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Biological Psychology Kalat 12th Ed > Chapter 7 > Flashcards

Flashcards in Chapter 7 Deck (42)
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1
Q

Why do we have a brain

A

to control our behavior. If we were stationary like a plant, we would not need a brain (like a plant)

2
Q

three types of muscles

A

smooth muscles: for organs
skeletal or striated muscles: control of body movement
cardiac muscles: control the heart

3
Q

muscle fiber - axon ratio

A

one muscle fiber can only have one axon, but one axon can control many fibers

4
Q

neuromuscular junction

A

synapse between motor neuron and muscle fiber. For all skeletal muscles acetylcholine is the neurotransmitter. It excites the muscle to contract

5
Q

antagonistic muscles

A

each muscle can only make one movement: contraction. relaxation is a lack of contraction. to move a limb in more than one direction requires antagonistic muscles, which work in opposite directions. The flexor for example brings your hand towards your shoulder, while the extensor straightens the arm.

6
Q

fast twitch and slow twitch fibers

A

fast twitch: fast contraction but also rapid fatigue

slow twitch: slower contraction but no fatigue

7
Q

aerobic

anaerobic

A

slow twitch fibers are aerobic because they continually use oxygen.
fast twitch fibers are anaerobic because they don’t need oxygen to function, but need it to recover from functioning (oxygen debt)

8
Q

proprioceptor

A

receptor that detects the position of movement of a part of the body

9
Q

stretch reflex

A

reflex caused by stretching of a muscle. It contracts back to its original position

10
Q

muscle spindle

A

Is a kind of proprioceptor.
Whenever the muscle spindle is stretched, its sensory nerve sends a message to a motor neuron in the spinal cord, which in turn sends a message back to the muscles surrounding the spindle, causing a contraction.

11
Q

Golgi tendon organs

A

also proprioceptors, respond to increases in muscle tension. Located at opposite ends of a muscle.
In short, a vigorous muscle contraction inhibits further contraction by activating the Golgi tendon organs

12
Q

Reflexes

A

Reflexes are consistent automatic responses to stimuli

13
Q

ballistic movements

A

ballistic movement, such as a reflex, is executed as a whole: Once initiated, it cannot be altered. However, most behaviors are subject to feedback correction

14
Q

central pattern generators

A

neural mechanisms in the spinal cord that generate rhythmic patterns of motor output.

15
Q

motor program

A

behavioral sequence that once begun, is fixed from beginning to end

16
Q

primary motor cortex

A

we know it already but again: anterior gyrus just anterior to the central sulcus. We can map our body on it, and it matches up nice with the sensory cortex, right on the other side of the central sulcus

17
Q

hierarchy for execution of movements

A

The motor cortex orders an outcome and leaves it to the spinal cord and other areas to find the right combination of muscles

18
Q

posterior parietal cortex

A

monitors the position of the body relative to the world. also important for planning movements

19
Q

supplementary cortex

A

inhibits habituated motor responses

20
Q

premotor cortex

A

most active directly before a movement

21
Q

prefrontal cortex

A

considers possible outcomes and thereby organizes our movements.

22
Q

antisaccade task

A

our eyes get naturally attracted to stimuli. In this task you have to look in the opposite direction, thereby inhibiting your reflex. Activates the prefrontal cortex and the basal ganglia

23
Q

mirror neurons

A

do not explain autism.

they get active when we see, imagine, or act out a movement. They are not essential for imitation.

24
Q

corticospinal tracts

A

there are two tracks, and they transport nearly all information between brain and spinal cord

25
Q

lateral corticospinal tract

A

primary motor cortex –> red nucleus (in midbrain) –> crosses to contralateral side
controls movements in peripheral areas such as hand and feet. The axons from the primary cortex directly project into the spinal cord. New axons join the tract at the red nucleus

26
Q

medial corticospinal tract

A

many cerebral cortex areas –> midbrain (vestibular nucleus) –> both sides of the spinal cord
controls bilateral movements such as walking, or banding

27
Q

the crebellum

A

for rapid movements that require timing

sensory perception of timing and rhythm of stimuli

28
Q

cerebellar cortex

A

the surface of the cerebellum

The cells are arranged in a regular pattern that enables them to produce outputs of precisely controlled duration

29
Q

purkinje cells

A

cells in sequential planes parallel to each other

send inhibitory messages down to the nuclei of the cerebellum

30
Q

parallel fibers

A

axons parallel to each other and perpendicular to the planes of purkinje cells. The excite one purkinje cell after another. The stronger the signal, the more purkinje cells get excited, the longer the duration of response in the purkinje cells. this is used to control the timing of movement

31
Q

nuclei of the cerebellum

A

clusters of cell bodies in the interior of the cerbellum

32
Q

direct and indirect pathway of the basal ganglia

A

in the book is complicated description of the details, which I will leave out here
direct: enhances selected movements
indirect: inhibits inappropriate competing movements
working of the indirect pathway is essential for learning

33
Q

basal ganglia

A

The term basal ganglia applies collectively to a group of large subcortical structures in the forebrain. It is crucial for the learning and initiating of new behavior.
It controls the vigor of movement based on input from the cortex, that tells the ganglia how rewarding an action is going to be

34
Q

readiness potential

A

a preparation for voluntary movements that occurs 500ms before your movement, and that occurs before the point in time where you notice a conscious decision. This does not mean that our decisions are not voluntary

35
Q

Parkinson’s disease

A

main symptoms: rigidity, muscle tremors, slow movements, difficulty initiating physical and mental activity
more common as people age, striking 1 percent to 2 percent of people over age 65

36
Q

neurological causes of parkinson

A

loss of neurons at the substantia nigra which leads to less dopamine releasing axons at the basal ganglia. This leads to an inhibition of the thalamus, which in turn leads to less vigorous voluntary movements.

37
Q

environmental and genetic causes of parkinson

A

genetics play a role for early onset of Parkinson, but this causation is not very clear. toxic chemical can also cause Parkinson, as well as head injury.
Coffee and cigarettes surprisingly decrease the risk for parkinson

38
Q

L-dopa treatment

A

is a treatment against Parkinson increasing dopamine in the brain. It works but not well, because the disease continues getting worse, only the symptoms get less. Furthermore it stimulates the whole brain creating unpleasant side effects

39
Q

other treatments for Parkinson

A

brain transplants: did not work well
stem cells: not ready yet
neurotrophin: promising but not ready yet

40
Q

Huntington’s disease

A

severe neurological disorder that strikes about 1 person in 10,000 in
Motor symptoms usually begin with arm jerks and facial twitches. Then tremors spread to other parts of
the body and develop into writhing
Gradually, the tremors interfere more and more with
walking, speech, and other voluntary movements
a lot of psychological disorders result out of it too
occurs at any age, but mostly 30-50

41
Q

huntington neurological cause

A

The disorder is associated with gradual, extensive
brain damage, especially in the basal ganglia but also in the cerebral cortex
Because the output from the basal ganglia is inhibitory to the thalamus, damage to the basal ganglia leads to increased activity in motor areas of the thalamus. That increase produces the involuntary jerky movements.

42
Q

heredity of huntington

A

is a dominant gene, the gene has been located and we can give a precise risk assessment. the wrong genes lead to a mutation of a protein called “huntingtin”