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Physiology Y2 > Motor System Physiology and Hypothalamus > Flashcards

Motor System Physiology and Hypothalamus Flashcards

1
Q

What is a motor unit?

A

The smallest units of motor control. Comprises a single alpha motor neurone and the collection of muscles fibres it innervates.
The number and type of fibres within a motor unit determines the amount of force that unit can generate.

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2
Q

Describe alpha motor neurones.

A

Each controls the contraction of a number of muscle fibres of the same type. Because the force depends on the total cross sectional area, alpha motor neurones that control a larger number of muscle fibres generate larger force than those that control fewer fibres.

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3
Q

What are the 3 main types of skeletal muscle fibre innervated by alpha motor neurones?

A
  • Type 1
  • Type 2a
  • Type 2b
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4
Q

Describe type 1 skeletal muscle fibres.

A

Slow twitch, oxidative phosphorylation, fatigue resistant, do not generate much force but are for sustained contraction, like anti-gravity muscles for sustained posture.

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5
Q

Describe type 2a skeletal muscle fibres.

A

Fast twitch, oxidative phosphorylation, relatively fatigue resistant, generate more force than slow twitch.

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6
Q

Describe type 2b skeletal muscle fibres.

A

Fast twitch, glycolytic metabolism, highly fatigable, high tension and a lot of force.

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7
Q

How does muscle tension increase with motor neurones firing?

A
  • Action potential firing rate also determines the amount of force produced by a muscle.
  • As motor neurone firing rate increases, there is not enough time for action potential to recover, so the force increases until fused tetanic contraction occurs, the maximum force that can be generated.
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8
Q

What is motor units recruitment?

A
  • Graded increases in force are obtained by the orderly recruitment of motor neurones.
  • Ordered recruitment by fibre type.
  • Force generated by a muscle is controlled by recruitment of alpha motor neurones.
  • Recruitment is the addition of an active motor neurone to an existing pool of active motor neurones.
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9
Q

How are motor units recruited?

A
  1. Smaller motor neurones controlling fewer muscle fibres fire first. Standing conditions, for example.
  2. Larger motor neurones controlling a greater number of fibres recruited as more force is required. Jumping and running, for example.
  3. So total force form a muscle increases.
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10
Q

Distinguish extrafusal and intrafusal muscle fibres.

A

Alpha motor neurone gives rise to end plates to muscle fibres in a muscle.

  • Intrafusal fibres generate this force and are spindle shaped.
  • Extrafusal muscle fibres are not within spindles but are controlled by alpha motor neurones.
  • Intrafusal are contractile and ends but central region is enclosed in a capsule/muscle spindle. Isolates it mechanically from surrounding muscle but is in parallel with extrafusal fibres.
  • If length of muscle changes lengths of intrafusal and extrafusal fibres changes in the same way.
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11
Q

What are Golgi tendon organs?

A

Gogi tendon organs have nerve endings between the collagen interwoven fibres. As tension on muscles increases, collagen fibres pull more and more, closing up gaps between the collagen fibres, squeezing the nerve endings and distort the membrane, increasing action potential fibres. So Golgi tendon organs are sensory to the tension and force, not length.

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12
Q

What are type Ia and II intrafusal fibres?

A

Type Ia fibres signal rate of change of stretch and so peaks and then decreases again when increasing and then decreasing length. But type II signals stretch directly so increases and decreases directly with length change.

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13
Q

What is the role of proprioceptive afferent fibres?

A

Information about length and tension needs to be transmitted quickly, because it provides feedback that is used to control movement.

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14
Q

What is the fibre group, modality and conductive velocity of primary muscle spindle receptor?

A

A-alpha (Ia)

Change of muscle length

75-120 m/s

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15
Q

What is the fibre group, modality and conductive velocity of secondary muscle spindle receptors?

A

A-beta (II)

Muscle length

35-75 m/s

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16
Q

What is the fibre group, modality and conductive velocity of Golgi tendon organ receptors?

A

A-alpha (Ib)

Active tension

75-120

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17
Q

What is the fibre group, modality and conductive velocity of joint capsule machnoreceptors?

A

A-beta

Joint angle

35-75

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18
Q

What is the fibre group, modality and conductive velocity of stretch sensitive free endings?

A

Aδ

Excessive stretch or force

5-35

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19
Q

Summarise the direction of information between muscle fibres and the spinal cord.

A

Extrafusal alpha motor neurones and gamma muscle spindles to motor nerve fibres from the spinal cord. Muscle spindles and Golgi tendon organs to sensory nerve fibres and on to spinal cord.

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20
Q

Describe the tendon jerk reflex.

A

Key part of the neurological exam:

  • Provides vital diagnostic information about the integrity of the neural pathway.
  • The monosynaptic tendon jerk reflex (stretch reflex) opposes changes in muscle length and helps to maintain the basal level of moto neurone activity that produces resting muscle tone.
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21
Q

What does the stretch reflex generate and how?

A

Generates muscle tone:

  • By opposing changes in muscle length, the stretch reflex helps to maintain limb position and muscle tone.
  • Changes in sensitivity of the stretch reflex change resting muscle tone.
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22
Q

What is the role of gamma motor neurones?

A

Gamma motor neurone activity changes the sensitivity of muscle spindles to match desired muscle length.

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23
Q

What signals are sent upon muscle contraction?

A

Signal sent to alpha motor neurones for contraction and similar signal must be sent to gamma motor fibres for increased tension to in muscle contraction so that length can still be altered.

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24
Q

What is the role of muscle spindles in motor control?

A
  • Movements are produced by alpha-gamma coactivation.
  • Alpha motor neurone activity signals force of contraction.
  • Gamma motor neurones activity signals desired muscle length, such as joint position.
  • Muscle spindles compare actual muscle length with desired muscle length.
  • The stretch reflex then corrects actual muscle length to desired muscle length.
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25
Q

What signals are sent when load on a muscle is increased?

A

Cause muscle shortening to either more or less of the desired length. If less muscle spindles are activated to increase Ia/II afferents to the spinal cord and then to alpha lower motor neurones, as well as parametric feedback to motor model in the cerebellum and then signals sent from here to upper motor neurones to the spinal cord.

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26
Q

Describe the clasp knife reflex.

A
  • Ib Golgi tendon organ afferents di-synaptically inhibit motor neurones controlling the homonymous muscle to limit the force produced.
  • Information also from cutaneous and joint receptors and descending pathways.
  • The sudden giving way of muscle tone in the clasp knife reflex is a physiological response – do not confuse with an abnormal absence of muscle tone.
  • Negative feedback so increasing tension causing reflex to decrease tension.
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27
Q

What is involved in medial descending tracts?

A

Upper motor neurones controlling axial and proximal musculature via alpha motor neurones – vital for postural responses and locomotion.

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28
Q

What are the roles of medial descending tracts?

A

Control of posture

Control of locomotion and reflexes, such as the startle reflex

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29
Q

What is the role of the tectospinal tract?

A

Tectospinal tract only projects as far as cervical level – controls reflex head orientation in response to visual or auditory stimuli.

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30
Q

What is involved in lateral descending tracts?

A

Upper motor neurones controlling spinal circuits of distal musculature. Goal directed movements such as reaching.

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31
Q

What is the rubrospinal tract?

A

Major lateral descending pathway in most mammals.

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32
Q

What is the lateral corticospinal tract?

A

Lateral corticospinal tract/pyramidal tract arises from large cortical neurones is more important in apes and carnivores.
Significant species differences in where tract terminates.

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33
Q

What does weakness or absence of stretch reflexes indicate in clinical assessment?

A

A disorder of the reflex arc = lower motor neurone dysfunction.

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34
Q

What do disorders of central descending control (UMN) present as?

A

Lead to hyperactive or hypoactive stretch reflexes and abnormal muscle tone. Upper motor neurones dysfunction results in abnormal muscle tone and increased/decreased speed/strength of tendon jerk reflex.

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35
Q

What does forebrain spasticity give rise to?

A

Spasticity, such as hyperactive stretch reflexes and resistance to repaid limb movement.

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36
Q

What does damage of midbrain level present as?

A

Decerebrate rigidity, hyperactivity in limb extensors.

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37
Q

What does a lesion at spinal level present as?

A

Spinal shock in which all spinal reflexes below the level of the transection are suppressed. Then reflexes return in hyperactive form.

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38
Q

What are the 3 basic requirements of posture?

A
  • The vertical projection of the centre of gravity must fall within its points of support (for a terrestrial animal)
  • Rigidity about joints – maintenance of muscle tone (stretch reflex)
  • Stretch reflex is fundamental to maintenance of posture.
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39
Q

What are the functions of the postural control system?

A
  • Maintenance of a stable stance by detecting and correcting deviations from stability
  • Anticipate the postural adjustments required during voluntary movement to prevent loss of stable posture.
  • Adapt to changing circumstances such as loss of a limb, or new motor tasks.
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40
Q

What is the postural system?

A

A set of basic reflexes (therefore rapid) and reactions (less rapid), which are coordinated and adapted by specific brain centres.

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41
Q

Distinguish reflexes and responses.

A

Reflexes are mediated at the spinal level, which makes them rapid, and they can still be observed in animals with rostral spinal damage.

Responses involve the forebrain and ascending and descending spinal tracts. They are less rapid than reflexes and dependent on functioning spinal tracts.

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42
Q

What does extensor postural thrust reaction test?

A

Cutaneous receptors in the feet sense the pressure acting on points of support. Reflex extension of the limb to support the weight.
If cutaneous receptors signal that a leg is bearing weight, then the extensor muscles are contracted to support weight. It is easier to move the limb if it is unloaded as a result.

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43
Q

Describe sway and hopping reactions.

A
  • Tilting of the body will cause unequal pressure distribution on the points of support, such as the feet.
  • Compensatory limb extension to resist the body sway (sway reaction)
  • Stepping or hopping reactions.
  • Hopping reaction is tested as part of the neurological exam.
  • Hopping reactions are important diagnostically because they can confirm that peripheral, spinal, ascending, central and descending aspects of the motor systems are functional.
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44
Q

What is the crossed extension reflex?

A
  • Noxious stimulus transmitted polysynaptically across to spinal cord
  • Ipsilateral flexion reflex
  • Contralateral limb extension
  • Withdrawal of limb from noxious stimulus and shifting weight on to other limb
  • Maintains postural stability
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45
Q

What are placing reactions?

A

Proprioceptive placing (normally tested by the knuckling response) and visual placing. These postural reactions test multiple aspects of motor system function, including forebrain circuits. Cover vision and see if dog can place foot on surface just by having contact with surface on dorsal paw. Can also place paw on dorsal aspect and see if animal will correct so that palmar/plantar is on the surface.

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46
Q

What are static orientation and dynamic cues?

A

SO: strong verticals and horizontals in visual field.

D: Large scale movement of the visual field, such as general upwards movement of visual field means that the animal is tipping forwards.

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47
Q

Distinguish the speed of visual and vestibular cues.

A
  • Visual cues are accurate and sensitive to small deviations but are slow due to the time required for visual processing.
  • Vestibular system also provides information about static and dynamic orientation which elicit vestibular reflexes. Faster but less sensitive.
  • Both provide information about the orientation and movement of the head but not the body.
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48
Q

Describe the vestibular and neck reflexes of a quadruped at normal position.

A

No neck or vestibular reflex. Muscle spindles supply information that head is in line with body and that head and body are upright.

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49
Q

Describe the vestibular and neck reflexes of a quadruped when one foot is off the ground and head and trunk are together.

A

Vestibular reflex elicits extension ipsilateral to tilt. Muscle spindles supply information that the whole animal has tilted sideways, activating vestibular reflex causing extension ipsilaterally and flexion contralaterally to prevent falling over sideways. Neck is in line with body.

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50
Q

Describe the vestibular and neck reflexes of a quadruped when one foot is off the floor and trunk and neck do not move together.

A

Neck reflex elicits extension contralateral to neck flexion. Muscle spindles supply information that head is vertical and body is tilted with respect to the head, so no vestibular reflex. Contralateral extension and ipsilateral flexion in respect to head tilt to maintain postural stability.

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51
Q

Describe the vestibular and neck reflexes of a quadruped where the head alone tilts.

A

Vestibular reflex ipsilateral extension and neck reflex contralateral extension cancel out. Vestibular and neck reflex happening at the same time. Postural maintenance despite head moving.

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52
Q

How do reticular and vestibular nuclei integrate and coordinate postural responses in the medial descending tracts?

A
  1. Spinal level – reflexes are helping correct deviations from normal posture – muscle tone, muscle spindles to stretch reflex, which oppose any changes to muscle length.
  2. Descending control – from vestibular nuclei from vestibulospinal tracts to control extensors to maintain posture. Heavy association with reticular formation so reticulospinal tracts feed into this also.
  3. Vestibular nuclei to postural stability and dynamic cues from visual cues. References to neck proprioceptors
  4. Static orientations cues via pons feed into reticular formation along with motor cortex with postural adjustment in voluntary movement.
  5. Cerebellum calibrates sensory information from all of these and has extensive connections with vestibular nuclei.
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53
Q

Describe adaptation to postural stability.

A
  • The stretch reflex opposes changes in muscle length
  • Reflexes need to be calibrated to ensure accuracy
  • Appropriate reflexes are reinforced
  • Inappropriate reflexes are suppressed
  • This calibration of reflexes is one of the roles of the cerebellum
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54
Q

What does locomotion in terrestrial animals require?

A

A rhythmic pattern of alternating flexor and extensor activity in each limb.

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55
Q

Describe spinal central pattern generators.

A

Basic patterns of locomotion are generated by spinal circuits.

Central pattern generators in the spinal cord generate rhythmic patterns of extensors and flexor neural activity. Does not require brain to regulate this activity, as it is in the spinal cord.

Flip-flip type arrangement based on mutual inhibition: flexor activity inhibits extensor activity during the swing phase and vice versa during stance. In order to do this, there must be sensory input to say that one phase is complete so the next can be switched to (otherwise more input for flexion would cause to get stuck in flexor EMG).

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56
Q

How does sensory feedback control the step cycle?

A
  • The leg needs to be fully extended and unloaded or the swing phase to be initiated in order to maintain posture.
  • Stimulation of Golgi tendon organ afferents from hip extensor muscle (signalling that the muscle is loaded) prevents flexor activity from initiating the next swing phase.
  • Other sensory feedback also influences step cycle, such as touching the dorsal surface of the foot during the swing phase leads to flexion up and over the obstacle.
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57
Q

What does increasing the stimulation of mesencephalic locomotor region increase?

A
  • Increases the speed of locomotion via reticulospinal tract
  • As speed increases, the gait changes.
  • This changes in the pattern of interlimb coordination are a property of the spinal circuits themselves.
  • So increased excitatory drive to spinal circuits via reticulospinal tract changes both speed and gait.
58
Q

How does locomotion cope with environmental variability?

A
  • Visual input
  • Postural reflexes
  • Experience

Feedforward visual input and experience are required to cope with the complexity of locomotion in the real world.

59
Q

How does the motor cortex deal with uneven terrain?

A
  • Feedforward control of locomotion – anticipatory adjustment of step cycle by descending projections from motor cortex.
  • Damage to motor cortex does not affect the ability to walk on smooth surfaces but disrupts ‘skilled walking’ involving a high degree of visuomotor coordination.
60
Q

Describe locomotion movements.

A

Rhythmical coordinated movements of limbs, wings or axial musculature, such as walking, flying, swimming. Is a phylogenetically old neural system regulated primarily by the medial descending tracts.

61
Q

Describe voluntary movements.

A

Initially slow and deliberate but become more rapid and smoother with practice, such as reaching for food, grasping a branch, pouncing on prey. They are initially slow and unrefined but become smoother and more rapid with practice. They are primarily mediated by lateral descending tracts.

62
Q

Name the stages of voluntary movement.

A
  1. Motivation for the movement
  2. Identification of the goal of movement
  3. Behavioural strategy to achieve the goal
  4. The planned motor action
  5. Sensory feedback
63
Q

Describe the motivation for voluntary movement.

A

This can be internally generated, such as hunger or exploration, or it can be sensory input. The neural basis for the motivation varies according to context but may involve regions such as the hypothalamus, nucleus accumbens and prefrontal cortex.

64
Q

Describe the identification of the goal in voluntary movement.

A

Normally involves a high-level sensory model of the world and the relationships among the features within it, which is a function of parietal cortex, along with the emotional significance of those features, which is a function linked o the amygdala and frontal cortex.

65
Q

Describe the behavioural strategy and execution for voluntary movement?

A

Function of the frontal cortex and especially prefrontal cortex along with basal ganglia.

The planned motor actions are executed by the motor cortex, brainstem motor areas and the spinal circuits they control.

66
Q

Describe the sensory feedback of voluntary movement.

A

Associated with performing the movement feeds back to either provide feedback control ongoing movement or parametric feedback, which updates, refines and adapts the motor model.

67
Q

How is the motor system organised?

A

Spinal circuits being controlled by the brainstem motor centres via the medial descending tracts

Both spinal circuits and brainstem motor areas, such as the medial reticular formation, are controlled by the motor cortex and are involved in the execution of movement.

68
Q

Describe the arrangement of the motor movement.

A
  • At higher levels of organisation, loops involved in the planning of movement.
  • One of these is from the cerebral cortex, via the basal ganglia and thalamus back to the motor cortex, which is involved in the selection and initiation of movement.
  • The second planning loops is from the cerebral cortex via the cerebellum and thalamus back to the motor cortex and is involved in the planning and rehearsal of planning movement.
  • Sensory feedback to spinal levels, brainstem and spinocerebellum is involved in the ongoing control of movement execution.
  • Sensory feedback coming via the somatosensory system into neighbouring primary motor cortex forming long-loop reflexes.
  • Sensory information also provides parametric feedback, which updates and fine tunes the motor model.
69
Q

Name the 3 regions of the motor cortex.

A

Primary motor cortex
Lateral premotor cortex
Supplementary motor area

70
Q

Describe the structure and function of the primary motor cortex.

A

Strip of cerebral cortex immediately adjacent to primary somatosensory cortex.
- Receives direct sensory input from both adjacent primary somatosensory cortex and parietal sensory association cortex.
- Stimulation of primary motor cortex results in relatively simple movements around individual joints.
- Stimulation of neighbouring points of the primary motor cortex results in movement of neighbouring joints on the body forming a somatotopic motor map, aligned with the somatotopic motor map in the somatosensory cortex.

71
Q

Describe the position and function of the lateral premotor cortex.

A

Immediately anterior to the lateral part of the primary motor cortex.

Stimulations results in more complex movements around several joints and stimulation.

72
Q

Describe the position and function of the supplementary motor area.

A

Anterior to the primary motor cortex and is found medially to lateral premotor cortex. Stimulation results in coordinated movement of different parts of the body that are used in movements such as climbing and leaping.

73
Q

What are the roles of the primary motor cortex?

A
  • Activity occurs prior to and during the execution of movement.
  • Activity not correlated with the position of limbs but rather with both the force and direction movement.
  • Damage to primary motor cortex does not prevent voluntary movement but does cause weakness of movement and reluctance to use the affected limb in paresis.
74
Q

What are the roles of the lateral premotor cortex?

A
  • Activity preceded movement by several hundred milliseconds, consistent with the role of these areas in the planning of movement.
  • Damage results in deficits in complex movements and difficulty in associating a sensory stimulus with a motor response.
  • This is because it is part of a planning loops with the cerebrocerebellum that is particularly involved in driving movements in response to external stimuli.
75
Q

What are the roles of the supplementary motor area?

A
  • Activity preceded movement by several hundred milliseconds, consistent with the role of these areas in the planning of movement.
  • Part of a loop including the basal ganglia, which is involved in the selection and planning of self-willed movements and learned sequences of movements, damage results in deficits in the coordination of voluntary movement between limbs.
76
Q

What are the basic roles of the basal ganglia?

A
  • Receive input from across cerebral cortex and they output via the thalamus back to motor cortex.
  • Have no direct projection to spinal levels and are involved in movement selection and planning and not execution of movement.
  • Involved in the initiation of self-willed movement.
77
Q

What is the problem with input to the basal ganglia and how is this overcome?

A

Overcoming for voluntary movement is the large number of possible trajectories of movement.

Which of the many is appropriate in a given context depends on weighting up a given situation’s risks and rewards from previous experience. This is part of the planning of voluntary movement to achieve a goal and involves frontal cortical areas.

78
Q

What do cortical inputs to the basal ganglia do?

A

Disinhibit thalamocortical circuits allowing appropriate internally generated, self-willed movements to be initiated, whilst suppressing unwanted movements.

79
Q

Describe disorders of the basal ganglia in veterinary medicine.

A

Less prevalent but are starting to be increasingly recognised, such as canine multiple system degeneration initially involves cerebellar symptoms of ataxia. If left to progress, degeneration of the basal ganglia occurs, leading to hypokinesia and difficulty in initiating movement. Hyperkinetic disorders are also seen in dogs and cats, such as paroxysmal dyskinesia, but often referred for abnormal behaviour rather than abnormal motor control.

80
Q

What is likely to underlie stereotypic behaviour?

A

The role of the basal ganglia in selecting certain patterns of behaviour and motor output is likely to underlie habit formation and stereotypic behaviour.

81
Q

Name the 4 main circuits through the basal ganglia.

A

Dorsal striatum
Oculomotor circuit
Prefrontal circuit
Limbic circuit

82
Q

Describe the role of the dorsal striatum.

A

Involved in a circuit to and from motor cortical areas, especially the supplementary motor area. It selects an appropriate motor action from all the possible motor action that could be selected to achieve the goal.

83
Q

Describe the oculomotor circuit.

A

Forming a loop with the supplementary eye fields in the frontal cortex of certain species including primates. Involved in selecting saccadic eye movements to move the point of gaze from 1 part of the visual field to another.

84
Q

Describe the prefrontal circuit.

A

Involves lateral prefrontal and orbitofrontal cerebral cortexes via the ventral striatum, which is involved in selecting an appropriate behavioural response to a given situation. Involved in reinforcement of rewarded behaviours.

85
Q

Describe the limbic circuit.

A

Involving the cingulate cortex, which mediates perception of internal body state, and orbitofrontal cortex, which is involved in selecting appropriate emotional responses and feelings.

86
Q

What is the vestibulocerebellum?

A

There is a distinct functional role of the flocculonodular lobe, referred to as the vestibulocerebellum, less so between the anterior and posterior lobes.

87
Q

What is the vermis?

A

Midline region of cerebellar cortex

88
Q

What is the spinocerebellum?

A

Intermediate part of the cerebellar hemisphere and vermis

89
Q

What is the cerebrocerebellum?

A

Spinocerebellum has distinct functions from the lateral parts of the hemispheres which are the lateral cerebellum/cerebrocerebellum.

90
Q

What is the vestibulocular reflex and disorders of this reflex?

A

Stabilises the retinal image during head movements.

Disorders of this reflex lead to jerky, repetitive nystagmus eye movements, which are signs of vestibular or cerebellar dysfunction.

91
Q

Describe the vestibulocular reflex pathway.

A
  1. Rotation of the head stimulates receptors in semi-circular canals of the vestibular system.
  2. Information conveyed to the vestibular nucleus.
  3. Excitatory pathway to oculomotor nuclei where it drives motor neurone output to oculomotor nuclei.
  4. Motor neurone output to the muscles controlling eye movement.
  5. Correct reflex will drive eye movement in the opposite direction of head movement, stabilising retinal image.
92
Q

How does the cerebellar cortex supply calibration for the vestibulocular reflex?

A
  • A copy of the vestibular information is conveyed via mossy fibres to granule cells in the cerebellar cortex.
  • Granule cells have an axon that bifurcates into parallel fibres synapsing on Purkinje cells.
  • Purkinje cells are GABAergic and inhibit the vestibulo-ocular reflex pathway in the vestibular nucleus.
93
Q

How is the vestibulocular reflex affected by transmission of the reflex loop?

A

If the transmission of the loop is increased, there is more inhibition on the vestibulo-ocular reflex and less eye movement for a given amount of head movement.

If transmission of the loop is decreased, there is less inhibition of the vestibulo-ocular reflex and more eye movement to counteract a given head movement.

94
Q

What is caused by eye movements performed inaccurately?

A
  • There is a slight blurring of the image on the retina.
  • This retinal slip generates an error signal to the inferior olive to excite climbing fibres.
  • Climbing fibres activity strongly depolarises the Purkinje cells.
  • Induces a decrease in the strength pf the excitatory input synapses from the parallel fibres.
  • Long lasting change in calibration loops, changing the amount of inhibition into the vestibulo-ocular reflex pathway.
  • Reflex made more accurate.
95
Q

What is the vestibulocerebellum?

A

The flocculonodular lobe. Receives input from the vestibular system and vestibular nuclei and output back to the vestibular nuclei. Calibrates postural reflexes and the vestibulo-ocular reflex.

96
Q

What does damage to the vestibulocerebellum lead to?

A

Damage leads to inaccurate stabilisation of gaze during head movements and often causes spontaneous or evoked nystagmus eye movements. Damage also causes postural instability with a wider than normal stance and an unsteady wobbly gait.

97
Q

What is cerebellar hypoplasia?

A

Cerebellum fails to develop properly. Balance problems. But the nervous system can compensate for the postural deficits over time.

98
Q

What signals does the spinocerebellum recieve?

A

Receives sensory inputs from all sensory systems.

99
Q

Where does the vermis output?

A

Via the fastigial deep cerebellar nuclei to the reticular formation and vestibular nuclei. Regulates ongoing movement via the vestibulospinal and reticulospinal tracts. Can project to oculomotor nuclei to calibrate saccadic eye movements.

100
Q

Where does the intermediate hemisphere/paravermis output?

A

Via the interposed deep cerebellar nuclei and thalamus to the primary motor cortex and red nucleus (midbrain). Enable regulation of ongoing movements via the corticospinal and rubrospinal tracts.

101
Q

What does damage to the spinocerebellum result in?

A

Ataxia, meaning all movements still occur but are performed inaccurately and oscillations are frequently observed, as desired limb positions undershoot and overshoot their targets.

102
Q

Where does the cerebrocerebellum/lateral cerebellum receive inputs and where does it output?

A

Receives contralateral input from parietal cortex and frontal cortex.

Outputs are contralateral via the dentate nucleus and thalamus to the primary cortex and lateral premotor area. Refines the motor models used in the planning and mental rehearsal of movements.

103
Q

What does damage to the cerebrocerebellum/lateral cerebellum result in?

A

Damage results in disruption of timing of movements, which can also lead to tremor, as well as the disruption of learning of new motor skills and the adaptation of existing ones to change circumstances.

104
Q

What is limb inertia.

A

Limbs have inertia so if a burst of flexor activity starts a movement, then an appropriately timed burst of extensor activity is required to stop the movement near at the desired position.

105
Q

How does the cerebrocerebellum/lateral cerebellum refine motor models?

A
  • When a new movement is first leaned, it is slow and inefficient.
  • Due to cerebrocerebellum, the motor system is able to build and refine the motor models of how it interacts with the world so that movements to achieve certain goals are available as preprogramed motor responses that are more rapid, fluid and effective than the initial movements.
106
Q

Describe the motor development of altricial species.

A

Such as dogs, cats and rabbits, have poor motor development and control when they are born and build and refine their motor models over the first few weeks.

107
Q

Describe the motor development of precocial species.

A

Such as sheep, are very well developed at birth, it does not take many hours for the cerebellar circuits of a wobbly new-born lamb to refine the motor models, reflexes and postural reactions that enable standing, suckling and escape from predators.

108
Q

What is the overall function of the hypothalamus?

A

The hypothalamus integrates information about internal state with information about external environment and produces a coordinated response. It is able to regulate physiological processes via control of the autonomic and endocrine systems and coordinate this with threats, opportunities and changes in the external environment via behavioural responses.

109
Q

Describe the endocrine output from the hypothalamus.

A
  • Via pituitary gland, located below hypothalamus.
  • Hypothalamic neurones indirectly regulate anterior pituitary hormone production via stimulatory and inhibitory factors released from hypothalamic neurones in the pituitary portal circulation.
  • Also synthesises and releasing the hormones arginine vasopressin and oxytocin directly into the systemic circulation at the posterior pituitary.
110
Q

Describe the positive feedback system of uterine contraction during parturition, which expels the foetus at birth, as an example.

A
  • Uterine contraction is dedicated to cervical stretch receptors, which signal to the hypothalamus that the foetus is stretching the cervix.
  • This neural feedback elicits the release of oxytocin into the circulation form the paraventricular nucleus of the hypothalamus via terminals in the posterior pituitary.
  • Circulating oxytocin enhances contractility of the uterus leading to further uterine contraction and further cervical stretch.
  • Positive feedback systems are unstable and will continue unless something actively stops them, such as the birth of the foetus.
111
Q

Describe blood osmolarity as an example of a negative feedback system.

A
  • Stimulates release of ADH/arginine vasopressin from neurones in the supraoptic nucleus of the hypothalamus at nerve endings in the posterior pituitary.
  • Increase water reabsorption in the kidney, but that on its own it may not be enough to restore blood osmolarity, this is where the coordinated response of the hypothalamus is important, as the hypothalamus will also drive thirst to elicit a behavioural response to increase the consumption of water,
  • Increased water intake and increased water reabsorption have a negative feedback effect to decrease blood osmolarity to maintain it within a physiological range.
112
Q

What is the OVLT?

A
  • Located in the anterior wall of the 3rd ventricle.
  • Is a circumventricular organ that is found around the ventricular system and contains osmoreceptors that monitor blood osmolarity.
  • Convey information to the median preoptic nucleus.
113
Q

What is the subfornical organ?

A
  • Another circumventricular organ located in the anterior wall of the 3rd ventricle.
  • Contains neurones that detect levels f the hormone angiotensin in the blood.
  • Convey information to the median preoptic nucleus.
114
Q

Where does the median preoptic nucleus receive information of blood volume?

A
  • Subfornical organ, providing information about circulating levels of angiotensin II, which is increased via the renin angiotensin system if blood volume falls, decreasing blood flow to the kidney.
  • Stretch receptors in the heart atria and conveyed to the hypothalamus via a neural pathway to the median preoptic area via the nucleus of the solitary tract.
115
Q

Where does the median preoptic nucleus receive information on blood osmolarity?

A

Information of blood osmolarity comes from OVLT osmoreceptors, which are effectively responding to changes in cell volume.

116
Q

If blood volume or osmolarity is low, what does the median preoptic nucleus do?

A
  • Drives release of ADH via supraoptic nucleus of the hypothalamus and thirst via the lateral hypothalamus.
  • Coordinated endocrine and behavioural endocrine response will help increase water intake and retain water via the kidneys.
  • Negative feedback effect to reduce blood osmolarity.
117
Q

What is done because increasing water intake not sufficient to restore fluid balance?

A
  • An appetite to increase salt intake can also be driven via the lateral hypothalamus.
  • Salt appetite is another behavioural response driven by the lateral hypothalamus and can be observed in many species that actively seek out sources of salt to lick.
118
Q

What are the consequences of delay in negative feedback systems in the osmolarity example?

A
  • Hypothalamus drives drinking behaviour, which has a negative feedback to reduce blood osmolarity.
  • Takes around 20 minutes for the water in the stomach to be absorbed into the blood.
  • By the time that the osmolarity of the blood was returned to normal to stop drinking, there would still be a lathe amount of water in the stomach.
  • Absorption of this excess water causes blood osmolarity to become too low.
119
Q

What is the role of satiety signals in osmolarity negative feedback delay?

A
  • Hypothalamus integrates that water is being consumed from a variety of visual, trigeminal and possibly gustatory sources via stretch receptors in the stomach, monitoring stomach distension.
  • This inhibits thirst promoting circuits in the lateral hypothalamus, suppressing drinking behaviour for long enough for absorption to occur.
  • Inhibitory decrease and osmoreceptors in the hypothalamus turn on thirst again as blood osmolarity is still too high.
120
Q

What role does the arcuate nucleus have in hunger and energy balance?

A

Contains neurones that express the neuropeptide Y (NPY) and AGRP.

These are excited by glucose sensitive neurones in the medulla when glucose levels are low. Also excited by ghrelin, secreted from the stomach when empty.

121
Q

What are the 2 outputs of NPY and AGRP neurones?

A

Output to paraventricular nucleus, which controls autonomic and endocrine responses to conserve energy. Decreases insulin secretion to spare glucose for the brain, decreased breakdown of fatty acids to conserve energy reserves and lower body temperature to reduce energy expenditure.

Lateral hypothalamus excite neurones expressing melanin concentrating hormone, MCH, and orexin/hypocretin. Excitatory effects on eating, facilitated by endocannaboids. Drives hunger.

122
Q

Describe the action of short term satiety signals.

A
  • Provided by eth sensory experience of eating food, its smell, taste, texture and appearance.
  • Also from the gut signalling food is present and being digested.
  • Via vagal afferents from stretch receptors in the stomach that sense gastric distension and taste receptors in the alimentary tract that sense the presence of digestion products such as glucose.
  • Release of cholecystokinin and peptide YYP, effects on the hypothalamus, and CKK signals indirectly by stimulating vagal afferents.
  • Inhibit NPY and AGRP neurones to turn off hunger and autonomic responses.
123
Q

Describe the action of long term satiety signals.

A
  • Leptin from adipose tissue.
  • Leptin receptors in brain, including the olfactory system, which decreases attractiveness of taste and smell of food.
  • Leptin effects on the feeding circuits of hypothalamus.
  • Inhibitory effect NPY/AGRP neurones.
  • Indirect effects via excitation of neurones in the arcuate that express CART and alpha MSH.
  • These send inhibitory projections to the PVN and lateral hypothalamus
  • Net results is increased inhibitory control of feeding more rapidly in the presence of high leptin levels, reducing food consumption.
124
Q

Describe generation of circadian rhythms.

A
  • All nucleated cells have a genetic clock in which levels of clock genes vary on around a 24 hour cycle.
  • Circadian functions controlled by local oscillators under the control of a pacemaker clock in the suprachiasmatic nucleus.
  • This is left synchronised with daily environmental changes via changes in light levels, sensed directly by retinal ganglion cells and transmitted to the suprachiasmatic nucleus via the retinohypothalamic tract.
125
Q

What is the function of pineal production of melatonin?

A

Provides a signal of day length. The hypothalamus of species that live at temperature latitudes is also sensitive to the seasonal changes in day length.

126
Q

Describe the action of melatonin in species living in high latitudes.

A
  • Produced by the pineal gland during darkness and inhibited by daylight.
  • The increase in melatonin is shorter in the long days of summer.
  • Length of melatonin pulses provides information to hypothalamic areas controlling GnRH release and activity of the hypothalamic-pituitary-gonadal axis to control seasonal reproduction.
127
Q

Distinguish species differences in the pineal gland.

A

Fish, amphibians, reptiles and some birds: pineal gland is itself sensitive to the daylight penetrating the skin and skull.

Mammals: pineal has lost this sensitivity to light, which means that a convoluted neural pathway is required to convey information about absolute light levels from the retinal ganglion cells to the pineal gland.

128
Q

What is the role of the paraventricular nucleus on sleep-wake cycle and seasonal breeding?

A
  1. Light stimulates melanopsin containing retinal ganglion cells which project via the retinohypothalamic tract directly to the suprachiasmatic nucleus.
  2. Excitatory pathway continues via the paraventricular nucleus of the hypothalamus.
  3. PVN projects via the spinal cord to inhibit sympathetic neurones in the superior cervical ganglion, which reduces melatonin production via projections to the pineal gland.
  4. Circulating melatonin in peripheral blood acts on receptors in the hypothalamus.
129
Q

How is seasonal breeding control different in non-mammalian vertebrates, including some bird species?

A

Not dependent on melatonin levels but is mediated by the activation of deep brain photoreceptors located within the hypothalamus itself which are sensitive to the low levels of daylight penetrating deep into the brain.

130
Q

Which sexual behaviours is the medial preoptic area of the hypothalamus responsible for?

A
  • Male mounting behaviour
  • Ventromedial nucleus of the hypothalamus drives female lordosis behaviour.
  • The hypothalamus is able to do this because it is integrating information about the internal body state, via receptors for circulating sex steroids, with external information about the availability of potential mates.
  • Drives maternal and paternal behaviour in response to sensory stimuli from offspring, which depends on priming by the hormonal changes during pregnancy and parturition.
131
Q

Name the 3 aspects to aggressive behaviour.

A
  • Overall baseline propensity for aggression
  • External sensory cues
  • Aggressive posturing or initiation of attack
132
Q

Describe the overall baseline propensity for aggression.

A

The internal motivation to initiate aggression, which is dependent on neurones in the ventromedial hypothalamus and circulating testosterone.

133
Q

Describe external sensory cues of aggression.

A

One off these is the external circadian rhythmicity signal from the superchiasmatic nucleus of the hypothalamus. This decreases the propensity for aggression during the first half of the rest period. Other sensory stimuli that elicit aggression in male mice include pheromones from a rival male.

134
Q

Describe aggressive posturing or initiation of attack.

A

Can be elicited by direct activation of neurones in the ventrolateral division of the ventromedial hypothalamus. Normal experimental activation of these neurones can bypass the dependence on hormonal state and external sensory cues and trigger aggression in appropriate contexts.

135
Q

Summarise what the lateral hypothalamus is responsible for.

A

Eating
Drinking
Sleep

136
Q

Summarise what the preoptic area is responsible for,

A

Ventrolateral = sleep
Thermoregulatory
Medial = male mounting behaviour, maternal and paternal behaviour

137
Q

Summarise what the ventromedial hypothalamus is responsible for.

A

Ventrolateral subdivision = aggression
Female lordosis sexual behaviour

138
Q

Describe consummatory behaviour.

A
  • Primary motivated that immediately satisfies a bodily or psychological need.
  • Sexual behaviour in the presence of a receptive conspecific, eating when food is available or drinking when water is available, taking shelter when cold if available.
  • These are controlled by the hypothalamus and integrated with autonomic and endocrine responses.
139
Q

Describe appetite behaviour.

A
  • Flexible, voluntary behaviour that anticipates goals and seeks out future opportunities.
  • For instance, seeking out and investigating conspecifics to establish whether they are sexually receptive, seeking food, water or shelter when they are not immediately available to consume.
  • This is controlled by the ventral striatum, including the nucleus accumbens.
140
Q

Describe the flexion withdrawal reflex.

A
  • Relatively fast – Aδ fibres by a polysynaptic spinal pathway.
  • Important in diagnosis and in judging depth of anaesthesia
  • Modulated by descending control from the brain
  • Excitation of flexor muscles by interneurone and excitation inhibitory neurone to inhibit extensor muscle.
141
Q

Describe cutaneous trunci/Panniculus reflex.

A
  • C8-T1 motor cell bodies
  • Lateral thoracic nerve outflow
  • Afferent input runs from muscle up spinal cord to C8-T1. You are testing where this afferent input might be interrupted
  • Cutaneous trunci muscle reflex contraction
  • Assess from L5 up to T3
  • Useful to determine location of a T3-L3 lesion
142
Q

What can central pattern generators allow, despite a spinal lesion?

A

Sensory input may be enough to generate basic walking pattern when supported and paws are down, despite no communication between limbs and brain.

Physiology Y2 (14 decks)

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