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Biological Psychology > Chapter 8: Movement > Flashcards

Chapter 8: Movement Flashcards

1
Q

three categories of muscle

A

Smooth
Skeletal/Striated
Cardiac

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2
Q

Smooth Muscle

A

controls digestive system and other organs

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3
Q

Skeletal/Striated muscle

A

controls movements of the body in relation to the environment

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4
Q

Cardiac Muscle

A

between other 2 categories with properties

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5
Q

Need for antagonistic muscles

A
  • important because there is no control to move the muscle in the opposite direction therefore you need another muscles to do that job
    ex) flexor and extensor
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6
Q

fast muscles and conditions under which each is most useful

A

Fast twitch: fast contraction, fast fatigue

-anaerobic no O2 therefore fatigue quickly due to needed O2 for recovery (oxygen debt, sprinting)

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7
Q

slow muscles and conditions under which each is most useful

A
  • slow contraction
  • no fatigue
  • to not fatigue because they are aerobic (use O2)
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8
Q

Proprioceptor

A

-receptor that detects position or movement of ta port of the body

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9
Q

Proprioceptor in muscle

A

-detect stretch and tension of a muscle and sends messages to enable spinal cord to adjust its signals

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10
Q

Muscle spindle

A

-receptor parallel to muscle that responds to stretch

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11
Q

Golgi tendon organ

A
  • responds to increase in muscle tension

- act as a brake against vigorous contraction

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12
Q

roles of the primary motor cortex in the control of movement.

A
  • elicits movement
  • axons extend to brainstem and spinal cord which generate impulses that control muscles
  • each spot does not control a specific muscle- they overlap
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13
Q

role of posterior parietal cortex in the control of movement.

A
  • planning movements
  • keeps track of body position relative to the world
  • controls aim
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14
Q

role of supplementary motor cortex in control of movement

A
  • planning and organizing rapid sequence of movements

- essential for inhibiting a habit when you need to do something else

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15
Q

role of premotor cortex in control of movement

A
  • most active right before a movement
  • receives info about target that body is directing its movement towards and info about body’s current position and posture
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16
Q

role of prefrontal cortex in control of movement

A
  • active during a delay before a movement
  • stores sensory info relevant to movement
  • considers probable outcomes of possible movements
17
Q

implications of the timing of the readiness potential before the person is aware of making a decision

A

Readiness potential- produced by motor cortex before any voluntary movement

  • on average 500ms before the movement
  • brain activity responsible for the movement begins before the person’s conscious decision
18
Q

functions and cellular organization of the cerebellum

A
  • contains more neurons than the rest of the brain combined
  • motor structure (balance, coordination, timing, aim)
  • help to tell if objects are same or different when in hands
  • any sequence of rapid movements that require timing
  • critical for certain aspects of attention
19
Q

organization of the cerebellum

A
  • receives input from spinal cord + sensory systems from cranial nuclei and cerebral cortex
  • neurons arranged in precise geometric pattern with multiple repetitions of same unit
20
Q

Purkinje Cells

A

-flat cells in sequential planes parallel to each other

21
Q

Parallel Fibres

A

-axons parallel to one another and perpendicular to planes of Purkinje Cells

22
Q

Action Potential Path in Cerebellum

A
  • Action potential from parallel fibre excites 1 purkinje cell after another
  • Purkinje cell transmits inhibitory message to cells in nuclei of cerebellum and vestibular nuclei in brainstem when it sends info to midbrain and thalamus
23
Q

Action Potential strength and distance in cerebellum

A
  • depending on which and how many parallel fibres are active they might only stimulate 1st few Purkinje fibres or a long series
  • more excited Purkinje= increase collective DURATION of response
  • only 1st Purkinje= short message to target cells
  • more than 1st= longer message to target cells
24
Q

Output of Purkinje cells

A

-timing of movement (onset and offset)

25
Q

Path in Cerebellum to brain

A

Parallel fibre -> Purkinje Cell (one after another)
l l
V V
inhibitory message . vestibular nuclei in
nuclei of cerebellum brain stem
l l
V V
midbrain thalamus

26
Q

list the structures that comprise the basal ganglia

A

Caudate Nucleus
Putamen
Globus Pallidus

27
Q

Pathway of Basal Ganglia

A 
Cerebral cortex 
l                     l
V .                 V
caudate .     putamen 
nucleus
               l
              V
    globus pallidus 
     l .                  l
    V .                 V . 
thalamus .      midbrain 
    l . 
   V
motor and prefrontal areas of cerebral cortex
28
Q

know the function of each and the general contribution of the whole system.

A
  • output from globus pallidus to thalamus = inhibitory
  • neurons show a lot of spontaneous activity
  • caudate nucleus and putamen tell globus pallidus to stop inhibiting
  • basal ganglia selects a movement by stopping it being inhibited
  • very important for self initiated behaviours
29
Q

know the function of each and the general contribution of the whole system.

A
  • output from globus pallidus to thalamus = inhibitory
  • neurons show a lot of spontaneous activity
  • caudate nucleus and putamen tell globus pallidus to stop inhibiting
  • basal ganglia selects a movement by stopping it being inhibited
  • very important for self initiated behaviours
  • have specialized cells for learning to stop and start a voluntary sequence of motions
30
Q

symptoms of Parkinson’s disease

A
  • rigidity, muscle tremors, slow movements, difficulty initiating physical and mental activity,
  • slow on cognitive tasks such as imagining events or actions
  • loss of olfactory is early (first symptom)
  • depression
  • memory loss
  • not paralyzed or weak
  • difficulty with spontaneous movement
31
Q

immediate physiological cause of Parkinson’s disease

A
  • gradual progressive death of neurons especially in substantia nigra
  • substantia nigra sends dopamine releasing axons to caudate nucleus and putamen
  • lose these axons and therefore lose dopamine
32
Q

genetic of Parkinson’s disease.

A

-genes have very small link

33
Q

environmental causes of Parkinson’s disease.

A
  • exposure to toxins
  • MPTP chemical that body converts to MPP+ accumulates in and destroys neurons that release dopamine
  • exposure to hazardous herbicides and pesticides
  • people who smoke cigarettes and drink coffee have less of a chance of developing Parkinson’s disease
34
Q

most common treatment for Parkinson’s disease and a problem with that treatment

A

-goal is to restore missing dopamine
-L-dopa=precursor to dopamine is a main treatment for Parkinson’s
Problems with L-dopa
-ineffective for some patients
-does not prevent continued loss of neurons
-unpleasant side effects (nausea, restlessness, sleep problems, low BP, repetitive movements, hallucinations, delusions)

35
Q

Other potential therapies for Parkinson’s

A
  • antioxidant drug to decrease further damage
  • drugs that directly stimulate dopamine receptors
  • drugs that inhibit glutamate or adenosine receptors
  • gene therapy : using virus to transfer into the brain a gene that increases dopamine synthesis
  • neurotrophins to promote survival and growth of remaining neurons
  • drugs that decrease apoptosis of remaining neurons
  • high frequency electrical stimulation of globus pallidus or subthalamic nucleus
  • possibility that transplanting brain tissue from aborted fetus would help
36
Q

describe the symptoms of Huntington’s disease

A
  • severe neurological disorder
  • arm jerks, facial twitches, tremors spread to other parts of body and develop into writhing
  • tremors start interfering with walking, speech, and voluntary movements
  • limited ability to learn and improve new movements
  • depression, sleep disorders, memory impairment, anxiety, hallucinations, delusions, poor judgement, alcoholism, drug abuse, sexual disorders
37
Q

immediate physiological cause of Huntington’s disease

A
  • gradual and extensive brain damage in caudate nucleus, putamen, globus pallidus, and cerebral cortex
  • genetic cause
38
Q

genetic cause of Huntington’s disease

A
  • results from dominant gene on chromosome #4
  • critical area of gene includes sequence of bases CAG which is repeated 11-24 times in most people, that repetition produces 11-24 glutamines
  • people with 35 CAG repetitions are considered safe
  • 36-38 repetitions might get it (probably not until old age)
  • 39+ repetitions are likely to get it
  • can predict whether a person will get it and when

Biological Psychology (15 decks)

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