Immuno 12 & 13 Cell Mediated Immunity

Front 1

CMI includes what effector cell?
what type of pathogen does it target

Back 1

CD8 cytotoxic T cells
Intracellular

Front 2

so a mature B cell has what surface BCR

Back 2

IgM
IgD

**both serve as membrane bound BCR

Front 3

arou double positive T cells immature or mature

Back 3

immature

Front 4

positive selection of T recognoizes what, what isnt recognized

Back 4

MHC is recog (now downreg CD4/CD8 down reg PRN)

Peptide is NOT recognized

**Ih MHC II binds, CD4 is kept and CD8 is down reg

Front 5

what do Th1 cells do
what do Th2 cells do

**its NOT just CTL in CMI, also Th

Back 5

th1: kill phagosomes infected with intracellular bug

Th2: kills parasites and allergens

Front 6

what tends to happen in a person who is CMI deficient

Back 6

they dont really have a whole lot of CTL (t cells in general)

lots of intracellular opprotunistic infections

Front 7

whats wrong in DiGeorgi Syndrome

Back 7

No thymus, No T cells (entire area from head to mediasteinum is affected)

**wont respond to skin test AG, no memory T cells

Front 8

what is it called when someone doesnt have a thymus

Back 8

DiGeorgi

*no thymus --> No T cells --> lots of infections, no rxn to skin AG tests bc NO memory cells

Front 9

what might be going on if someone doesnt respone to skin rxn AG tests

Back 9

no memory cells

DeGeoige: no Thymus, No T cells

Front 10

waht is the fx of CTL
Th?

Back 10

capture ENDOgenouse AG with MHC I

Th does EXOGenous with MHC II (APC)

Front 11

what are three things the the cytokines from Th do

Back 11

1. Acitvate (proliforate/diffferentiate) T and B cells
2. Activate mscro
3. Inflammation

Front 12

what are important cell surface markers for T cells that do signal transduction

Back 12

CD3 zeta

Front 13

what cell has CD3 and zeta, what doies it do

Back 13

T cell

**signal transduction (zeta is analogous to the Iga and Igb on BCR)

**the CD4 (th) or CD8 (CTL) also do signal transduction

Front 14

what cell has CD28, what does it do

Back 14

T cells

**Co stimulation

Front 15

what is the inhibitory signal on T cells

Back 15

CTLA4

Front 16

what cell has CTLA 4, what does it do

Back 16

T cells, signal inhibition

Front 17

what are LFA 1 adn VLA4, how does their fx differen from CLTA 4

Back 17

FLA 1 and VLA 4 are adhesion mulocules on T cells

CTLA 4 is also on T cells but it inhibits hte ssignal that was created by CD3, zeta, and CD4 or CD8

Front 18

what do T cells need to have FLA1 and VLA4

Back 18

so that they can interact thghtly with APC and have AG be presented to them

Front 19

there are 7 molecules on T cells, what are they

Back 19

CD3: signal
Zeta: signal
CD4/CD8: signal
CD28: co stim
LFA1: adhesion
VLA4: adhesion

**CD44 and cD25 also expressed to commit to the T lineage early on

Front 20

Do APC presenet to BOTH Th and CTL

Back 20

sure thing

Front 21

what is the big picture for T cell actication

Back 21

APC presents 2 signals to the T cells.

**presents to both Th adn CTL

Front 22

what does actication of a T cell lead to?

Back 22

proliforation of T cells with a single specificity!

**LOTS of T cells that recognize the SAME AG

Front 23

where does T cell activation occur?
what kinds of T cells are activated?
what happens once activated?
Who activates them, how?

Back 23

2 lymph tissue
Th and CTL
Proliforation
APC with TWO activation signals (Both signals come from the APC)

Front 24

how are T cells acticated and what happens once they are activted

Back 24

an APC give a T cell 2 signals for activation, this allows the T cell to proliforate so that there is an arms full of T cells with the same AG specificity to attack teh AG. Effector t cell fx include: Th: activate macro, T and B and inflammation. and CTL: kill infected cells

Front 25

what is teh first signal for T cell activation

Back 25

TCR binds MHC

TCR matches the AG MHC, then CD4 or Cd8 will also bind

Front 26

what is the second signal for T cell activation

Back 26

CD28 on T cell binds to the B7 on APC

**this is the step that acticates the T cell via intracellular signal transduction

Front 27

what step (1 or 2) does the actual activation

Back 27

second

1. MHC: AG binds to the TCR: CD8/4 and STABILIZE

2. THe APC B7 and CD28 on T can occur and actually cause activation of the T cell

Front 28

why must the T cell FIRST adhere to the APc adn THEN its activated via CD28/B7.

Back 28

First turn on the engine, then step on the gas

**its a safe guard :)

Front 29

what makes dendrites such a good activator of T cells in a primary immune response

Back 29

they have CONSTITITIVE expression of MHC and B7

Front 30

wht APC is a really good T cell activator, why

Back 30

Dendrites, they always have MHC nad B7

MHC for 1st step
B7 for second step

**other APC need to be activated themselves, macrophages need activation by IFNg to express B7 for the second step of activation

dendritic is good for niaeve T
macro is good for effector T

Front 31

how do dendritic cells and macrophages compare in terms of theri ability to APC?

Back 31

1. Dendrites, the best, they ALWAYS have MHC nad B7 (both are required for the 2 steps of T cell activation)

2. Macrophages, pretty good but require IFNg in order to express B7 which is required for the second step of T cell activation

**dendritic are good for activating Niaeve T in primary response

**macro are good at effector T cells

Front 32

what role does IFNg in T cell activation

Back 32

acts on macrophages to express B7, required for the 2 step of T cell activation

**macro are better at stim effector T cells.

Front 33

is LFA 1 and VLA4 part of the 1 or 2 step of T cell activation

Back 33

1- adhesion

Front 34

what happens when there is no B7/CD28 interaction

Back 34

ANERGY

*no second signal, no T cell activation

**this limits the nu,ber of cells that can actually activate a t cell

Front 35

what is anergy

Back 35

unresponsive T cells, they get the 1 signal but not the second


**no B7 for the co stimulation required in the second step of activations

**only a limited number of cells (APC) have B7, limits the number of cells that can activate a t cell

Front 36

ok so we have all of this stuff going on extracellularly to activate T cells (TCH, MHC< CD4, B7:CD28) what happens in the cell when this hapens

Back 36

signal transduction is activated

1. NFAT
2. NFkB
3. AP1
**all work together to make IL2

Front 37

what does CD4/8 actually bind to

Back 37

the MHC on the APC

Front 38

what are the 3 TF that are made in repsonse to the extracellular 2 step T cell activation? what do they do

Back 38

NFAT
NFkB
AP1

**all work to make IL2

Front 39

how is IL2 made,

Back 39

made by the T cell. So we have the 2 step activation path that causes signal transduction, this makes NFAT, NFkB, and AP1, these TF then work to make IL2

Front 40

in addition to secretion of IL2 by the T cell in response to activation what else happens

Back 40

the T cell also makes an IL2 receptor for itself

**IL2 is an autocrine signal, made BY the T FOR the T

Front 41

is IL2 required for T cell activation?

Back 41

sure is!

Front 42

so the T cell has received two activation signals (MHC:AG::TCR:CD4/8) it makes IL2 and IL2R. Then what?

Back 42

IL2 makes cyclins which activate activation

Front 43

what must happen in order for IL2 to bind T cell

Back 43

needs a high affinity IL2 receptor, this means that only activated T cells will be able to bind IL2 and stim proliforation via cyclins

Front 44

so... we have had
1. 2 step activation
2. production of TF (NFAT, NFkB, AP1)
3. Production of IL2 & IL2R
4. several rounds of replication

what happens next

Back 44

we then make T cells with CTLA4

**CTLA4 is in inhibitory signal that binds to B7 on the APC to stop the signal

Front 45

what 2 things on the T cell can bind to By on the APC

Back 45

1. CH28, the normal thing for co stimulation. ACTIVATOR

2. CTLA 4, only expressed after several rounds of IL2/cyclin induced proliforation. Out competes CH28 and acts as an INBITORY signal to stop proliforation

Front 46

wht stops t cell proliforation after it has been activated

Back 46

CTLA 4 is expressed on the T cell after several rounds of proliforation. this binds to B7 on the T cell to block the 2 co stim signal! INHIBITS proliforation

Front 47

what part of T cell activation can be manipulated to help in cancer

Back 47

IL2

**take some T cells from cancer, show them IL2 to increase the T cell numbers and then put them back into the cancer (tumor)

Front 48

what 2 drugs inhibit T cell activation? how do they work

Back 48

1. cyclosporin
2. tacrolimus

**they prevent NFAT, no NFAT no IL2. no IL2, NO T CELL ACTIVATION

**recall NFAT, NFkB and AP1 are all required to act as TF for IL2 synthesis

Front 49

what is one method of immunosupression useing T cells

Back 49

inhibit activation by blocking IL2

**cyclosporin and tacrolimus can prevent NFAT, no NFAT no IL2, no IL2 no T cell response

Front 50

what does it mean that several days after activation T cells proliforate into a CLONE of AG specific T cells and will further differentiate

Back 50

they become EFFECTOR: helper or cytotoxic. Primary IR

they become MEMORY: secondary IR

Front 51

what are the 3 types of Th, what do they respond to, what do they secrete

Back 51

TH1 cell mediated. IFNg
Th2 HUMORAL. IL4 IL5 IL13
Th17 inflammatory, microbial. IL17

Front 52

what Th cell controls

Humoral response
Cell Mediated

Back 52

th2 (IL4 IL5 IL13) humoral
th1 (IFNg) cell mediated
th17 (TH17) inflammatory/microbial

**recall IFNg was also the cytokine that activates macro to express B7

Front 53

name the Th cell that secretes these sytokins

IL4 IL5 IL13
IL17
IFNg

Back 53

Th2 (humoral)
TH17 (imflammation/microbes)
TH1 (cell mediated)

**recall that IFNg is also the cytokine that activates macrophages to express B7

Front 54

what determines if Th1 Th2 or Th17 is made

Back 54

the cytokines and AG that are around in the early IR

Front 55

name the early stumulus that induces the Th cell. (AG and cytokine)

Th1
Th2
Th17

Back 55

Th1: cell mediated, bacteria fungis viria (intracellular bugs), IL12 IFNg

Th2: humoral, Parasites/allergens. IL4

Th17: inflammatory, some microbial. no known AG. IL6 and TGFb

Front 56

if IL12 and IFNg are around that Th cell will be made? what AG will stim this

Back 56

Th1

**intracellural bugs. bacteria, virus, fungi

**cell mediated immunity

Front 57

if IL4 is around what Th is made. what AG will also stim this

Back 57

Th2

**parasites and allergens

**humoral immunity

Front 58

if IL6 and TGFb is around what Th is made. what AG will also stim this

Back 58

Th17

**no known AG

**inflammatory and SOME microbial

Front 59

wr know that IFNg and IL12 will caure Th__ formation. where do these cytokines come from

Back 59

Th1: cell mediated response

IL12: from macro and dendrites after they eat up infected things

IFNg: secreted by Nk cells (recall macro secretes IL12 to tell Nk to make IFNg, IFNg in return helps macro as APC and phsgocytic cell)

Front 60

what is the cool feed forward mech of Th1 differentiation

Back 60

IL12 secreted by macro.dendrites stim Th1, it also atim Nk to make IFNg. IFNg also stim Th1

**once Th1 are activated, they also secreted IFNg to aid in Th1 differentiations

Front 61

we know that Il4 stim Th___. the IL4 comes from...

Back 61

Th2: humoral

IL4 is from Th2 itself. When we have Th cells that want to differentiate and there are NO APC SECRETING IL12 then we get IL4 adn thus Th2.

**IL4 also comes from mast cells when there are allergens/parasites

Front 62

which cytokine acts as an autocrine growth factor in the differentiation of Th cells

Back 62

IL4 to make Th2

*when there are no APC's around to secrete IL12 they default to make IL4 and Th2

**keep in mind where there are allergans/parasites IL4 is also secreted

Front 63

we know that IL6 and TGFb cause differntiation of TH___. what makes IL6 and TGFb and how do the 2 work together

Back 63

17: inflammatory cytokine made by LOTS of cells

TGFb: also made by lots of cells at mucosal surface

**together they make T cells secrete IL21 and act as autocrine signals for Th17

Front 64

Il 21 does what?

Back 64

well the combination of the proinflammatory IL6 and the TGFb at mucosal surfaces causes T cells to make IL21, the IL21 induces differentiation into Th17

Front 65

where do EFFECTOR T cells act

Back 65

site of infection in the periphery

** can be activated in Ln and then home to the periphery via CAMS or can be activated in the periphery and just stay there

Front 66

what is teh primary fx of Th1 cells? what do they secrete? how do they specifically do their Fx

Back 66

phago intracellulat infections. Recall cell mediated modulator

IL2 (recall makes cyclins for proliforation)
IFNg
TNF

1. Activate PMN, NK, Tc
2. Stim B cell production of opsinizing AB

Front 67

Wht Th would activate PMN, NK, and Tc. And also increase opsinizing Ab from B cells

Back 67

Cell mediated Th1

Front 68

how does a Th1 stim a macrophage? (Th1 does cell mediated, so we want to kill intracellular things with macro phago)

Back 68

Th1 secrete IFNg and they have CD40L (CD154)

APC has CD40 and so can bind to the CD40L on the Th1.

This binding btwn macro and Th1 increases the phago ability of the macro

Front 69

what does CD40 and CD40L do? what cells

Back 69

CD40 on macro can bind to the CD40L (Cd154) on Th1 cells. This increases the phago/APC ability of macro

Front 70

hoe do Th1 stim B cells

Back 70

make AB for opsinization. CMI

**Th1 secrete IFNg which makes plasma cells make IgG for opsinization

class switching stim by IFNg from Th1 to make IgG for opsinization and compliment activation

Front 71

the Th1 secretes IL2, IFNg TNF and CD40L. what do they all do

Back 71

IL2: make better CTL

IFNg: stim B cells to make igG for opsinization and compliment activation

TNF: extravasation

CD40L: expressed on Th1 and binds to the CD40 on macro to increase the phago and APC ability of macro

Front 72

what role does the IFNg and IL2 play in Th1 doing its cell mediated respinse

Back 72

activates/differentiates niaeve T cells into CTL

Front 73

if an APC provides BOTH activation signals to a nieve Tc is Th1 required

Back 73

nope

*Th1 can secrete IFNg and IL2 to activate CTL

Front 74

what does the production of TNF from Th1 do to help the Th1's CMI

Back 74

makes BV express more CAMs to ptomote extravasation

Front 75

what cytokine from Th1 helps get cells into the site of infection

Back 75

TNF

**increase CAM's on BV so WBC can get where they need to be

Front 76

what Th makes opsinizing AB, what makes non opsinizing

Back 76

OPsinizing: Th1, IgG, IFNg

Non Opsinizing: TH2

Front 77

what are the 4 cytokines made by Th2? what causes them to be secreted (what type of AG do they respond to?)

Back 77

IL4: mast cell, AB production
IL13: mast cell, AB production
IL5: eisinophile activation
IL10: supress macro

**allergens, parasites, helminthic

**activate B calls, eisoinophiles, and mast cells. INHIBIT MACRO

Front 78

what Th cell inhibits macro

Back 78

Th2

Front 79

what type of resonse is elicited against allergens/parasites/worms? what Th cell? what cells involved

Back 79

humoral
Th2
eosinophile, mast cell, inhibit macrophages

Front 80

what Th cell helps with inflammation, what are the 3 cytokines they produce? what is the effector fx

Back 80

Th17

IL17
IL21
IL22

Not really a whole lot known about the effector fc og TH17 but they promote inflammation: acute phase protein, chemokines to attract WBC, IL6 proinflammatory cytokines

Front 81

what are the 3 general effector fx of Th17? and the cytokines

Back 81

promote inflammation

IL17: chemokines to attract WBC where they need to go on BV (recall TNF from Th1 has a similar fx)

Front 82

the TNF from Th1 and the IL17 from Th17 have similiar Fx, wht is it

Back 82

attract WBC to the BV for extravasation

IL21: induce other cells to make proinflammatory cytokines like IL6

IL22: make acute phase proteins

Front 83

what is the Fc of CTL, MHC? can more than 1 CTL bind to same target

Back 83

KILL, direct cell contact to fight intracellular pathogens as well as cancer

MHC I

more than 1 can bind

**TCL have 2 mechs for killing

Front 84

what are the 2 mechs for likking by CTL

Back 84

1. Degranulation, same as NK
2. FAS:FASL

Front 85

describe the degranulation method of likking by CTL

Back 85

same as NK.

1. Perforin causes a pore to form in the membrane of an infected cell

2. Granzymes: serine esterase, activates caspase apoptitic path

Front 86

what cells have FAS what has FASL

Back 86

FAS: ALL nucleated cells
FASL: T cells that dont have granules for the granular killing mech. ACTIVATED CD8

Front 87

how do effector CTL know what cells to kill since ALL cells have FCL

Back 87

only the cells that need to be likked will also be recognized by TCR:MHC I

Front 88

explain the FAS FASL mechanism of killing

Back 88

CTL (CD8) when activated has FASL.

If the TCR MHC match and there is ALSO binding of FAS FASL the caspase pathway for apatosis is stim

Front 89

what 2 things can activate caspase path for apoptosis, what cell type will stim this

Back 89

CTL (CD8 T cells)

when T cell finds its AG:MHC target cell it can also bind FAS FASL (on T) which leads to apoptosis

CTL can also have granules with perforin and grnauzymes that kill

Front 90

where does maturation of T cells occur, where does differentiation

Back 90

Maturation: thymus

Differentiation: 2 lymph organ

Front 91

what are teh 2 subselts of T memory cells

Back 91

central memory: home to 2 lymph tissue and proliforate fast when they see AG to make lots of effector cells

Effector: home to peripheral tissue and secrete cytokines, not lots of proliforation. initial RAPID.

Front 92

what T memory cell doesnt proliforate alot, what does it do? where does it do it

Back 92

effector

makes cytokines in the peripheral tissue (mucosa especially)

Front 93

what T memory cells does LOTS of proliforation? whre does it do this

Back 93

central memroy

secondary lymph tissue

**go to the 2 lymph tissue and proliforate rapidly on exposure to AG to make lots of effector T cells

Front 94

dont confuse effector t cells (TH1 TH2 CTL)
and effector memory

Back 94

effector memory go to the peripheral tissue and make LOTS of cytokiens without much differentiation

Front 95

what helps memory T cells stay around for a long time

Back 95

IL7 stim low levels of proliforation

Front 96

____ stimultes prodution of Th1 which makes ____

____ stimultes prodution of Th2 which makes ____

____ stimultes prodution of Th17 which makes ____

Back 96

IL12 IFNg::: IFNg, IL2, TNF, CD40L

IL4:::: IL4 IL5 IL13 IL10

IL6 TGFb::: IL17 IL21 IL22

Front 97

the TH17 cytokines are made when ____ are made initially and cause what

Back 97

IL6 TGFb

IL17: stim inflammation
IL21: CTL activation
IL22: increase APR, IL10

Front 98

the Th2 sytokines are made when ______ in isitially secreted and cause what

Back 98

IL4

IL4 & IL13: B to make IgE
IL5 eosinophile activation
IL10 macro inhibition

Front 99

the Th1 cytokines are made when ____ is intiially secreted, and cause what

Back 99

IL12 IFNg

IFNg: macro activation and IgG
IL2: CTL activation
TNF: PMN activation

Front 100

TNF causes what

Back 100

PMN activation

Front 101

wht increases IgG, IgE

Back 101

IgG, Th1 with IFNg

IgE: IL4/IL13 from Th2

Front 102

name the direct path for the motor loop of the BN
tell if each step is + or -, overall is it + it -

Back 102

cortex to striatum (putamen) +
striatum to internal GP -
Internal GP to thalamus -
thalamus to cortex +

Overall it is an excitatory stim

Front 103

name the indirect path for the motor loop of the BN

Back 103

cortex to putamen (striatum) +
Putamen to external GP -
External GP to subthalamic nucleus -
Subthalamic to internal GP +
Internal GP to thalamus -
Thalamus to Cortex +

**overall it is an inhibitory pathway

Front 104

what are the 2 differences btwn the direct and indirect paths

Back 104

1. indirect: from putamen to GP uses EXTERNAL,

2. from GP it goes to subthalamic nucleus instead of directly to the thalamus

Front 105

what is the excitatory NT used? inhibitory

Back 105

Glut
GABA

Front 106

what are the corticostriate projections of the motor BN tract? what NT is used, excitatory or inhibitory? is it the same for the direct and indirect

Back 106

input from cortex to the striatum (putamen)

GLut, Excitatory

same for both

Front 107

from what areas of the cortex does info in the corticostriate come from

Back 107

primary motor cortex
premotor cortex
supplementary cortex


*corticostriate is from cortex to striatum (putamen, + glut, same for both

Front 108

what are the striatopallidal projections

Back 108

in the motor loop of BN its the second neuron in both the direct and indirect path,

-, uses GABA


projection from putamen to the GP

Direct: internal GP, sub P
Indirect: external GP, enkephalin

Front 109

what additional NT is used in the direct path in the striatopallidal projections? indirect

Back 109

Sub P
Enkephalin

Front 110

when is sub p or enkephalin used

Back 110

in the motor loop of the BN
in the projectin from putamen to GP (striatopallidal projections)

Direct: GABA + Sub P, net (-)
Indirect: GABA + enkephalin, net (-)

Front 111

where is the striatopallidal proojection for the direct, indirect path

Back 111

Direct: putamen to internal GP, sub P

Indirect: putamen to external GP, enkephalin

Front 112

what is the pallidothalamic projection? what NT is used

Back 112

output from GP into the thalamus

for the direct path this is a direct thing, from int GO to VA/VL nuclei in the thalamus


GABA (-)

**the indirect also has a pallidothalamic projection that is inhibitory but it receives + info from the subthalamic nucleus

Front 113

is the pallidothalamic projectino from the internal or external GP? indirect and direct

Back 113

in BOTH cases its from internal to VA/VL with GABA

BUT...
Direct is straight from putamen (-) and the indirect is from teh subthalamic nucleus (+)

Front 114

in the internal GP does the direct/indirect receive + or - stimuli

Back 114

Direct: -
Indirect + (so MORE GABA will be released, this has the effect of inhibiting the whole path...details to come)

Front 115

waht are the thalamocortical projections, what NT is used.

Back 115

from the VA/VL of the thalamus to the cortex (premotor, supplementary, primary)

GLUT +++

Front 116

does the thalamosortical projection for the direct and indirect path change?

Back 116

nope, both are from VA/VL to primary motor, premotor and supplementary motor and use GLUT as an ++ NT

BUT...
overall the Direct is ++ and indirect is ---

Front 117

what are niagrostriatal projections? what NT, + or -

Back 117

in the BN motor loop its from the sus niagra pars compacts to the putamen (striatum)

Dopamine in BOTH cases but depending on the receptor can be + or -

*overall effect is to increase to contrast. ie excitatiry is MORE excitatory and inhibitory is MORE inhibitory

Front 118

so info form the sub niagra pars compatct can influence the direct and indirect path, for each what NT is used and how does it affect the path

Back 118

Direct: +, increases the path. MORE excitatory

Indirect: -, decreases the path. MORE inhibitory

BOTH USE DOPAMINE

Front 119

in what part of the BN motor loop is dopamine used?

Back 119

the nigrostriatal projection

**dopamine from the sub niagra pars compacts influences the direct and indirect paths in opposite ways due to the receptors.

Idirect: -
Direct: +

Front 120

what path has a pallidosubthalamic projection, what does it do?

Back 120

indirect, detour

from external GP to subthalamic (then you go from subthalamic to internal GP (subthalamopallidal projection)

**GABA, inhibitory

Front 121

what is the subthalamopallidal projection

Back 121

from the subthalamic nucleus to the internal GP in the indirect path

**this is ++, glut

Front 122

what are the names of the projections in the indirect path that get info from the GP to the subthalamic, are they + ot -

Back 122

Pallidosubthalamic: external GP to Subthalamic nucleus, GABA -

Subthalamopallital: subthalamic to INTERNAL GP, GLUT +++

**this detour makes the indirect pathway inhibitory

Front 123

what part of the motor loop is the accelerator? brake

Back 123

direct path (increase motor OUTput from cortex)

indirect path (decrease motor OUTput from cortex)

Front 124

what path increases motor output from cortex

Back 124

direct

Front 125

what effect does dopamine have on the motor loop

Back 125

increases contrast btwn the indirect (inhibitory) and direct (excitatory) path

enhance movement bu increaing force/speed of movement.

info from sub niagra, degenerates in parkinsons

Front 126

what enhances movement bu increasing speed/force of movement

Back 126

dopamine adn influence in sub niagra

**missing in parkinsons

Front 127

what path activates agonist mm, and what inhibits antagonists

Back 127

role of basal nuclei is to do this via
direct
indirect

Front 128

what determines normal basal nuclei fx

Back 128

balance btwn the thalamic disinhibition by direct and SUBTHALAMIC disinhibition by the indirect

??????????

Front 129

the balance of thalamic disinhibition and subthalamic disinhibition does what

Back 129

determines normal BN fx

?????