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BPK306 > Midterm 3 > Flashcards

Midterm 3 Flashcards

1
Q

what is the role of the somatosensory system? what type of information does it provide?

A

provides information about the CNS about the state of the body and its contact with the environment
- exteroceptive: senses looking at outside world
- proprioceptive: movement of our body
- enteroceptive: internal messages (gut)

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2
Q

where are receptor potentials generated in the somatosensory system?

A

distal tips of a first-order neuron (cell bodies in the dorsal root)
- first-order neuron is unipolar

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3
Q

what information does the dorsal column medial lemniscus (DCML) carry? where does it cross? what fibres is it composed of?

A

fine discriminatory touch, proprioception, vibration
- crosses at medulla
- type III and IV afferents

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4
Q

what information does the spinothalamic tract carry? where does it cross? what fibres is it composed of?

A

pain, temperature, crude touch
- crosses at level of spinal cord (enters through ipsilateral dorsal horn but crosses to contralateral lateral tract)
- type III and IV afferents (smaller diameter than DCML neurons, making their transmission slower)

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5
Q

what is a dermatome?

A

a given dorsal root (sensory neurons) supplying a specific cutaneous region

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6
Q

what are the types of sensory afferents in the skin?

A

glabrous skin:
- Meissner’s corpuscles (superficial)
- Pacinian corpuscles (deep)
- Merkel’s disk (superficial)
- Ruffini endings (deep)
hairy skin:
- hair and nerve fibres
- free nerve endings

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7
Q

what type of afferents are Meissner’s corpuscles?

A

FA1: fast-adapting, small receptive field
- sensitive to rate of change (fire when stimulus intensity is changing)
- fires more because smaller receptive field

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8
Q

what type of afferents are Pacinian corpuscles?

A

FA2: fast-adapting, large receptive field
- sensitive to rate of change (fire when stimulus intensity is changing)
- fires less because larger receptive field

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9
Q

what type of afferents are Merkel’s discs?

A

SA1: slow-adapting, small receptive field
- sensitive to pressure + rate of change of pressure
- sustained firing due to sustained touch
- increased firing during change, sustained firing after change

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10
Q

what type of afferents are Ruffini endings?

A

SA2: slow-adapting, large receptive field
- sensitive to pressure + rate of change of pressure
- sustained firing due to sustained touch

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11
Q

in the DCML, where does each type of neuron synapse?

A
  • first-order neurons enter spinal cord and project to dorsal column medial nuclei of the medulla
  • second-order neurons decussate at the medulla and then project to thalamic nuclei
  • third-order neurons located in thalamus project to S1
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12
Q

what afferents are responsible for fast vs slow pain in the ST?

A
  • fast: III
  • slow: IV
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13
Q

in the ST, where does each type of neuron synapse?

A
  • primary afferents project to secondary afferents in spinal cord (they decussate)
  • secondary afferents project to tertiary afferents in the VPI thalamus and then to S1 + other areas for emotional responses
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14
Q

what kind of ion channels do free nerve endings of nociceptors possess?

A

transient receptor potential (TRP) ion channels
- chemo-, mechano-, and thermo-sensitive

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15
Q

what TRP channel is heat sensitive? cold sensitive?

A
  • heat: TRPV1
  • cold: TRPM8
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16
Q

what receptors do incoming afferent pathways receive their proprioceptive information from?

A

muscle spindles and golgi tendon organs

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17
Q

what is the myotatic (stretch) reflex? how many synapses does it have? what is its pathway?

A

knee-jerk (patellar reflex) -> monosynaptic
- Ia fibres originate in the muscle spindle and enters the dorsal root
- one branch passes directly to the ventral horn and synapses directly with alpha motorneurons innervating the same muscle containing the muscle spindle (contracts)
- other branch synapses on an inhibitory interneuron neuron that inhibits the antagonistic pair

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18
Q

what is the net result of the myotatic (stretch) reflex?

A

the agonist (rectus femoris) is excited (contracts) and the antagonist (semitendinosus) is inhibited (relaxes)
- extension of leg at knee

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19
Q

what kind of channels are involved in muscle spindle information transmission?

A

mechanically gated TRP channels open in response to rapid, transient stress (ex. unexpected disruption to an ongoing movement) to produce graded receptor potentials

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20
Q

what does the myotatic (stretch) reflex regulate? what is Westphal’s sign?

A

regulates muscle length, keeping muscle length constant
- when a muscle lengthens, alpha motorneuron activity increases, causing muscle fibres to contract and resist the stretch
- Westphal’s sign: absence of patellar reflex; may occur with lower motor neuron lesions (b/c doesn’t require CNS input)

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21
Q

what fibres mediate the effect of a tendon tap?

A

dynamic fibres - sensitive to velocity of change

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22
Q

what fibres mediate the effect of bending a limb?

A

slower, therefore tonic fibres - sensitive to amplitude and duration
- always firing but fire more in response to increased force/length of movement

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23
Q

what is the inverse myotatic reflex? how many synapses does it have? when does it occur? what is its pathway? what is the net effect?

A

opposite of the stretch reflex; used to prevent hyperextension -> disynaptic
- occurs with extension at the knee (rec fem is extensor, semitend. is flexor)
- Ib afferent fibres in GTOs within rec fem enter spinal cord and synapse onto:
1) interneurons that inhibit the motor neurons of the extensor (rec fem)
2) interneurons that excite the motor neurons of the flexor (semitendin.)
extensor relaxes and flexor contracts (flexion of leg at knee)

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24
Q

what is the function of the inverse myotatic reflex?

A

functions to maintain posture
- during prolonged standing, extensor fatigues, leading to decreased force in GTO
- reduced firing in 1b afferent will disinhibit extensor, helping to reduce loss in force due to fatigue

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25
Q

how does GTO force influence the function of the inverse myotatic reflex?

A
  • with increased GTO force, due to inhibitory neurons, reflexes increases motor neuron firing to the flexor and decreases firing to the extensor
  • if muscle tension declines, and GTO force is reduced, GTO firing decreases (decreased inhibition of extensor)
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26
Q

what is the flexor (crossed-extensor) reflex? when does it occur?

A

type of withdrawal reflex (ex. stepping on a painful stimulus) - flexion usually brings limb closer to body away from the painful stimulus
- legs have opposite things going on
- involved in central pattern generation; used in locomotion with repetitive circuits (ex. walking- rhythmic activity)

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27
Q

what triggers the crossed-extensor reflex?

A

in response to stepping on a painful stimulus, nociceptors detect the pain and transmit it through flexor reflex afferents (FRAs) that are type III and IV fibres (slow, small diameter, unmyelinated)

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28
Q

what are the pathways involved in the crossed-extensor reflex?

A

afferent input from FRAs enter the spinal cord and synapse onto:
1) excitatory interneurons to activate alpha motorneurons that innervate ipsilateral flexors
2) inhibitory interneurons to inhibit alpha motorneurons to ipsilateral extensors
3) commissural interneurons to produce the opposite effect on the contralateral side, which allows for shifting of weight (reciprocal innervation)

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29
Q

what is reciprocal innervation?

A

contraction of one muscle (or group) is accompanied by simultaneous inhibition of the antagonistic muscle (or group)
- achieved by inhibitory interneurons

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30
Q

what is the net effect of the crossed-extensor reflex?

A

ipsilateral flexion and contralateral extension
- flexion to move leg away from painful stimulus
- extension to shift balance to the other foot

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31
Q

what is recurrent inhibition?

A

permits a negative feedback mechanism that activates when flexor motor neuron is overactive -> prevents muscular damage from overexcitation and tetanus
- involves Renshaw cells (RCs): specialized inhibitory interneurons

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32
Q

what is an example of recurrent inhibition?

A
  • in response to extensor muscle being used too much, extensor provides feedback to RC which inhibits the alpha motor neuron innervating the extensor (reduces firing)
  • RC inhibits Ia inhibitory interneuron of flexor alpha motor neuron -> disinhibition excites flexor to reduce/take on the extensor load
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33
Q

how does tetanus toxin affect RCs?

A

tetanus toxin targets RCs
- inhibits release of GABA/glycine from RCs, causing alpha motor neurons to overexcite
- causes tetanus/rigid paralysis

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34
Q

what is the musculotopic organization of the ventral horn of the spinal cord?

A
  • motor neurons that supply axial muscles (proximal) are medial; motor neurons that supply limb muscles (distal) are lateral
  • motor neurons to flexors are dorsal to those tha innervate extensors
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35
Q

what are the lateral descending pathways?

A
  • lateral corticospinal tract (90% of corticospinal tract)
  • rubrospinal tract
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36
Q

lateral corticospinal tract: where does it originate? where does it decussate? where does it end? what musculature does it supply?

A
  • originates in the frontal lobe (layer V) motor cortex and projects ipsilaterally through internal capsule into the medulla
  • crosses in the medullary pyramids
  • descends contralaterally and synapses on interneurons or motor neurons in the lateral ventral horn
  • controls distal musculature -> fine independent movement of distal limbs and dexterity
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37
Q

rubrospinal tract: where does it originate? where does it decussate? where does it end? what musculature does it supply?

A
  • originates in the red nucleus of the midbrain, where it decussates and descends through the pons and medulla
  • neurons terminate in lateral portions of the spinal cord grey matter and excite motor neurons mainly via interneurons
  • mainly controls upper limb flexors
  • integrates input from cerebellum and motor cortex
  • minor in humans
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38
Q

what are the medial descending pathways?

A
  • medial corticospinal tract (10% of corticospinal tract)
  • vestibulospinal tract
  • reticulospinal tract
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39
Q

medial corticospinal tract: where does it originate? where does it decussate? where does it end? what musculature does it supply?

A
  • originates in the frontal lobe (layer V) motor cortex and projects ipsilaterally through internal capsule into the medulla
  • descends ipsilaterally past medulla and into the spinal segment where is decussates
  • supplies proximal muscles
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40
Q

vestibulospinal tract: where does it originate? where does it decussate? where does it end? what musculature does it supply?

A
  • originates in the lateral/medial vestibular nuclei; receives input from semicircular canals and otolith organs
  • does not cross
  • descends to ipsilateral spinal segments and supplies motor neurons of trunk and extensor muscles important for postural control (ex. gastroc)
  • regulate movement of axial and proximal limb muscles
  • postural adjustments in response to angular and linear accelerations of the head
  • lesions can cause inabilities to maintain posture or move limbs away from body
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41
Q

reticulospinal tract: where does it originate? where does it decussate? where does it end? what musculature does it supply?

A

medullary:
- originates in the medulla, has both ipsilateral (largely) and contralateral components
- contralateral components decussate in medulla
- end on interneurons that control voluntary and reflex axial and limb muscles; largely inhibitory
pontine:
- originates in pontine reticular formation
- largely uncrossed; ends on interneurons
- controls axial proximal extensor muscles that support posture; reflexes responses and muscle tone
- influence activity of intercostal and phrenic nerves (component in breathing) + role in CPG

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42
Q

what symptomology is a result of lesions in lateral descending pathways?

A
  • weakness of distal muscles (ex. fingers)
  • paralysis (negative sign)
    -Babinski - dorsiflexion of big toe instead of curling
  • spasticity if RtS is also damaged (positive sign)
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43
Q

what symptomology is a result of lesions in medial descending pathways?

A
  • reduced tone of postural muscles + gross movement
  • loss of righting reflexes (reflexive fixing posture)
  • locomotor impairment (ex. gait)
  • frequent falling
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44
Q

what are capsular strokes?

A

strokes in the internal capsule -> deficits in corticospinal pathways

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45
Q

what are the types of postural reflexes (brainstem reflexes not involving cortex)?

A
  • tonic neck reflexes: activated by muscle spindles in neck muscles; observed in newborns (fencing reflex - causing opposing movements in opposite sides of the body; ex. flexion in one leg + extension in the other); absent shortly after birth
  • vestibular reflexes originating in the inner ear
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46
Q

what is an example of a vestibular reflex?

A

righting reflex: rotation of the head activates receptors that send commands via the VS tract, which activates postural support muscles (head tilts to the left, postural support is increased on the left - prevents falling)

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47
Q

how does brainstem control contribute to locomotion?

A
  • cortical influence of CPGs is mediated by projections to locomotor regions in the brainstem
  • primary locomotor region in the brainstem = midbrain locomotor region -> receives input from the motor cortex and projects to the reticulospinal tract
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48
Q

what motor areas are within the frontal cortex?

A
  • FEF: frontal eye field (eye movements)
  • PMA: premotor area (planning, spatial guidance)
  • primary motor cortex (M1): projects via LCS; execution of movement
  • posterior parietal cortex: sensory info pooled here and sent to SMA and PMA
    process are paralleled, not hierarchical
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49
Q

how does the brain control motor movement?

A
  • target of movement isolated by sensory info in parietal cortex, transmitted to PMA and SMA, where planning occurs and motor decisions are made
  • information is transmitted to M1, which initiates signals carried by descending tracts (mostly LCS)
  • 2 modulatory systems:
    • cerebellum
    • basal ganglia
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50
Q

what are the general functions of the cerebellum? what are its 4 nuclei?

A
  • functions in learning and execution of motor movements
  • oversight of movement (compares executed movement with intended movement)
  • fastigial, globose, emboliform, dentate
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51
Q

what are the general functions of the basal ganglia? what are its nuclei?

A
  • movement when a movement should be made (correct timing)
  • do not receive input from spinal cord
  • fires before movement occurs -> thought to influence movements that are to be made
  • globus pallidus and putamen: body movements
  • caudate: body/eye movements
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52
Q

what are the 3 lobes of the cerebellum?

A
  • vestibulocerebellum (flocculonodular lobe)
  • spinocerebellum (anterior lobe)
  • cerebrocerebellum (posterior lobe)
53
Q

what is the function of the vestibulocerebellum?

A

inputs from the vestibular nucleus; responsible for eye movement, balance, muscle tone

54
Q

what is the function of the spinocerebellum?

A

proprioceptive input from the spinal cord, as well as visual and auditory; responsible for control of posture and balance, anticipating future position
- control of trunk

55
Q

what is the function of the cerebrocerebellum?

A

inputs from cortex (via pons: pontocerebellar fibres); responsible for control of reaching rate and force of movement; acts as a “break” to keep from shooting past an object or from oscillating about an object (ie damping)
- limb muscle control

56
Q

what kind of control does the cerebellum have?

A

ipsilateral due to double crossing
- first in cerebellar efferent, then in descending motor pathway

57
Q

what are the 2 major inputs to the cerebellum? what is the major output?

A

inputs:
- climbing fibres
- mossy fibres
output
- Purkinje cells that project to deep cerebellar nuclei, which provide input to the rest of the brain

58
Q

how do mossy fibres provide input to Purkinje cells?

A

excitatory: synapse indirectly on Purkinje cells - first synapse on granule cells that project as parallel fibres -> parallel fibres synapse onto Purkinje cells
- deliver proprioceptive/motor-related info to cerebellum (info about current state of events - baseline/status quo)
- arise from multiple sources
- high frequency (firing all the time)

59
Q

how do climbing fibres provide input to Purkinje cells?

A

excitatory: synapse directly on Purkinje cells
- modify pattern from mossy fibres; alter responsiveness of Purkinje cells to mossy fibres; timing function (motor learning)
- arises solely from the inferior olive nucleus (ION)
- detects errors: activates ION which activates CFs
- low frequency (fires only in response to errors)

60
Q

what kind of firing results in Purkinje cells as a result of mossy fibre input?

A

mossy fibre input causes single APs in PCs (simple spike)
- no direct role in shaping movement
- simple spikes are involved in generating ongoing movement; mismatches activate inferior olive and leads to LTD of active PFs

61
Q

what kind of firing results in Purkinje cells as a result of climbing fibre input?

A

climbing fibre input causes burst of APs in PCs (complex spike)
- alter sensitivity to MF -> LTD
- alters responsivity of PCs to mossy fibre input
- the adjustment of synaptic weight affects activity in the future; no error = system remains as it is (no CF firing); with error = LTD (CF firing present)

62
Q

what is the mechanism of PF-PC LTD?

A

PF-PC is postsynaptic as a reduction in the # of functional AMPARs by clathrin-mediated endocytosis; 3 requirements for induction:
1) CF input contributes to LTD via Ca2+ influx through Cav channels opening in PCs during complex spikes (release moderate levels of Ca2+ b/c CF is low frequency -> LTD due to moderate stimulation
2) PFs release glutamate that act on both mGluR1s (causes AMPAR endocytosis) and AMPARs
3) PKC also though to be involved

63
Q

why is it believed that the reverse BCM rule applies to PF-PC LTD? why is this not true?

A
  • believe that weak conditioning stimulation induces LTP/strong stimulation (due to CF input) leads to LTD
  • not true: MF is high frequency, CF is low frequency -> burst of CF activity still gets you moderate (low) Ca2+ activity, inducing LTD
64
Q

what kind of motor impairments manifest due to cerebellar damage?

A
  • grossly impaired movement
  • defects in rate, range, and force of movement
  • ipsilateral motor deficits
  • intention tremor
  • past pointing (not a clean movement to the target)
  • dysdiadochokinesia (inability to perform rapid and alternating movements; pronate/supinate)
65
Q

what clinical manifestations arise based on the cerebellar lobe damaged?

A
  • flocculonodular: nystagmus, vertigo, balance
  • anterior: ataxia (uncoordination of gait), balance and trunk control issues
  • posterior: limb control issues, dysmetria (inability to control movements), decomposition (inability to complete movements)
66
Q

what is the direct pathway of the basal ganglia?

A

overactivity used to enhance motor activity
- cortical motor areas release glutamate onto caudate/putamen
- caudate/putamen releases GABA onto GPi
- inhibition of GPi reduces GABA release onto thalamus, exciting it
- thalamus released glutamate onto cortical motor areas, allowing for increased SC and brainstem activity and limb movements

67
Q

what is the indirect pathway of the basal ganglia?

A

overactivity used to reduce motor activity
- cortical motor areas release glutamate onto caudate/putamen
- caudate/putamen releases GABA onto GPe; exciting GPi in 2 ways:
1) reduces GABA release of GPe onto subthalamic nucleus, increasing glutamate release onto GPi
2) reduces GABA release of GPe onto GPi
- excited GPi releases GABA onto thalamus, reducing excitatory glutamate release onto cortical motor areas
- reduced output onto SC and brainstem, reducing limb movements

68
Q

what causes Parkinson’s disease?

A

degeneration of the substantia nigra pars compacta pathway
- normally excites direct pathway through excitatory D1 pathway and inhibits indirect pathway through inhibitory D2
- degeneration causes indirect pathway to overpower direct pathway -> constitutive inhibition
- net effect: over-excitation of GPi, more inhibition of thalamus, inhibition of cortical areas and motor movement

69
Q

what is the symptomology of Parkinson’s disease?

A

hypokinetic: movements cannot be executed smoothly
- rigidity, slowness, difficulty with stability and gait, bradykinesia

70
Q

what causes Huntington’s disease?

A

degeneration of the GABAergic projections from the caudate/putamen onto GPe
- causes overinhibition of GPi, less inhibition of thalamus, increased excitation of the motor cortex -> constitutive activity

71
Q

what is the symptomology of Huntington’s disease?

A

hyperkinetic: shaking, jerky involuntary movements (chorea)

72
Q

what muscles are involved in horizontal eye movements? what nerves control these muscles?

A
  • medial rectus controlled by oculomotor nuclei (CN III)
  • lateral rectus controlled by abducens nuclei (CN VI)
73
Q

what are the types of eye movements?

A
  • vestibuloocular (keeps image stable when head moves)
  • optokinetic reflex (keeps image stable when image moves)
  • saccades (rapid eye movements)
  • smooth pursuit (prolonged continuous observation of a moving target)
  • nystagmus (alternating slow and fast movements)
  • vergence (eyes move together)
74
Q

what brainstem centres control horizontal eye movements?

A

gaze centres in the paramedian pontine reticular formation (PPRF) near the abducens and vestibular nuclei

75
Q

what is the optokinetic reflex? what does it depend on? what cells are involved?

A
  • activated by movement of a scene, requires visual input
    ex) watching a train move
  • retinal image slips away from proper position
  • detected by motion-sensitive ganglion cells
  • eye movements will follow the slipping image and stabilize it on the retina
  • often produces perception of movement
  • often occurs with fast saccadic-like movements to produce nystagmus
76
Q

what does nystagmus consist of?

A
  • OPK follows the slipping image and stabilizes it on the retina
  • saccades snap eyes back to the next target
  • nystagmus is alternating between OPK and saccades
77
Q

what is the vestibuloocular reflex (VOR)? what does it depend on? what cells are involved?

A
  • keeps eyes trained on the target as the head moves; requires motor input
  • stable visual scene on the retina achieved when VOR produces eye movement that is equal and opposite to the movement of the head
  • initiated by hair cells in the vestibular apparatus
  • not dependent on visual stimulus or light
  • depends on rotational head movement
78
Q

what is the cross point for oculomotor and abducens nerves?

A

medial longitudinal fasciculus (MLF)

79
Q

which vestibular nuclei is relevant in VOR?

A

medial

80
Q

what is the inhibitory pathway in response to the head rotating left?

A

activation of left semicircular canals -> vestibular afferent -> inhibitory ipsilateral neuron -> inhibits abducens -> left lateral rectus and right medial rectus relax

81
Q

what is the excitatory pathway in response to the head rotating left?

A

excitatory contralateral neuron -> excites abducens -> left medial rectus and right lateral rectus contract

82
Q

how does sound reach the cochlea?

A

sound (compression and decompression) waves strike the tympanic membrane and cause movement of the ossicles (malleus, incus, stapes) in the middle ear -> transmits sound to cochlea

83
Q

what does the vestibule consist of?

A
  • otolith organs (utricle and saccule): linear accelerations
  • semicircular canals (3): rotation
84
Q

what cells are involved in the vestibular apparatus? where do they project to?

A

primary vestibular afferents (specialized receptor cells) of the vestibular nerve (CN VIII)
- CN VIII projects to the vestibular nuclei in the medulla, some fibres project directly to the cerebellum

85
Q

what are characteristics of the semicircular canals? where do afferents project? how do they interact with descending tracts?

A
  • 3 coplanar semicircular canals
  • filled with endolymph
  • detects angular movements or rotational accelerations of the head
  • afferents project to the vestibulocerebellum; vestibulospinal tract allows body to make postural adjustments to maintain balance if equilibrium is disrupted
  • trigger head and eye movements to stabilize visual image on retina
86
Q

where does semicircular canal activation occur? what structures are present here?

A

ampullary crest
- ampulla: outswelling of semicircular canal where it joins the vestibule; contains ampullary crest (endothelium)
- cupula: gelatinous structure that crosses the ampulla and occludes its lumen; contains vestibular hair cells
- innervated by primary vestibular afferents

87
Q

what causes hair cell depolarization in the cupula?

A

angular acceleration of the head causes fluid movement to bend the cupula and cilia of the hair cells within, resulting in hair cell depolarization

88
Q

what are the effects of head movement in semicircular canals?

A

polarization of hair cells
- when bent towards the kinocilium (tallest hair cell), hair cells depolarize and release glutamate/aspartate
- when bent away from the kinocilium, hair cell hyperpolarizes
ex) when you move your head to the left, left semicircular canals have increased firing and right semicircular canals have decreased firing

89
Q

what are characteristics of the otolith organs? how do they signal information?

A
  • hair cells oriented in different directions detect accelerations in different directions
  • gelatinous mass (otolith membrane) containing CaCO3 crystals (otoliths) -> provide weight and amplifies movement
  • inertia due to head movements bends stereocilia in different directions, resulting in the perception of acceleration as depolarization of hair cells
90
Q

what is the composition of endolymph?

A

similar to ICF
- high in K+, low in Na+
- 145 mM K+, 2 mM Na+

91
Q

what channels are involved in depolarization of hair cells? how do they open? what is the ion flux when they open? what NT is released?

A

bending of cilia towards the tallest kinocilium causes mechanically-gated TRP channels to open
- depolarization of hair cells causes K+ influx resulting in increased NT (glutamate) release and firing rate at the vestibular afferent

92
Q

how is vestibular information transduced to the cortex?

A
  • vestibular afferents project to the brainsteam via CN VIII
  • cell bodies in Scarpa’s ganglion
  • project to vestibular nuclei (VN) via the vestibular nerve in medulla and pons
  • afferents end in VN
  • VN project through MLF to oculomotor nuclei (control over eye movements; VOR)
93
Q

where else does vestibular information project (other than vestibular nuclei)?

A
  • collaterals to cerebellum (vestibulocerebellum)
  • vestibulospinal tract (trunk and neck muscles/balance and equilibrium)
  • to thalamus to mediate conscious perception of vestibular activity
94
Q

what is the symptomology of Meniere’s disease?

A
  • nystagmus accompanied by vertigo and nausea
  • brain interprets difference between L and R vestibular systems as motion
  • abnormal eye movement, tinnitus, hearing loss, and related psychological effects
95
Q

what is Meniere’s disease?

A
  • overproduction of endolymph that makes you feel like you’re moving all the time
  • can cause rupture of the vestibular apparatus (semicircular canals)
  • causes mixing of endolymph and perilymph -> transduction cannot occur efficiently
96
Q

what are the parts of the ear that are important for hearing?

A
  • external auditory meatus: funnels sinusoidal waves
  • tympanic window: waves hit this and it acts like a drum to move ossicles
  • ossicles (malleus, incus, stapes): convert energy from tympanic window to oval window (mechanical energy converted to fluid waves)
  • eustachian tube: filters fluid in middle ear (supposed to be air-filled)
  • cochlea
  • auditory nerve (CN VIII)
97
Q

what is the structure of the cochlea?

A
  • basilar membrane separates fluid filled cavities
  • cochlear duct (scala media) contains endolymph and organ of Corti
  • hair cells at the basilar membrane detect fluid movement
  • stereocilia: set of cilia embedded in the tectorial membrane
98
Q

what are the fluid-filled cavities of the cochlea? what are they composed of?

A
  • vestibular duct (scala vestibuli): perilymph (standard ECF)
  • cochlear duct (scala media): endolymph
  • tympanic duct (scala tympani): perilymph
99
Q

how is sound transduced in the cochlea?

A

fluid wave displaces basilar membrane -> mechanically stimulates hair cells that convey frequency-dependent information to cochlear afferents via NT release (glutamate)
- sound waves transduced by organ of Corti

100
Q

where are hair cells situated in the cochlea?

A

hair cells sit on the basilar membrane within the organ of Corti and the cilia of the hair cells are embedded in the tectorial membrane that overlays the basilar membrane

101
Q

how do fluid waves reach the organ of Corti? what is its structure and composition?

A
  • vibration of tympanic membrane -> movement of ossicles -> vibration of oval window -> fluid waves in cochlea
  • upward shear forces cause stereocilia to bend towards the tallest cilium, which depolarizes the hair cell
  • innervated by CN VIII; cell bodies of primary auditory afferents in spiral ganglion
102
Q

how does the basilar membrane move? what happens when it moves?

A
  • net potential for K+ influx causing depolarization
  • cilia arranged in order of height connected via tip links
  • tallest cilium is tethered to the tectorial membrane
  • fluid movement displaces the basilar membrane relative to the tectorial membrane causing the cilia to bend to the tallest cilium
  • tip links act as levers to open K+/Ca2+ channels (TRP1A)
103
Q

what are receptor potentials called in the cochlea? what happens when they are produced?

A

cochlear microphonic potentials: produced in hair cells in response to TRP1A channel K+ influx
- causes glutamate release -> excites primary cochlear afferent nerve resulting in AP generation

104
Q

how does the composition of the basilar membrane change as distance increases from the oval window? why is this significant?

A

TONOTOPIC ORGANIZATION
- at the base (oval window): very narrow and stiff -> transduces high frequencies (20k Hz)
- 100x stiffer than apex
- at the apex: increased width and floppiness -> transduces low frequencies (200 Hz)
- 5x thicker at apex
width, stiffness, and flexibility of the basilar membrane differ along its length

105
Q

what is the place theory of hearing?

A

our perception of sound depends on where each component frequency produces vibrations along the basilar membrane

106
Q

what is labelled line coding (relevant to hearing)?

A

sound of a specific frequency will be transduced on a specific part of the basilar membrane, which will travel to a specific part of the cortex
- this same sound will be perceived the same every time

107
Q

how is sound transduced to the cortex?

A
  • auditory information initiated in hair cells (cochlear microphonic potentials) is transmitted to cochlear afferent cells resulting in APs
  • afferents project via CN VIII to the cochlear nuclei of the brainstem
  • neurons in the ventral and dorsal cochlear nuclei decussate to the contralateral superior olivary nuclei and project to the inferior colliculus and then to the medial geniculate nucleus of the thalamus
  • from thalamus, acoustic radiation fibres project to the auditory cortex in the temporal lobe
108
Q

which ion channel was thought to be responsible for
cochlear microphonic potentials? what evidence
supported and what evidence refuted this notion?

A

TRP1A
1) transcription of TRP1A occurs during sound transduction at hair cells
2) TRP1A antibodies show that the channel localizes at the tips of cilia (where you would expect to see them)
3) if you knockdown TRP1A expression, you turn down mechanotransduction

109
Q

what happens to TRP1A knockout mice?

A

display normal hearing; mice did exhibit hypersensitivity to pain, thus TRP1A is part of the transduction machinery associated with nociception of environmental irritants and endogenous compounds that elicit pain

110
Q

how many smells are there? how many tastes are there?

A
  • ~400 different odor receptors
  • 5 elementary taste qualities
111
Q

what 3 cranial nerves innervate taste buds?

A
  • facial nerve (CN VII)
  • glossopharyngeal nerve (CN IX)
  • vagus nerve (CN X)
112
Q

what are the 5 tastes? what type of receptors are used for each? what are the primary ligands activate them?

A
  • salty: ion channel, sodium chloride (Na+ of NaCl)
  • sweet: GPCR, sucrose
  • sour: ion channel, hydrochloric acid (H+)
  • bitter: GPCR, quinine
  • umami: GPCR, monosodium glutamate (MSG)
113
Q

what are the type of chemoreceptors in taste buds?

A
  • type I: supporting cells, salt sensing
  • type II: sweet, bitter, and umami sensing; metabotropic
  • type III: salty and sour sensing; ionotropic
114
Q

what are basal cells in taste buds?

A

give rise to new chemoreceptors (stem cell pool for renewal of themselves and other chemoreceptors)
- chemoreceptors have a 10 day lifespan

115
Q

how does signal transduction occur in type II chemoreceptors?

A
  • sucrose, quinine, or MSG binds GPCRs, activating gustducin
  • second messenger pathways are activated (PIP2 converted to IP3 and DAG) causing Ca2+ release from stores (ex. ER)
  • increased Ca2+ leads to Ca2+ mediated-NT release of ATP which excites primary gustatory neurons
116
Q

how does signal transduction occur in type III chemoreceptors?

A
  • Na+ (salty) and H+ (sour) enter through ion channels
  • causes depolarization -> results in opening of Ca2+ channels
  • Ca2+ mediated-NT release of serotonin excites primary gustatory neurons
117
Q

how is spicy or minty transduced as taste?

A

thermosensitive TRPV1 channels expressed in receptor cells open in response to heat and also in response to capsaicin (chili pepper extract) (heat-gated, spicy)
- TRPM8 is cold gated (minty) -> chemically gated by menthol (ex. toothpaste tastes cold b/c activates this channel)

118
Q

how does taste reach the primary gustatory cortex?

A
  • cell bodies of taste fibres in CN VII, IX, and X reside in the geniculate, petrosal and nodose ganglia, respectively
  • afferent fibres enter medulla and synapse in the nucleus tractus solitarius (NTS)
  • secondary neurons in the medulla project to the pons
  • pontine neurons project to the ventral posterior medial (VPM) thalamus (largely uncrossed)
  • from thalamus, neurons project to primary gustatory cortex for taste sensation
119
Q

what other areas of the brain does gustation project to?

A
  • pontine taste area projects to lateral hypothalamus (homeostasis, motivation, feeding behaviour)
  • pontine taste area projects to amygdala (emotion/reward)
120
Q

why do we taste salty and sour faster than sweet and bitter?

A

salty and sour are ionotropic which are faster than metabotropic

121
Q

how is olfaction (smell) transduced?

A
  • odorant molecules dissolve in mucus layer and bind an odorant receptor (GPCR)
  • activates Golf which is similar to the Gs pathway
  • activates AC which converts ATP to cAMP
  • cAMP opens CNGs, allowing Na+ and Ca2+ influx (non-selective)
  • Ca2+ opens ANO2 channels (Ca2+-dependent Cl- channel), causing Cl- efflux and further depolarization
  • produces receptor potentials in olfactory receptor cell (bipolar neuron)
  • receptor potentials sum to produces APs at the axon hillock (soma) that propagate down the axon to towards the olfactory bulb
122
Q

what creates the concentration gradient in an olfactory cell?

A
  • Na+/K+-ATPase (2 K+ in, 3 Na+ out)
  • NKCC1 (Na+-K+-Cl- cotransporter) -> secondary active transport, uses Na+ gradient)
    • K+ stays in the cell but Na+ kicked out via Na+/K+-ATPase
123
Q

what are olfactory chemoreceptors?

A

neuronal receptors (exception to the special sense rule, which usually have specialized receptor cells)
- bipolar neurons with cilia containing GPCRs that detect odorant molecules that dissolve into overlaying mucus
- 10^6
- short lifespan and are continually replaced

124
Q

what are supporting cells in the olfactory mucosa?

A

act as a stem cell pool that can differentiate into neuron receptor cells + provide support

125
Q

how does COVID affect your sense of smell?

A

support cells express ACE2 receptors that COVID hijacks
- causes communication problems between support cells and neuronal receptor cells of olfaction
- cannot replace constantly overturned neurons
- impairs cell support + ability to generate new neurons

126
Q

what cells are responsible for lateral inhibition in the olfactory bulb?

A

periglomerular cells (interneurons)
- inhibit other smells to amplify the actual smell

127
Q

what is the olfactory bulb?

A

where primary neurons synapse onto secondary neurons

128
Q

what is the pathway of smell information?

A

olfactory nerves -> olfactory bulb -> olfactory tract -> olfactory cortex (bypasses the thalamus)

129
Q

what other brain regions does olfaction have connections with?

A
  • hippocampus (memory)
  • amygdala (emotion)
  • hypothalamus (homeostasis and motivation)
  • reticular formation (visceral responses)

BPK306 (4 decks)

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