process the same information, often in collaboration with primary sensory cortex

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26
Q

Primary somatosensory cortex (S1)

A

in postcentral gyrus

receives information from the opposite side of the body

parts if the body especially sensitive to touch have large representations in s1 compared with less sensitive areas

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27
Q

sensory homunculus

A

the size of each body part reflects the proportion of s1 devoted to that part

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28
Q

the use of one sensory system influences perception from

A

another sensory system

humans detect visual signals more accurately if accompanied by a sound

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29
Q

association areas

A

process a mixture of inputs from different modalities

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30
Q

synesthesia

A

when seeing a number evokes a colour, or music becomes a taste

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31
Q

three components of pain experience

A

the sensory-discriminative dimension (throbbing, gnawing, shooting)

the motivational-affective (emotional) dimension (tiring, sickening, fearful)

an overall cognitive-evaluative dimension (no pain, mild. excruciating)

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32
Q

nociceptors

A

on free nerve endings specialized to detect damage

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33
Q

substances in injured tissue:

A

serotonin, histamine, and various enzymes and peptides can stimulate nociceptors

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34
Q

Peripheral Mediation of Pain

A

damaged cells release substances that excite free nerve endings that function as nociceptors

action potential generated in the periphery can reflexively excite blood vessels and mast cells to produce inflammation

stimulated mast cells release histamine and a chloroquine-like molecule

information enters through dorsal root and synapses on neurons in dorsal horn

pain fibers release glutamate as a transmitter and substance P as a neuromodulator in the spinal cord. the dorsal horn cells then send information across the midline and up to the thalamus

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35
Q

SCN9A gene

A

encodes a sodium channel expressed in free nerve endings that serve as nociceptors

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36
Q

study of capsaicin TRPV1

A

the chemical that makes chili peppers spicy hot

TRPV1 receptor, or vanilloid receptor 1, detects the spicy heat

belongs to a larger family of proteins called transient receptor potential (TRP) ion channels

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37
Q

TRPM3

A

detects even higher temperatures than TRPV1, but does not respond to capsaicin

found on A-delta fibers, which are large diameter myelinated axons, so the action potentials reach spinal cord quickly

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38
Q

Nerve fibers that possess TRPV1 consist of:

A

thin, unmyelinated fibers called C-fibers

initial sharp pain from burning yourself is conducted by fat A delta fibers activated by TRPM3 receptors, and the long-lasting dull ache after arises from slower C fibers and their TRPV1 receptors

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39
Q

Substance P

A

a peptide that selectively boosts pain signals and remodels pain pathway neurons

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40
Q

pain information is integrated in the:

A

cingulate cortex

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41
Q

neuropathic pain

A

neurons continue to directly signal pain and amplifies the pain signal, in the absence of any tissue damage

e.g. phantom limb pain

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42
Q

gate control theory

A

hypothesizes that “spinal gates”– modulation sites at which pain can be facilitated or blocked– control the signal that gets through the brain

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43
Q

analegesia

A

absence of pain

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44
Q

endorphins

A

bing to specific receptors in the brain to reduce pain

this action is pronounced in brainstem region called the periaqueductal gray

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45
Q

transcutaneous electrical nerve stimulation

A

mild electrical stimulation is applied to nerves around injury sites to relieve pain

we know that TENS acts at least in part by releasing endogenous opioids

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46
Q

placebo effect

A

placebos work by activating the brains endogenous opioid system

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47
Q

acupuncture

A

resembles a placebo

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48
Q

stress activates:

A

both an opioid-dependent form of analgesia, which can be blocked by naloxone

endogenous analgesic systems allow a wounded individual to fight or escape rather than be overwhelmed with pain

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49
Q

placebo

A

may activate endorphin-mediated pain control

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50
Q

hypnosis

A

alters brains perception of pain

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51
Q

stress

A

uses both opioid and non-opioid mechanisms

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52
Q

cognitive

A

may activate endorphin-mediated pain control system

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53
Q

opiates

A

bind to opioid receptors in periaqueductal gray and spinal cord

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54
Q

spinal block

A

blocks pain signals in the spinal cord

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55
Q

anti-inflammatory drugs

A

block chemical inflammatory signals at the site of injury

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56
Q

cannabinoids

A

act in nociceptor endings, spinal cord, and brain

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57
Q

TENS/mechanical

A

on large fibers, blocks or alters pain signal to brain

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58
Q

central gray

A

electrically activates endorphin-mediated pain control systems, blocking pain signal in the spinal cord

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59
Q

motor plan

A

a complex set of commands to muscles that is established before an act occurs

60
Q

Electromyography

A

track simple movements that make up and act by recording the electrical activity of muscles as they contract

61
Q

antagonist muscle group

A

When one muscle group contracts, it stretches the other group— they are antagonists. E.g.bicep and tricep.

62
Q

synergists

A

Muscles that act together to move a limb are synergists

63
Q

At the neuromuscular junction,

A

the neurotransmitter acetylcholine (ACh) is released.

64
Q

The motor neuron, together with all muscle fibers it innervates, is known as a

A

motor unit. Some motor units are bigger than others, e.g.thigh muscle vs face muscles)
The fibers respond to the release of ACh triggering the molecular events that cause contraction.

65
Q

Proprioception

A

the collection of information about body movements and position.

66
Q

muscle spindle

A

is a capsule, buried in other muscle fibers, that contains intrafusal fibers—it responds to stretch.

67
Q

Golgi tendon organs

A

are sensitive to muscle tension. Golgi tendon organs detect overloads that threaten to tear muscles and tendons and may cause sudden relaxation (dropping something you cannot carry).

68
Q

The Stretch Reflex Circuit

A

a weight dropped into the hand stretches the biceps muscle

the stretch excites the muscle spindle, which sends action potentials to the dorsal spinal cord

the action potentials synapse onto motor neurons in the spinal cord that cause the biceps to contract, restoring the arm to its original position

the muscle spindle also excites interneurons, causing the triceps to relax when the bicep contracts

69
Q

the pyramidal system

A

consists of neuronal cell bodies within the frontal cortex and their axons, which pass through the brainstem, forming the pyramidal tract to the spinal cord

70
Q

extrapyramidal system

A

tracts outside the pyramids of the medulla, they and their connections are lumped together as the extrapyramidal system

lesions interfere with systems that regulate and fine-tune motor behaviour

projections pass to the spinal cord via specialized motor regions (retiuclar formation and red nucleus) of the midbrain and brainstem. the basal ganglia are an important point of origin for extrapyramidal projections

71
Q

M1

A

the primary motor cortex occupies a single large cortical gyrus: the precentral gyrus

M1 will cause movement in the corresponding region of the right side of the body

72
Q

The Supplementary motor Cortex and Premotor cortex together make up the:

A

nonprimary motor corte

73
Q

Supplementary Motor cortex:

A

seems important for the initiation of movement sequences

74
Q

Premotor cortex

A

seems to be activated when motor sequences are guided by external events

75
Q

In M1recordings from monkeys making arm movements, commands can be observed:

A

M1 cells change firing rate according to the direction of the movement.
*Each cell has one direction that elicits the highest discharge rates. *An average of neuronal activity allows scientists to predict the direction of arm movements.

76
Q
A
77
Q

Motor cortex damage can cause

A

plegia(paralysis) or paresis (weakness) of voluntary movements.

78
Q

A subregion of premotor cortex (F5) contains cells called

A

mirror neurons.

these neurons fire before making a movement as when observing another individual make the same movement

79
Q

The basal ganglia

A

are a group of interconnected forebrain nuclei that modulate movement
*Caudate nucleus, putamen, and globus pallidus
*With inputs from the substantia nigra and subthalamic nucleus

help control the amplitude and direction of movement and are important in
- initiation of movement
- movements performed by memory rather than by sensory control

80
Q

The cerebellum receives inputs from

A

sensory sources and other brain motor systems.
*Guides movement through inhibition
*Helps fine-tune skilled movements

81
Q

Damage to extrapyramidal systems impairs

A

movement

Common symptoms of cerebellar damage include abnormal gait and posture, especially ataxia(loss of coordination) of the legs.

82
Q

Decomposition of movement

A

describes gestures that are broken into segments instead of being executed smoothly.

83
Q

Parkinson’s disease

A

caused by progressive loss of dopaminergic cells in the substantia nigra, which results in slowed movement, tremors in the hands and face, rigid posture, and reduced facial expression.

84
Q

Huntington’s disease

A

caused by progressive damage to the basal ganglia, especially the caudate and putamen, which results in increasingly excessivemovement, beginning with clumsiness and twitches of the fingers and face.

85
Q

Amplitude, or intensity, measured in

A

decibels(dB) and perceived as loudness

86
Q

Frequency, measured in

A

number of cycles per second, or hertz(Hz), and perceived as pitch

87
Q

sound from a musical instrument contains

A

A fundamental—the basic frequency

Harmonics—multiples of that frequency

Timbre—characteristic sound quality of an instrument, determined by the intensities of its harmonics

88
Q

External ear

A

Pinna—collect sound waves

Ear canal (or auditory canals)

The shape of the external ear modifies the character of sound frequencies that reach the middle ear

89
Q

Three ossicles

A

—the malleus, incus, and stapes—connect the tympanic membrane(eardrum) to the oval window.

90
Q

Sound waves in the air strike the

A

tympanic membrane and cause it to vibrate with the same frequency as the sound.
This vibration also causes ossicles to move, which amplifies vibrations. These vibrations are crucial for converting vibrations in the air to movements of fluid in the inner ear.

91
Q

cochlea of the inner ear

A

converts vibrations into neural activity

92
Q

The cochlea has three parallel canals:

A

Scala vestibuli(vestibular canal)
*Scala media (middle canal)
*Scala tympani (tympanic canal)

93
Q

round window

A

a membrane that separates the tympanic canal from the middle ear

94
Q

Organ of Corti

A

a receptor system in the scala media

has three main structures:
*Sensory cells, or hair cells
*supporting cells
*Terminations of the auditory nerve fibers
The basilar membrane is the base of the organ of Corti.

95
Q

Sound vibrations cause the basilar membrane to

A

ripple

96
Q

different parts of the basilar membrane respond to different frequencies:

A

high frequency: have greatest effect at the base, where is it narrow and relatively stiff

low frequency: produce larger response near apex, where it is wider and more flexible

97
Q

sterocillia

A

tiny hairs protrude from each hair cell

Stereocilia are connected to each other by tip links—tiny fibers that open ion channels when the stereocilia bend.
*A depolarization of the hair cell occurs and neurotransmitter is released.

98
Q

inner hair cells

A

a single row near the central axis

99
Q

outer hair cells

A

three rows

100
Q

vestibulocochlear nerve

A

cranial nerve VIII contacts the bases of the hair cells

101
Q

IHC afferents

A

convey action potentials that provide sound perception to the brain.

102
Q

IHC efferents

A

lead from the brain to the IHCs, allowing the brain to control responsiveness of IHCs.

103
Q

OHC afferents

A

convey information to the brain about the mechanical state of the basilar membrane, not sounds themselves.

104
Q

OHC efferents

A

lead from the brain to OHCs, allowing the brain to modify the stiffness of the basilar membrane, thus sharpening and amplifying sounds.

105
Q

Auditory signal pathway from cochlea to cortex

A

Auditory nerve fibers from IHCs terminate in the cochlear nuclei.

The cochlear nuclei then send information to the superior olivary nuclei.

Superior olivary nuclei pass this information, from both ears, to the inferior colliculi—the primary auditory centers of the midbrain.

Outputs of the inferior colliculi go to the medial geniculate nuclei of the thalamus.

Pathways from here extend to auditory cortex.

IHC-cocholear nuclei-superior olivary nuclei-inferior colliculi-medial geniculate nuclei of the thalamus- auditory cortex

106
Q

auditory pathways have tonotopic organization

A

They are arranged in a map of low to high frequency. At higher levels, auditory neurons are excited by certain frequencies and inhibited by neighboring ones, resulting in the ability to discriminate tiny differences.

107
Q

sound mainly activates the

A

primary auditory cortex (A1)

108
Q

differences in frequency are important for our sense of pitch

A

frequency - a physical property of sound
pitch - our subjective perception of sound

109
Q

place coding

A

pitch is determined by the location of activated hair cells

the base of cochlea responds to high frequencies and signals treble, and activation of receptors near apex which responds to low frequencies, signals base

110
Q

temporal coding

A

encodes the frequency of auditory stimuli in the firing rate of auditory neurons

111
Q

infrasound

A

less than 20 Hz

112
Q

ultrasound

A

More than 20,000 Hz

113
Q

interaural intensity difference

A

result from the intensity of a sound

depending on the species, intensity differences occur because one ear is pointed more directly towards the sound source or because the head casts a shadow, preventing sounds originating on one side (off-axis sounds)

the head shadow effect is most pronounced for higher frequencies

114
Q

interaural temporal differences

A

differences between the two ears in the time of arrival of sounds

one ear is always a little closer to an off-axis sound than the other ear is

onset disparity: the difference between the two ears in hearing the beginning of a sound

ongoing phase disparity: the continuing mismatch between the two ears in the time of arrival of all the peaks and troughs that make up the sound wave

115
Q

spectral filtering

A

The structure of the external ear can reinforce some frequencies, anddiminish others

116
Q

Heschl’s gyrus

A

the primary auditory cortex where music is first processed

117
Q

amusia

A

lifelong inability to discern tunes or sing

associated with abnormal function in right frontal lobe and impoverished connectivity between frontal and temporal cortex

118
Q

Conduction deafness

A

disorders of the outer or middle ear prevent sounds from reaching the cochlea

119
Q

sensorineural deafness

A

hair cells fail to respond to movement of the basilar membrane; no action potentials fired
*Caused by genetic mutations, infections, ototoxic effects of drugs, loud sounds
*Damage to hair cells can result in tinnitus, a persistent ringing in the ears

120
Q

central deafness

A

damage to auditory brain areas such as by stroke, tumors or traumatic brain injury

121
Q

word deafness

A

selective difficulty recognizing normal speech sounds; normal speech and hearing of nonverbal sounds

122
Q

cortical deafness

A

difficulty recognizing all complex sounds, verbal or nonverbal; rare

123
Q

Parts of the vestibular system:

A

*Semicircular canals—three fluid-filled tubes, connected to the utricle and saccule

Canals (tubes) are oriented in three planes of head movement:
1. Nodding(pitch, y-axis)
2. Shaking(yaw, z-axis)
3, Tilting(roll, x-axis)

*Ampulla—enlarged chamber at the base of the canals; contains hair cells

124
Q

receptors in the utricle and saccule provide

A

acceleration and deceleration signals

125
Q

head movements initiate flow of fluid in:

A

semicircular canal of the same plane, which deflects stereocilia in the ampulla, signaling movement in the brain

126
Q

Many vestibulocochlear nerve fibers terminate in the

A

vestibular nuclei in the brainstem; some project directly to the cerebellum.

127
Q

motion sickness

A

too much vestibular excitation

128
Q

sensory conflict theory

A

sickness occurs when we receive contradictory sensory such as between vestibular and visual input

one hypothesis is that nausea evolved to rid the body of ingested toxins that presumably triggered dizziness

129
Q

five basic tastes

A

salty, sour, sweet, bitter, umami

130
Q

three kinds of taste papillae

A

circumvallate, foliate, fungiform

131
Q

taste buds

A

embedded in the papillae, extend microvilli into a pore where they can contact tastants

132
Q

salty

A

Sodium (Na+) ions enter taste cells via sodium channels, causing depolarization.
*A second salt sensor is TRPV1 (transient receptor potential vanilloidtype 1), which increases sensitivity to Na+and alsodetects cations of other salts in food.

133
Q

sour

A

Acids release hydrogen ions (H+) and taste sour.
*Sour taste cells all seem to contain the same type of ion channel that allows an influx of protons, which depolarizes the cell.
*The same receptor detects carbonation in drinks

134
Q

sweet, bitter and umami

A

all activate second messangers within the cell

135
Q

sweet

A

detected by a heterodimer of T1R2 and T1R3

136
Q

bitter

A

detected by T2R receptors
*Each bitter-sensing cell produces most or all of the different bitter receptors.
*High sensitivity to bitter evolved to detect poison.

137
Q

umami

A

meaty-savory flavor—is detected by two types of receptors:

*Metabotropic glutamate receptor that responds to glutamate: Stimulated by monosodium glutamate (MSG), a flavor enhancer

*Receptor that is a combination of T1R1 and T1R3: Responds to most dietary amino acids

138
Q

gustatory system

A

extends from the tongue to brainstem nuclei, to the thalamus, and ultimately to the somatosensory cortex

The brain may simply monitor which specific axons are active to determine which tastes are present.
*May be a labeled line system *
Other four tastes remain intact when receptors for one taste are inactivated

139
Q

olfaction

A

sense of smell

140
Q

anosmia

A

inability to smell

141
Q

olfactory epithelium

A

types of cells in epithelium: supporting cells, basal cells, receptor neurons

142
Q

odorants

A

inhaled molecules that interact with olfactory receptor proteins on the dendrites

143
Q

olfactory neurons differ from neurons of the brain:

A

incredible diversity of receptor subtypes

die and are replaced in adulthood

144
Q

olfactory bulb

A

each olfactory axon extends onto this bulb of the brain

the axon terminates on a specific glomerulus, which receives information from one specific class of odorant recpetors

145
Q

glomeruli

A

organized like a map, adjacent glomeruli receive input from the receptors that are closely related

146
Q

olfactory information is conveyed to the brain via

A

mitral cells which extend from glomeruli in the olfactory bulbs to various regions of the forebrain

PSYCH 2220 B Midterm (3 decks)

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