Basal Ganglia And The Cerebellum

Front 1

what are the 5 nuclei of the Basal ganglia?

Back 1

Caudate
Putamen
Globus Pallidus(internal/external)
Subthalamic
Substantia Nigra (reticulata/compacta)

Front 2

what are the major inputs of the basal ganglia? from where to where?

Back 2

Corticostriatal to the striatum caudate and putamen

Front 3

What is the substantia nigra compacta and reticulata?

Back 3

They are nuclei of the basal ganglia

Front 4

What are the subthalamic nuclei part of?

Back 4

It is part of the basal ganglia

Front 5

What is the major out puts? Are they excitatory or inhibitory? What structures do they affect?

Back 5

They are all inhibitory outputs, and they arise from the substantia nigra reticulata, GPI and they inhibit the superior colliculus and thalamus

Front 6

The superior colliculus and thalamus are inhibited by 2 Basal ganglia outputs what are they?

Back 6

The Nigra reticulata and the Globus Pallidus

Front 7

The striatum recieves inputs from what structure of the BG?

Back 7

The cortico striatum

Front 8

The two structures of the BG that link inputs and outputs are what?

Back 8

The subthalamic and globus pallidus external

Front 9

What do the globus pallidus external and subthalamic structures of the BG do to inputs and out puts?

Back 9

They link them

Front 10

What does the substantia nigra pars compacta do?
How does parkinsons' affect this structure?

Back 10

It modulats nerons in the striatum wth DA, and a person with Parkinson's has these neurons that die

Front 11

What structures does the BG modulate to affect movements?

Back 11

THe PMA and SMA in area 6

Front 12

The BG affects area 6 in the motor cortex, specifically PMA SMA that in turn modulates another area in the mortor cortex, what is that area?

Back 12

Area 4 MI

Front 13

How is the loop that the BG, thalamus and motor cortex organized?

Back 13

Like everything in the brain parrallel.

Front 14

A patient comes in and suffers Hypokinesia or hyperkinesia this can be a result from damage to what brain structure? and what are these two disorders?

Back 14

The Basal ganglia damaged.
hypo reduced movement,
hyper uncontrollable or excessive movement.

Front 15

For the BG what is the direct pathway?

Back 15

In the cerebral cortex, glutamate binds and exites neurons that project an excitatory response to D1 receptors that require GABA (inhibitory) and substance P NTs to send an inhibitory response that inhibits the GPi and SNr from inhibiting the thalamus that affects motor movement.

Front 16

When D1 receptors are excited by GABA and substance P what is their affect? (in BG)

Back 16

The directly inhibit GPi and SNr from inhibiting the thalamus.

Front 17

In the basal ganglia what inhibits GpI and SNr?

Back 17

The excitation of D1 receptors

Front 18

Where are D1 receptors located?

Back 18

in the striatum of the BG

Front 19

What is the indirect pathway in the BG?

Back 19

Glutamate binds to D2 receptors that are active by the enkephalin, and gaba NT, this in turn sends a inhibitory response that can target D1 receptors preventing them from inhibiting the GPi/SNr so that it can inhibit the thalamus, AND it can inhibit the Globus Pallidus external from inhibiting the Subthalamic nucleus. The STN can therefore excite the GPi/SNr to inhibit the thalamus causing reduced movement.

Front 20

In the BG the Globus Pallidus Externa is excited/inhibited by what? Which NT does it use? and what does it do to what structure :)

Back 20

its excited under normal circumstances, but it is inhibited by D2 receptors in the striatum. It uses Enk and Gaba. It is excited under normal cirucmstances to inhibit the Substhalamic Nucleus. When it is inhibited it does not inhibit the STN and there fore the STN can cause the GPi/SNr to inhibit the thalamus and inhibit movement

Front 21

In the BG what is the STN? what is its NT? and what does it do to what structure?

Back 21

The Subthalamic Nucleus has excitatory neurons driven by glutamate. This is inhibited by GPe normally, and wil not excite the GPi/SNr from inhibiting the thalamus.

Front 22

What is the indirect pathway activation do?

Back 22

it increases BG inhibition on the thalamus blocking movements

Front 23

What does activation of the direct pathway do?

Back 23

It decreases basal ganglia inhibition of the thalamus and allows movements to go forward.

Front 24

In the BG how are Outputs and inputs acting?

Back 24

Outputs are inhibitory, inputs are excitatory.

Front 25

How does the basal ganglia allow movement to go forward and block other movements? How does it use both pathways together?

Back 25

It uses inhibition of the thalamus to prevent movements and reduces this inhibition for certain movements.
By working together the body picks and chooses which movements it applies.

Front 26

What structures elicit the direct pathway? 2of them

Back 26

Caudate/putamen

Front 27

What structure elicit the indirect pathway

Back 27

the Subthalamic Nucleus.

Front 28

Who discovered parkinsons"? When? Waht did he do?

Back 28

James Parkinsons 1817 made a complete description, the shaking palsy.

Front 29

3 differences between normal and Parkinson's pts.

Back 29

The amount of DA receptors decreases
Flouro dopa is decreased
and so are Dopamine reuptake transporters, in Cd: gone in Pu gone..ect.

Front 30

How many DA (%) neurons do you lose before you develop parkinson's?

Back 30

about 80-90%

Front 31

People that are in their 80's lose about ____% of their DA neurons, but in order to develop parkinsons they need to lose _____% in the _____ Keep at it ya old farts.

Back 31

40%
80-90%
substantia nigra pars compacta.

Front 32

In parkinsons disease the BG pathway is screwed up. Describe this pathway:

Back 32

D1 receptor neurons are less active allowing GPi/SNr to inhibit the thalamus.
There are no SNc DA neurons. the indirect pathway becomes more active:
it results in bursting with no more tonic inhibition. Normally there is no correlation with spiny neurons, but with the disease there is correlation with the actiity of other GPi neurons causing this bursting affect.

Front 33

What are the receptors on spiny neurons

Back 33

D1

Front 34

What are the pharmacolgical treatments for Parkinsons?

Back 34

Levadopa (L-Dihydroxyphenalalanine) converted to DA by DOPA decarboxylase.
also COMT inhibitors (entacapone) to block L-Dopa DA agonist ropinirole (Requip) and pramipexole (mirapex)
Ach inhibitors such as benztropine (congenitor) and trihexyphindyl(artane) because there is a ratio that the body keeps of DA:ACh

Front 35

benztropine (congentinor and trihexyphenidyl (artane)?

Back 35

ACh inhibitors that can be given to pts with parkinsons

Front 36

Catechol-o-methyltransferase inhibitors

Back 36

Given to Parkinsons pt that block LDOPA conversions outside the brain.

Front 37

Dyskinesias

Back 37

abnromal movements such as head wobble. Usually side effects of LDOPA

Front 38

Too much LDOPA causes

Back 38

unctonrollable dyskinesisas

Front 39

In the video why was the old lady kicking...and really sensitive?

Back 39

because of her tx for parkinsons

Front 40

What is DBS?

Back 40

deep brain stimulation to tx parkinsons, electrode in the brain, battery in the chest.

Front 41

Huntingtons disease/chorea

Back 41

CAG repeats, degeneration off neurons in caudate, uncontrollable choreatic movements Autosomal dominant, if a parent has it 50% chance of you getting it.
IT15
greater than 40 CAG repeats.
Affects Basal Ganglia.

Front 42

What is the genetic component of Huntingtons

Back 42

CAG repeats:
Autosomal Dominant mutation on short arm of chromosome 4
IT15 it makes htt protein.

Front 43

Ppl with 35-40 CAG repeats

Back 43

may get huntingtons but there is a reduced penetrance

Front 44

wwhat is htt

Back 44

huntingtin protein that causes the symptoms of huntingtons disease.

Front 45

How does huntington affect mitochondria?

Back 45

ppl with huntington have fewer and poorly working mitochondria

Front 46

What is the Ca+2 dependent increase in synaptic transmission related to?

Back 46

In huntington's disease it means the neurons keep working themselves to death.

Front 47

How does huntington's disease affect the function of mitochondria? 2 ways

Back 47

By inhibiting PGC-1alpha that is important for the biosynthesis and oxidative phsophorylation
and by impairing II, II, IV e- transports and binds to Sp1-mediated gene transcription.

Front 48

Who has a serpentine tongue

Back 48

snakes and ppl with huntingston

Front 49

Where are over 50% of the neurons located?

Back 49

in the cerebellar cortex.

Front 50

Where does the cerebellar cortex preject its axons?

Back 50

deep cerebellar nuclei

Front 51

Where do inputs of the cerebellum come from? 4 places

Back 51

inf. olive, dorsal nucleus of clark, pontine nuclei, vestibular nuclei.

Front 52

what does the word cerebellum mean? What does the cerebellum do?

Back 52

little brain
coordinate movements.
arbor vita= tree of life.

Front 53

What are the 4 saggital zones of the cerebellum

Back 53

vermis, intermediate
lateral/hemisphere
flocculonodular lobe

Front 54

vermis, whats it do where does it send shit to?

Back 54

gets visual, auditory, vestibular, somatosensory sensory inputs. Modulates posture, locomotion, eyemovements
sends to the Fastigial in the deep cerebellar

Front 55

Intermediate what does it recieve, what does it do? where does it send shit to?

Back 55

gets somatosensory input from limbs.
Modulates movements of distal limbs
sends to interposed deep cerebellar nuclei

Front 56

Hemisphere lateral: what does it do, wehre does it get info from, and where does it send this info?

Back 56

from cerebral cortex, sends to dentate nuclei deep in cerebellum. Modulates the activity of teh cerebral cortex.

Front 57

What input does the Fastigial nuclei receive? who sends it?

Back 57

input from the vermis on auditory, vestibular, somato sensory

Front 58

What input does the interposed nuclei receive? Who sends the input?

Back 58

input on the somatosenroy information of the limbs from the intermediate region

Front 59

What input does the Dentate nuclei receive? Who sends it?

Back 59

input on the cerebral cortex from the lateral/hemisphere portion of the cerebellum

Front 60

What aprt of the cerebellum monitors the cerebral cortex?

Back 60

the lateral/hemisphere

Front 61

what part of teh cerebellum modulates posture locomotion and eye movements

Back 61

vermis

Front 62

Information from various limbs are sent to what part of the cerebellum

Back 62

the intermediate

Front 63

What is flocculonodular lobe?
Where does it send info? what info does it get? What does it do?

Back 63

It is part of the cerebellum: gets vestibular and visual sensory input, sends it directly the to brain/vestibular nuclei

Front 64

Where does the cerebellum receive informaion about intedned movements from?

Back 64

the motor cortex via pontine nuclei

Front 65

Where does the cerebellum receive informaion about actual movements from?

Back 65

The somatosensory cortex and spinal cord also by pontine nuclei

Front 66

How does the cerebellum do its function of coordinated control?

Back 66

It takes the intended and actual movements and makes corrections

Front 67

The cerebellum acts on the MI cortex area 4 through inputs to ______(____) and by acting on ________neurons that receive M1 inputs.

Back 67

thalamus(ventrolateral nucleus caudal)
red nucelus

Front 68

The cerebellar cortex has 5 types of cells:

Back 68

Purkinje
granule
stellate
basket
golgi

Front 69

Which cells of the cerebellar cortex inhibit

Back 69

purkinje
stallate
basket
golgi

Front 70

which cells of the cerebellar cortex excite

Back 70

the granule (most common) cells excite
the "neurons" of the deep cerebellar nucleus also excite, they excite other neurons outside the cerebellum

Front 71

Purkinje cells

Back 71

inhibit deep CNN and get excitatory inputs from granule cells (parrallel fibers) and the inferior olive (climbingfirbers)

Front 72

How many granule cells synapse purkinje cell

Back 72

about 80,000
a parallel fiber synapses once or twice on 300-400 purkinje cells.

Front 73

cLIMbing fibers connect to what? How many does it contact?

Back 73

it connects to one purkinje cell, but climbs all over the tree and contacts a few purkinje cells. ??? WTF?
they are inferior olive

Front 74

Stellate cells

Back 74

inhibit pcells

Front 75

baskate cells

Back 75

inhibit pcells

Front 76

Golgi cells

Back 76

inhibit mossy fibers / granule cells

Front 77

Complex spikes occur in response to what?

Back 77

a climbing fiber action potential
Coltage dependent Ca^+2 channels. Ca+2 causes depolarization

Front 78

Simple spikes occur in response to what?

Back 78

Parallel fiber/ granule cell inputs they are standard Na+ AP.

Front 79

What do simple spikes show?

Back 79

Detailed information about movements and sensory stimuli

Front 80

What provies and error signal that alters the synaptic strength of parallel fiber synapses.

Back 80

Complex spikes. They may be the neural basis for motor learning.

Front 81

What are the 3 categories of movement abnormaliteies associated with cerebellar disorders?

Back 81

Hypotonia
intention tremor
Ataxia

Front 82

Tremor at rest vs intention tremor.

Back 82

Tremor at rest 4hz for parkinsons
Intention tremor is in cerebellar dysfunction and gets worse as the patient attempts to terminate the movement. It is a result of misjudgement of corrections for mistakes in movement trejectory.

Front 83

Rigidity

Back 83

increased muscle tone in parkinsons disease

Front 84

micrographia

Back 84

reduced size of letters with prolonged writing

Front 85

hypophonia

Back 85

softer speech and vocal hesitation

Front 86

gait disturbances

Back 86

small steps narrow based gait.

Front 87

Cardinal features of parkinsons

Back 87

tremor at rest
rigidity
bradykinesia
postural instabiity

Front 88

Ssecondary features of parkinsons

Back 88

Micrographi
hypophonia
gait disturbances

Front 89

Pt has reduced muscle tone and there is diminished resistance to movement of limbs, what is probably wrong with them? (it's not the same as muscle weakness) What part of their ns is most likely damaged?

Back 89

hypotonia cerebellar is broke.

Front 90

Ataxia refers to lack of coordination in voluntary movements and is broken down into 4 groups:

Back 90

Delays of initiating movements
Dysmetria: errors in the size of movements
Errors in the rate of repetitive movements
Decomposition of movement in which multi joint actions are poorly coordinated.

Front 91

What is dysdiadochokinesia

Back 91

inability to make rapid or alternative movements and inability to coordinate antagonistical pairs of muscles.

Front 92

Person is asked to say gagagaga they say gjaofdslfjawoign...wtf?

Back 92

They have speech disfunction probably due to cerebellar dmg, and dysarthia.

Front 93

Spinocerebellar ataxia 1 SCA1

Back 93

caused by cag repeats 39-91 in the ATXN1 gene chromosome 6 just like HD it is autosomal dominant.

Front 94

CAG repeats huntingtons vs dysarthia:

Back 94

Dysarthia 39-91 ATXN1 gene chromosome 6
HD greater than 40 Triplet repeats on the IT15 on chromosome 4

Front 95

intention tremor has damage to their left cereebellum, which is

Back 95

left side, ipsilateral.

Front 96

Person has cerebral cortex damage on his left side brain which side of the body would they expect to find problems?

Back 96

contralateral, or the right side..

Front 97

The prism test where the girl couldn't do the prism test where water bends the light. what is the point of this video?

Back 97

To watch the girl unable to adapt and hit the rod. Due to motor learning dysfunction that is due to cerebellum damage.