Section 3 Lecture 4 Flashcards Preview

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Flashcards in Section 3 Lecture 4 Deck (79):
1

Which portion of the brain is the BG in?

Forebrain

2

BG is involved in:

M control, cognitive fxn, and emotional or affective fxn

3

Fxn of the BG in terms of what info travels through and to where:

To control excitatory drive to cortex

4

What is the extrapyramidal system:

BG (does not operate independent of cortex, this is an old view)

5

What is the striatum composed of?

Caudate and putamen

6

What is the BG composed of?

Caudate, putamen and Globus pallidus

7

T or F? The substantia nigran and the subthalamic nucleus are both part of the BG.

F. Neither are.

8

Main fxn of SN:

dopamine released, altering the functional level of the striatum

9

Damage to BG:

involuntary moves or slowness of movement (bradykinesia)

10

BG diseases or disorders:

PD, ADHD, tourette's, Restless Leg syndome, Tardive dyskinesia, Huntington's, dystonias

11

PD facts:

typical onset: 60+, more men than women, progressive, but slow, can live for 20+ yrs

12

There is degeneration of this in PD:

substantia nigra

13

Specific cell population affected in PD:

substantia nigra degeneration of neurons, loss of dop input to striatum, caudate and putamen

14

Causes of PD:

unknown, genetic factors? Not a single gene mutation, would be genetic contribution or influence

15

Post-infectious PD:

got it after a flu virus, some viral influence (in this case at least)

16

Biochemical link to PD:

depression

17

Cognitive affects of PD:

dementia, sometimes

18

Motor symptoms of PD:

combo of + and - effects: tremor AT REST (esp hands and mouth), bradykinesia, akinesia

19

cerebellar lesions lead to:

tremors when movements are activated

20

Symptoms of PD:

motor, affective (depression), cognitive (dementia), tremor, brdykinesia, akinesia

21

Absence of movement, especially self-initiated moves, i.e. lack of facial expression, swinging arms when walking):

Akinesia

22

Are the motor symptoms connected to PD pos or negative?

both

23

How to induce PD in animals:

MPTP

24

BG is especially important in what type of moves?

self initiated movements

25

The ability to walk and swing arms with legs (assoc moves) is lost with the disease:

PD

26

T or F? Excitation and inh are intrinsic properties of dopamine.

F. They are not

27

Is PD slow or fast progressing?

slow prog

28

What is DBS and explain how it works.

deep brain stimulation: electrodes, subthalamus n., like a pacemaker

29

What led to the discovery of MPTP and what does it damage?

attempts to make heroin,MPTP damages SN

30

Effects of MPTP:

destroys neurons in substantia nigra

31

T or F? Most neurogenic disease aren't found in animals.

T

32

Death of neurons in the sub nigra lead to what?

gradual loss of dopamergic input to caudate and putamen

33

Cause of PD:

not known

34

Tx for PD:

l-dopa, tissue/stem cell implants, lesion in pwy, or DBS

35

Why can't we give dopamine to tx PD?

bc it wont pass BB barrier, give a precursor

36

Experimental procedure to tx PD:

Implant cells that will synthesize dopamine,

37

Goal in the tx of PD:

block or reduces abnormal drive to MC, disrupt abnormal activity in the BG

38

What happens w the removal of dopamine?

too much excitation in one place, too little in another.

39

Recent development that will help our understanding of PD:

we now have animal models of PD

40

PD involves the synapse bw:

SN to striatum

41

Transporter protein takes up:

serotonin, dopamine

42

Stimulant drugs act by:

changing dop levels, reuptake of dop at synapse is terminated by a "transporter" i.e. coin works on dop transporter

43

T or F? Dopamine is involved only in the M system.

F. other cell groups synthesize and release dop

44

Lack of sufficient dopamine reuptake can be related to:

transmitter concentrations, receptors, or transporters

45

How do the serotonin levels in depressed people compare with those of non-depressed people?

the same, receptor function may be inhibited

46

Subtypes of dopamine receptors:

D1-D5

47

Which subtypes of dopamine receptors are found in the hypothalamus?

D3 and D5

48

Which subtypes of dopamine receptors are found in the corpus striatum?

D1 and D2

49

What is neurological basis of shizophrenia:

too much dopaminergic action in the frontal lobe (hypothesis)

50

Dopamine receptor blockers:

neuroleptics, used to be tx for schizo, i.e. Chlorpromazine (Thorazine) and Haloperidol (Haldol)

51

Long term use of neuroleptic drugs for schizo can lead to:

motor disorders: tardive dyskinesia (invol mouth, face and hand moves) or tardive dystonia (abnormal m. tone or postures)

52

Which lobes of the brain are implicated in schizo?

frontal

53

Newer drugs for schizophrenia:

atypical antipsychotics, act on dop receptors in cerebral cortex (frotal lobe) and not subsets in the BG (tx cortical and does not interfere with M systems use of dopamine) Also used to tx bipolar disorder

54

Symptoms of atypical antipsychotics:

weight gain and diabetes

55

List of atypical antipsychotic Dx:

Risperdal (Risperidone), Olanzapine (Zyprexa), Quetiapine (Seroquel), Ziprasidone (Geodon), Aripiprazole (Abilify), Paliperidone (Invega), Lurasidone (Latuda)

56

T or F? ADHD is a M system disorder.

F.

57

What NT is implicated in ADHD?

dop, fxnal dopamine deficiency (hypothesis)

58

T or F? ADHD is a lifelong disorder

F, mainly. "symptoms MAY continue into adulthood"

59

Fxn of ritalin (methylphenidate) or adderall:

increase dopamine levels (adderral increases NE as well)

60

What is the biomarker for ADHD?

There isn't one

61

Rital fxns by:

acting on the dop transporter

62

Adderall fxns by:

inc the release of dop and NE

63

Tourette's is a movement disorder assoc w this part of the brain:

BG

64

T or F? The tics that come with Tourett'es an be suppressed and controlled.

F. Can't control but can suppress

65

T or F? Tourette's is a single gene disorder

F. Hereditary, but not a single gene

66

Is Tourettes' more prevelant in men or women?

Men 3:1

67

What is the neurological basis of Tourette's?

Too much functional dopamine (hypothesis)

68

Tx or Tourette's

dopamine receptor blockers, ie Haldol (still?)

69

Typical age of onset of Tourette's:

childhood, often w ADHD

70

T or F? Restless Leg Syndrome has M symptoms only.

F. Sensory and motor symptoms

71

RLS is a disorder of what part of the brain?

BG (hypothesis)

72

Tx for RLS:

increase synthesis of dopamine (L-dopa carbidopa = Sinemet) or mimic the action of dopamine (ropinirole, pramipexole, and rotigotine)

73

Symptoms of RLS are more pronounced:

at night

74

Who are affected by RLS more, men or women?

Women

75

What portion of the brain is involved with Huntington's?

BG disease:

76

T or F? Huntington's a dopamine disorder.

F

77

What is going wrong in the brains of pts with Huntington's?

Death of cells in caudate and putamen (the striatum)

78

Does Huntington's have a genetic basis?

Yes, 1 in 10,0000

79

How is Huntington's passed geneticlally:

Autosomal dominant