Ch 7 Flashcards

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1
Q

Muscles and Their Movements [placeholder]

A

Vertebrate muscles fall into 3 categories

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2
Q

Smooth muscles

A
  • control internal organs (intestines)
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3
Q

Cardiac or heart muscles

A

.

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4
Q

Skeletal or striated muscles

A
  • control movement of body in relation to the environment
  • long cylindrical with stripes
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5
Q

Neuromuscular junction

A
  • synapse of motor neuron with muscle fiber
  • axons release acetylcholine at synapse, Ach excites the muscle to contract (move)
  • each muscle can move in one only direction and in absence of acetlycholine it relaxes
  • movement in the opposite direction requires another set of antagonistic muscles: flexor to raise arm and extensor to lower arm
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6
Q

Myasthenia Gravis

A
  • is autoimmune disease
  • immune system anti-bodies attack acetylcholine receptors;
  • If Ach can’t work on the receptors, muscles can’t contract
  • Symptoms are weakness and rapid fatigue of muscles
  • Motor neurons compensate by pumping out more Ach – not good for our motor neurons to constantly produce maximum acetylcholine
  • treated by drugs that inhibit acetylcholinesterase to prolong acetylcholine
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7
Q

fast twitch fibers

A

: fast contractions, easily fatigued, used when sprinting

  • Fast twitch fibers are anaerobic – they do not require oxygen at the time of movement
  • Also produce lactate and phosphate, which accumulate and make our muscles fatigued
  • slow twitch fibers: slow contractions resistant to fatigue, used when talking or walking
  • Slow twitch fibers are aerobic – they use oxygen in their movements
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8
Q

anaerobic

A

– they do not require oxygen at the time of movement

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9
Q

aerobic

A

they use oxygen in their movements

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10
Q

Muscle Proprioceptor

A
  • receptor that is sensitive to the position or movement of a muscle. Proprioceptors detect the stretch and tension of a muscle and send messages to the spinal cord to adjust its signals
  • Sometimes when a muscle is stretched, a stretch reflex occurs, which is the spinal cord sending a reflexive signal to contract it
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11
Q

muscle spindle

A

type of proprioceptor sensitive to stretch. It senses stretch of muscle and sends feedback to motor neuron to contract. This helps us to walk and hold things. (Contact!)

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12
Q

golgi tendon organ

A
  • type of proprioceptor sensitive to increases in muscle tension, sends message to inhibit motor neuron and brake contraction (too much muscle contraction can actually tear the muscle) (Don’t Contract!)
  • loss of proprioception
  • no automatic control from sensors
  • requires constant visual monitoring to provide feedback
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13
Q

Voluntary and Involuntary Movements [placeholder]

A

.

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14
Q

Reflexes

A
  • consistent, automatic responses to stimuli (e.g., the stretch reflex or constriction of pupil to light)

—> infant reflexes include rooting, grasp, and Babinski

  • Reflexes are considered ballistic movements because they cannot be altered once started
  • Most movements, e.g., walking, are a combination of voluntary and involuntary muscle control
  • involuntarily adjust to irregularities in road and automatically swing your arms unless you tell yourself not to.
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15
Q

Sensitivity to Feedback

A
  • Many movements are rhythmic in nature (e.g., birds’ wings flapping)
  • These types of movements are controlled by Central Pattern Generators
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16
Q

Central Pattern Generators

A
  • neural mechanisms in the spinal cord that generate rhythmic patterns
  • They’re started by a stimulus then the pattern determines the frequency of movement, e.g., cats scratch themselves 3-4 times/sec
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17
Q

Motor Program

A
  • is a fixed sequence of movements caused by CPGs – in general, once started, they continue automatically until their completion
  • Sometimes they’re there when we’re born, sometimes we learn them
  • Ex: mouse washing face, gymnast with complex movements, yawn
  • automatic patterns may be disrupted when thinking about them, e.g., typing or playing piano
18
Q

Role of Cerebral Cortex

A
  • Remember, the primary motor cortex (precentral gyrus) is involved in controlling our movements
  • But nothing there is directly attached to muscles, and the information has to follow several paths to get to them
  • Cerebral cortex important for complex actions such as writing

—> less complex movements e.g., coughing, laughing, crying are controlled by subcortical areas

  • Stimulation of primary motor cortex elicits movements in corresponding body area
19
Q

Areas Near the Primary Motor Cortex [placeholder]

A

.

20
Q

Posterior parietal cortex

A
  • keeps track of position of body relative to environment. Integrates our senses and motion
  • if damaged we can describe what we see but can’t walk toward it, pick it up, or step over object (what pathway was that from the vision chapter?)
21
Q

Primary somatosensory cortex

A
  • is main receiving area for touch and other body information
  • responds to shape of object and grasping, lifting or lowering
  • For example, if I put a door knob and a drawer handle, both attached to a board, under a cover, by touching it, you would know how to hold it in order to exert action on it. This is governed by your primary somatosensory cortex
22
Q

Areas Near the Primary Motor Cortex [placeholder] {small info dump}

A
  • The prefrontal, pre-motor, and supplementary motor cortices all help us prepare to move. They all send messages to the primary motor cortex which then instigates the movement
23
Q

Prefrontal cortex

A
  • active when planning and calculating possible outcomes of a movement
  • damage results in badly planned movements, showering with clothes on, salting tea instead of food, etc.
24
Q

Premotor cortex

A
  • is active during preparations for a single or few movements
  • receives information about target and body location
  • Works in conjunction with the posterior parietal cortex
25
Q

Supplementary motor cortex

A

active during preparations for a rapid series of movements; typing, dancing, speaking, playing musical instrument

26
Q

Connections From Brain to Spinal Cord [placeholder]

A
  • Messages from brain reach the medulla and spinal cord through 2 tracts (pathways) dorsolateral or ventromedial
27
Q

Dorsolateral (pyramidal tract)

A
  • originate from primary motor cortex, surrounding areas and red nucleus (small area of midbrain primarily responsible for control of arm muscles)
  • in “pyramids” of medulla, axons cross over to opposite side of spinal cord
  • controls movement in our body’s periphery: hands, fingers, toes
  • damage here means loss of fine movements
28
Q

Ventromedial tract

A
  • includes axons from the primary and supplementary motor cortex and other areas of the cortex
  • Go to both sides of the spinal cord because axons control bilateral movement of the neck, shoulders, trunk, large leg muscles (can move the fingers on one hand independently, but can’t just turn one side of your neck or walk with one leg)
  • damage here impairs walking, turning, bending, standing up and sitting down
  • **most movements require a combination of both the dorsolateral and ventromedial tracts (throwing a ball)
29
Q

Role of Cerebellum [info dump]

A
  • Also very important for motor control
  • Has more neurons than rest of brain
  • Processes information about guiding movement, not the movement itself

Damage causes:

  • Difficulty with sequences that require accurate aiming and timing, e.g., tapping rhythm, speaking, writing, playing musical instrument
  • Difficulty with finger-to-nose task: initial rapid movement may strike face or hold segment of task may waver
  • Clumsiness, slurred speech, inaccurate eye movements
  • Since this is an area that alcohol typically affects first, these are good tests of intoxication!
30
Q

Cellular Organization in Cerebellum [placeholder]

A
  • Receives input from the spinal cord, each of the sensory systems, and from the cortex
  • All this info eventually reaches the cerebellar cortex (surface of the cerebellum)
31
Q

Purkinje cells

A
  • are very flat and exist in sequential planes
32
Q

Parallel fibers

A
  • are perpendicular to the planes of the Purkinje cells
  • Action potentials in parallel fibers excite one Purkinje cell after another
  • Then Purkinje cells send messages to the nuclei of the cerebellum (clusters of cell bodies at the bottom of the cerebellum)
  • This works to control the timing of a movement (the more Purkinje cells excited, the longer the duration of the behavioral response)
33
Q

Role of Basal Ganglia [placeholder]

A

.

34
Q

Basal ganglia

A

: group of large subcortical structures in the forebrain

  • caudate nucleus and putamen receive sensory input from thalamus and cortex
  • globus pallidus sends information to the thalamus where it goes on to the motor and premotor cortices
  • As a whole they store sensory information to guide movements, learn rules and organize sequences of movements into a smooth, automatic whole

—> Organize action sequence into chunks or units like learning to drive a car (habit learning)

—> OCD has been linked to increased activity of the BG – one theory is that this area may be responsible for habit formation, and so perhaps over activity is linked to excessively strong, life-dominating habits

35
Q

Parkinson’s Disease

A

Symptoms include:

  • Some cognitive slowing
  • some depression
  • Most defining symptoms: rigidity, muscle tremors, slow movements and difficulty initiating physical and mental activity
  • Onset typically after age 50, strikes about 1% of population
  • Gradual progressive death of neurons especially in the substantia nigra, an area of the brain that sends dopamine axons to the caudate nucleus and putamen

—> Symptoms begin when neurons decrease 20%-30%

—> decrease in dopamine results in decreased excitation of motor involved areas of the brain

36
Q

Substantia nigra

A
  • an area of the brain that sends dopamine axons to the caudate nucleus and putamen
37
Q

Parkinson’s Disease cont.

A

Possible Causes:

  • Genetics appear to play a small role

—> early onset in identical twin good predictor for other twin but less so after 50 years of age

—> 5 genes more common in patients but no specific gene for disease

  • one cause is exposure to toxins, e.g., MPTP designer drug which destroys dopamine releasing neurons

Smoking and caffeine decreases risks

—> inconsistent findings as to why, though

—> Certainly don’t start smoking to lessen your chances of getting Parkinson’s!!!

38
Q

Treatment for Parkinson’s

A
  • Most common treatment – L-Dopa
  • If we know Parkinson’s results from a DA deficiency, then we need to restore the missing DA. But DA can’t cross the blood brain barrier, so they got creative
  • L-Dopa is a precursor for dopamine that crosses blood-brain barrier
  • Once in the brain, neurons convert it to DA
  • effective in early to intermediate stages but some patients do not benefit at all
  • does not stop progression of the disease, may do harm
  • side effects: nausea, restlessness, sleep problems, low blood pressure, hallucinations, and delusions
39
Q

Other Treatment for Parkinson’s

A

One or more of following usually combined with L-Dopa:

  • drugs: e.g., dopamine receptor stimulants, drugs that decrease apoptosis,
  • electrical or surgical destruction of globus pallidus (tends to blocks the tremor, but very risky)
  • neurotrophins to promote growth of remaining neurons
  • cell transplants

—> most successful with substantia nigra cells transplanted from rat fetuses into young rats

—> slight benefits with human fetal brain transplants to patients

—> neurotrophins (even from pigs) may help if researchers can get them past blood-brain barrier

40
Q

Huntington’s Disease

A
  • Severe neurological disorder striking 1 in 10,000
  • Extensive damage to caudate nucleus, putamen, and globus pallidus, and some in the cerebral cortex from severe neuronal degeneration
  • Symptoms most often appear between 30-50 years
  • Earlier the onset, the worse the progression, eventually this will kill you

—> begin with jerky arm movements, then facial twitch, later tremors spread and develop into writhing

—> cannot learn new or improve movements

—> includes depression, memory impairment, anxiety, hallucination

—> No known treatments 

41
Q

Huntington’s Disease

A

Cause: dominant gene. If one of your parents has it, you have a 50% chance of getting it.

  • Would you want to know or not know? A Presymptomatic Test can look at your genes and let you know with almost perfect accuracy whether or not you will get it
  • The gene produces a protein, which attaches to certain neurons and destroys them