Bsci 453 Exam 3

Front 1

overall organization of neural structures involved in the control of movement

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Back 1

Front 2

draw knee tap reflex

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Back 2

Front 3

where are lower motor neurons located?

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Back 3

Front 4

how was the organization of lower motor neurons determined?

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Back 4

Retrograde transport of tracer molecules from muscle back to motorneuron
Cell bodies shows that different groups of motorneurons innervate each muscle

Front 5

talk about what motor neurons innervate in regards to a single spinal column

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Back 5

Front 6

what is a motor unit?

what does it innervate

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Back 6

A “motor unit” is a single motorneuron and all of the muscle cells that it innervates

Front 7

how many motor neurons is a muscle innervated by?

Back 7

A muscle is generally innervated by several different “types” of motor neurons, each contacting muscle fibers (cells) with distrinct properties, creating different types of motorunits.

Front 8

compare the force and fatigability of three different motor units in regards to grams of force and time

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Back 8

begining is where motor neuron was stimulated

Front 9

recruitment of motor neurons in cat under different conditions

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Back 9

As the use to which the muscle is put changes, so different motor unit types
are recruited by the nervous system to drive contraction

Front 10

the effect of stimulation rate on muscle tension

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Back 10

a.p. frequency in the motor unit determines contraction strength.

Front 11

diagram of increase in voluntary force and number of motor neurons
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Back 11

Different motor units generate different ranges of force and so are active during
Different strengths of contraction

Front 12

So the nervous system controls muscle contraction by:

Back 12

1) recruiting the right types of motor unit for a task

2) varying the a.p. frequency within those motor units by controlling the rate of a.p’s in the motorneurons

Front 13

2 examples of control of motorneuron activity at the spinal cord level?...no picture

Back 13

spinal reflexes

e.g. the stretch reflex – serves to maintain
limb position despite varying loads.

e.g. holding a mug while it is being filled with beer

Front 14

draw stretch eflex circuitry

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Back 14

muscle spindles detect stretch of muscle...

A motor neuron comes from spinal cord and drives main conraction

Spindle afferent goes to spinal cord and activity increases with stretch

Gamma motor neuron regulates activity of spindle afferent

Front 15

draw the mug reflex response

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Back 15

Stretch activates spindle sensory
neurons

Spindle sensory neurons activate flexor
Muscle alpha motoneurons
(and inhibit extensor motorneurons)
Arm is raised! Beer is saved!!!!!

Front 16

stretch reflex circuitry negative feedback loop....mug example

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Back 16

Front 17

draw role of gamma motor neuron diagram

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Back 17

Gamma activity prevents spindle from becoming floppy and
“silent” during voluntary contraction – maintains usefulnesss of reflex
even during contraction

Front 18

what do spinal reflexes allow?

Back 18

So spinal reflexes are feedback circuits that allow muscles to respond rapidly
to changing loads.

Front 19

what is another role for local spinal circuits?

ex?

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Back 19

Another role for local spinal circuits is in rythmic generating patterns of activity – like those created during walking
- spinally-transected cats show ryhtmic firing of motor neurons while“walking” on a motor-driven treadmill

each limb has its own central pattern generator responsible for alternating flexion and extension

transection of spinal cord proves following...

Rythmic, alternating, muscle contractions
Are still recorded despite the transection
Of the spinal cord
- Rhythm must be locally generated

see 6b of 11/18 for picture

Front 20

example of central pattern generators?

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Back 20

lobster is the picture

cat walking


the pattern is retained without future input.

Front 21

basal ganglia

Back 21

The basal ganglia (or basal nuclei) are a group of nuclei in the brain interconnected with the cerebral cortex, thalamus and brainstem. Mammalian basal ganglia are associated with a variety of functions: motor control, cognition, emotions, and learning. In modern use the term 'ganglia' is in this instance considered a misnomer; 'ganglion' refers to concentrations of neural nuclei in the periphery only (for example those of the autonomic nervous system), and the term 'basal nuclei' is preferred.

Front 22

how does the brain control the action of muscles?

Back 22

1) pathways from brainstem (upper motor neurons) to the spinal cord...lower motorneurons

2)Pathways from cortical (also called upper) motorneurons to the spinal (lower) motorneurons
...direct and indirect

3)modulated by basa ganglia

4)modulated by cerebellum

Front 23

draw 4 descending projections from the brainstem to the spinal cord

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Back 23

11/25

1c and 1d

Front 24

draw direct cortical projection pway

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Back 24

Note:
Neurons in left cerebral
Hemisphere drive
Spinal motorneurons on the
Right hand
Side of the body

Motor cortex driving right
Hand side of body is
Just in front of sensory cortex receiving
Info from right
Hand side of body

11/25 2b

more lateral when linking w/ spinal cord in comparison to indirect pway

Front 25

indirect cortical projection

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Back 25

more medial when linking to spinal cord

Front 26

lateral and medial view of primary motor cortex.

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Back 26

Front 27

topographic map of they body musculature in the primary motor cortex

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Back 27

much more coarse in comparison o somatosensory tract

Front 28

diagram showing the influence of a single cortical upper motor neurons on muscle activity

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Back 28

11/25

3c and d

Front 29

when are cortical neurons active?

Back 29

just before movement begins

Front 30

two major structures that modulates cortical motorneurons activity

Back 30

basal ganglia

cerebellum

Front 31

motor components of the human basal ganglia

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Back 31

from caudate to nigra reticulata is basal ganglia cells.

basal ganglia is a group of cells.

Front 32

draw feedback loop of human basal ganglia

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Back 32

The basal ganglia seem to be
Involved in a feedback circuit that
Controls cortical motorneuron activity

loop from thalamus is feedback loop

MN: C N call pat while he's on a sub globing N with a thalamus that's cool

Front 33

basal ganglia and one thing it is involved in

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Back 33

saccadic eye movement is fast eye movement that searches for stuff

substantia nigra pars reticulata is active when fixating a target

1)GABAergic neurons activate caudate

2)this decreases retiulate output.

Front 34

the the apikes of the 2 cells responsible for saccadic eye movements and describe

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Back 34

brown is superior colliculus and this occurs during saccadic eye movement

light blue is substantia nigra which is normally spontaneously active and allows one to fixate on a target.

Front 35

components of the brainstem and diencephalon related to the cerebellum

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Back 35

Front 36

diagram of functional organizatin of inputs to the cerebellum

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Back 36

Front 37

neuronal pway of functional organization of inputs to the cerebellum

Back 37

Front 38

summary diagram of motor modulation by the cerebellum

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Back 38

Front 39

talk about vestibulo-ocular reflex in monkeys and show experiment

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Back 39

Resetting is not
learnt after
cerebellar damage
Eyes still do
Not follow target

1)eyes follow target
2)eyes do not follow target
3)eyes follow target


reflex operates to move the eyes as the head moves so that image remains stable

minifying spectacles cause eyes to move too far. The brain accounts for this in time and it causes eyes to move less.......in cerebellar damage there will not be this learnt response.

Front 40

habituation

Back 40

decrease in response to repeated stimulus presentation

Front 41

sensitization

Back 41

generalization of an aversive stimulus to non-aversive stimuli

aversive: unpleasent stimuli

Front 42

picture of Aplysia californica

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Back 42

Front 43

draw cells of aplysia californica

Back 43

Front 44

draw 2 sets of graphs that show habituation and sensitization in Aplysia gill

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Back 44

12/02 1d, 2a

Front 45

synaptic mechanisms underlying short-term sensitization in aplysia californica

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Back 45

this type is heterosynaptic facilitation

Front 46

show motor neuron epsp after activating siphen sensory neurons at 0min 20 min and 50min and then stimulating tail nerve at 51 min

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Back 46

3 first 3 parts are when the siphen sensory neurons are activated

Front 47

presynaptic depression

Back 47

-Depletion of the presynaptic NT vesicles

-Inactivation of N-type Ca2+ channels

Front 48

mechanism for presynaptic enhancement underlying behavioral sensitization for short term.

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Back 48

PKA enhances glutamate release

short term changes occur because of post-translational mmodifications

Front 49

rule for short-term changes in synaptic strength

Back 49

Short-term changes in synaptic strength are mediated by post-translational modifications

Front 50

Mechanism of presynaptic enhancement underlying behavioral sensitization long term

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Back 50

caused by changes in gene expression...aka mediated by protein synthesis.

Front 51

long-term change synaptic strenght rule

Back 51

Long-term changes in synaptic strength are mediated by protein synthesis (translation +/- transcription)

Front 52

what were lessons learned from a slug

Back 52

-short-term changes in synaptic strength are mediated by posttranslational modifications

-long-term changes in synaptic strength are mediatedby protein synthesis (translation +/- transcription)

-”memory molecules/cognitive kinases”

Front 53

genetics of learning and memory in the fruit fly.....2 things

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Back 53

Classical conditioning in
Drosophila: pairing an aversive
stimulus (shock or bright light)
with an odor results in
avoidance of that odor

graph shows that mutant flies were bad at learning

MUTANTS ARE DEFICIENCIENT IN PKA SIGNALING........

Gene mutated in rutabaga is adenylyl cyclase

Gene mutated in DUNCE is a phosphodiesterase (PDE) degrades cAMP

BIDIRECTIONAL DISRUPTION = UNCOUPLING PKA
ACTIVATION FROM EXPERIENCE

Front 54

mechanisms of synaptic plasticity.....4

Back 54

HETEROSYNAPTIC = ACTIVITY AT ONE SYNAPSE REGULATES THE STRENGTH AT ANOTHER (DIFFERENT) SYNAPSE

HOMOSYNAPTIC = ACTIVITY OF A SYNAPSE REGULATES THE STRENGTH OF THAT
(SAME) SYNAPSE

-Presynaptic (change in the amount of NT released)

-Postsynaptic (change in the response to the NT released)

Front 55

draw membrane potential diagram of homosynaptic short-term plasticity......

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Back 55

1)increase in curve: facilitation

2)decrease in curve: depression

3) no change: rest

4) 30 seconds later: post-tetanic potentiation


shows that communication outlasts tetanus.

Front 56

potentiation

Back 56

improvement in communication between 2 neurons

Front 57

PRESYNAPTIC SHORT-TERM FACILITATION

Back 57

STIMULATION FREQUENCY > CA2+ BUFFERING CAPACITY

= SUMMATION OF PRESYNAPTIC CALCIUM

= INCREASE IN P

Front 58

PRESYNAPTIC SHORT-TERM DEPRESSION

Back 58

STIMULATION FREQUENCY > VESICLE RECYCLING

= DEPLETION OF NEUROTRANSMITTER VESICLES

= DECREASE IN P

Front 59

POST-TETANIC POTENTIATION

Back 59

HIGH FREQUENCY STIMULATION PHOSPHORYLATES SYNAPSIN

= RELEASE OF SYNAPTIC VESICLES FROM RESERVE POOL

= INCREASE IN SYNAPTIC VESICLES IN ACTIVE POOL

= INCREASE IN P

Front 60

reserve pool diagram

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Back 60

Front 61

homosynaptic short-term plasticity location

Back 61

presynaptic locus

Front 62

homosynaptic long-term plasticity location

Back 62

postsynaptic locus

Front 63

mammalian hippocampus purpose

Back 63

encodes spatial information

consolidates short-term into long-term memories

Front 64

learning

Back 64

change in behavior over repeated trials

Front 65

memory

Back 65

retention of something learned (time)

Front 66

experiment in mice that showed need for hippocampus

Back 66

morris water maze experiment.

-mice were placed in a kiddy pool with mercy water so that they could not see platform

-the room had visual cues so that they new their location

-after 10 trials, mice were able to find the platform with ease so that they could rest

-results showed need for hippocampus because in hippocampus lesioned samples, they showed no improvement in finding the platform.

12/02 8d if needed.

Front 67

draw rodent hippocampus

Back 67

Front 68

experiment that showed long-term potentiation of schaffer collateral-CA1 synapse

Back 68

12/04 lecture see 1b,c,d as well

path 1 had a high frequency stimulus....path 2 did not

.....tetanus is what occured in response to their own stimuli strength

Front 69

how is LTP caused?

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Back 69

by pairing presynaptic and postsynaptic activity

a single stimuli does not increase synaptic strength....this only occurs when the CA1 is depolarized by applying current pulses through the recording electrode

also see12/04 2b

Front 70

talk about NMDA receptor and LTP

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Back 70

the nmda receptor channel can open only during depolarization of the postsynapic neuron from its normal resting level.

depolarization expels mg2 from the nmda channel allowing current to flow into the postsynaptic cell.

this leads to ca2+ entry, which in turn triggers LTP

Front 71

draw signaling mechanism underlying LTP of NMDA channel

Back 71

during glutamate release, the NMDA channel opens only if the postsynaptic cell is sufficiently depolarized. CA2+ enters the cell throug the channel and activates postsynaptic protein kinases.

These postsynaptic kinases trigger a series of reactions that leads to insertion of new AMPA receptors into the postsynaptic spine, thereby increasing the cell's sensitivity to glutamate.

Front 72

requirement for LTP

Back 72

presnaptic activity

postsynaptic depolarization

Front 73

Why is LTP a good model for memory formation?

Back 73

-Activity-dependent

-Shows specificity and associativity

-many manipulations that degrade memory degrade LTP

Front 74

specificity vs. associativity

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Back 74

in B, pathway 2 does not have LTP unless

Front 75

draw the current that would be seen before and after LTP that caused AMPA channels to be inserted

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Back 75

Front 76

what would appear if you fluoresced a cell and looked at it after LTP?

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Back 76

spines would be present...this is what the arrows are

Front 77

experiment that shows role of protein synthesis for maintaining LTP

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Back 77

repetitive high frequency stimulation ...arrows...induces LTP that persists for many hours in A...

In B, Treatment with anisomycin, an inhibitr of protein synthesis, causes LTP to decay within a few hours after the hih-frequency stimulation

Front 78

short-term vs. long-term NMDA LTP diagram with both in one

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Back 78

Front 79

Long-term synaptic depression in the hypocampus

Back 79

a low-amplitude rise in calcium concentration in the postsynaptic CA1 neuron activates postsynaptic protein phosphatases, which cause internalization of postsynaptic AMPA receptors, thereby decreasing the sensitivity to glutamate released from the Schaffer collateral terminals.

Front 80

association cortices

Back 80

Underlie cognition “To know the world”

To attend to, identify/recognize , and plan for interaction w/external stimuli or internal motivation.

Front 81

lateral and medial views of the human brain showing extent of the association cortices

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Back 81

blue is assoiation cortices which is much bigger area in omparison to primary sensory and motor areas

Front 82

canonical neocortical circuitry diagram

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Back 82

thalamus, other cortical areas, and brainstem modulatory systems on the right side of picture are inputs

each circuitry has inputs and outputs

Front 83

methods of non-invasive imaging

Back 83

CT: serial X-rays; better for hard than soft tissue

PET: positron emission; accumulation of radioactive metabolites

fMRI: magnetic resonance; functional anatomy

EEG: electrical activity; physiological response

Front 84

experimental strategies to localize a function (3)

Back 84

-lesion studies

-non-invasive imaging in humans

-stimulate/record from experimental animals

Front 85

damage to parietal cortex can cause what?

Back 85

deficits of attention

cause inattention or neglect of something

right lesion, affects left side

Front 86

3 tasks that prove someone has a lesion in parietal cortex and name?

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Back 86

contralateral neglect syndrome

also the picture with the lines where the patient has to cross out all lines, but only crosses out the right sides

remember, a left side lesion of parietal cortex will affect the right side of view.

Front 87

what is more important for attention, the right or left parietal hemisphere?

Back 87

a right parietal lesion results in severe left neglect, whereas a left parietal lesion leads to only minimal right neglect due to preserved attention within the right hemisphere.

Front 88

draw PET scan revealing metabolic activity of parietal cortex on both sides during activation

Back 88

shows that right parietal lobe is much more highly active....

Front 89

neuroanatomy of attention....draw the different types of lesions

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Back 89

12/9 2d 3a

Front 90

different lobes of brain and where a recording via electrode would test for attention

Back 90

would find it in the parietal lobe

Front 91

procedure that showed response to stimuli is mediated in parietal lobe in monkeys

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Back 91

12/9

3d, 4a

Monkey had recording electrode surgicall placed in head.

A stimuli was placed on the screen: pair of simultaneously illuminated targets

When animal paid more attention to stimuli, it was given more juice

The more juice a particular monkey received, the more they would focus on the screen, and the more their parietal cortex would be active.

Front 92

two words to explain what temporal cortex does?

Back 92

identification/ recognition

Front 93

Agnosia

Back 93

not knowing

----different from the case where one can't draw the left side of the house: these patients do not know that the left sides exists.

Agnosia patients can see the image, but are unsure of its place in the world

object generally

Front 94

prosopagnosia

Back 94

face blindness; can see faces and can have perfect vision , but are unable to recognize faces from one another

.....faces are described as blurred often times

.....often times can look out of the corner of their eyes to recognize faces

Front 95

what would be shown of the brain during an fMRI during a face recognition exercise

Back 95

increased activity in the right temporal lobe

Front 96

monkey face experiment

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Back 96

12/9 5c,d

electrode was place in the inferior temporal cortex for recording

1) in one set the monkey had the highest response in frontal views of the face

2) in another set, it responded best to profiles

Front 97

180 of face picture

Back 97

shows columnar organization of object representations in the inferotemporal cortex...each column(going down) has a certain point of view that it works best at.

Front 98

inferior temporal cortex location

Back 98

Front 99

dorsolateral prefrontal cortex
picture

purpose

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Back 99

planning

Front 100

experiment showing activity in the prefrontal cortex

Back 100

when experiment is performed with no food as a reward, there is less activity in the prefrontal cortex

12/9 6d if you want to see a.p

Front 101

explain a neuropsychological testing test

Back 101

wisconsin card sorting

1)4 cards are already sorted
2) after 10 correct trials, examiner will say wrong and the patient must sort in some other method

...individuals with frontal lobe lesions have trouble with this because of deficits in planning.

Front 102

brain size and intelligence

Back 102

-smarter animals tend to have larger brains overall and in comparison to their total body size

-this study done among humans is very controversal because of racial issues

...hard to determine what exactly constitutes smarts between humans.

Front 103

synaptic plasticity

Back 103

potential for synaptic function (strenght) to be regulated by experience (activity)

Front 104

experiment that showed that pathway of a particle from the eye

Back 104

-used radioactive amino acid labeling

1)tissue fixed
2)sectioned
3)placed on glass slides
4)coated with photographic emulsion
5)radioactive decay will show up as silver grains to form in the emulsion

Experiment showed where the pathway actually goes....

From eye to lateral geniculate nucleus to layer 4 in primary visual cortex.

Front 105

experiment that shows deprivation in a kittens eye versus in an adult cat eye

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2 important points

Back 105

1 is only right eye......7 is only left eye.....in between is a combinatino of both

results showed that if a kittens eye was sutured, it would not get better once removed....


In an adult it would get better if removed.

see 12/11 page 2 if needed.

key points...
1) the juvenile cortex is more plastic than adults

2)vision is required for normal development of visual system.

Front 106

3 vs 6 days in deprivation in the kittens eye

Back 106

Front 107

what did hubel and weisel receive a nobel prize for

Back 107

1) function of cortex regulated by experience

2) plasticity highest during postnatal critical period

-no changes in response properties of RGC's

No changes in the response properties of the thalamus

Front 108

enriched environment vs standard environment (7)

Back 108

“Enriched environment” paradigm results in::::

Enhanced cortical thickness!!

Enhanced brain weight!!

CREB-mediate gene expression expression

Enhanced dendritic branching

Enhanced oligodendrocyte to neuron ratio

Enhanced number of synapses per neuron



essentially standard environment leads to impoverished conditions

enriched environment leads to stimulating conditions....

Front 109

talk about london taxi driver case

Back 109

results showed that taxi cab drivers had a larger posterior hippocampal section than that of non-taxi cab drivers.

...this is because this area is used to remember spatial information

....likewise when comparing taxi cab drivers among each other, drivers who had been on the job longer had larger posterior hippocampal sections.

see 12/11 5a if needed

Front 110

draw memory flow diagram

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Back 110

Front 111

areas that, when damaged, tend to give rise to declarative memory disorders

Back 111

hippocampus is most important

called amnesia

Front 112

talk about the case of H.M. and what occured and what was removed

Back 112

-performed surgery in which the amygdala, uncus, hippocampal gyrus, and anterior two-thirds of the hippocampus were removed.

-he performed well at everything, but he was unable to form declarative memories.

Front 113

conncections between the hippocmpus and possible declarative memory storage sites

Back 113

memory is not stored in the hippocampus, but instead only integrated

Front 114

dementia

Back 114

Dementia (from Latin de- "apart, away" + mens (genitive mentis) "mind") is the progressive decline in cognitive function due to damage or disease in the body beyond what might be expected from normal aging.

Front 115

Talk about Alzeimer's disease

Back 115

Alzheimer’s disease: most common form of progressive dementia

10% of people over 65; 45% of people over 85

Only 1% (early onset) AD has clear genetic basis
(presenilin 1 and 2, apolipoprotein E)

Early signs: retrograde amnesia, progress to anterograde amnesia

** personality changes

Late signs: Language skills, problem solving, judgement

Definitive diagnosis is only post-mortem

Front 116

amnesia

Back 116

Amnesia (from Greek Ἀμνησία) is a condition in which memory is disturbed. In simple terms it is the loss of memory. The causes of amnesia are organic or functional

Front 117

plaques are...

tangles are...

Back 117

extracellular

intracellular

Front 118

talk about histological hallmarks of AD

Back 118

In 1907, in the first report, Alois Alzheimer described senile plaques (SP) and neurofibrillary tangles (NFT)
SP are found in neocortex, hippocampus and in several subcortical areas
NFT density correlates with disease duration and severity of dementia.

Front 119

draw difference between neurofibrillary tangle and plaques

Back 119

Front 120

draw the signaling pathways and processing of things in AD patients

Back 120

12/11

7b,7c,6c

6c.....
Molecular and cellular processes presumed to participate in AD pathogenesis. Aｧ peptides produced by neurons and other brain cells aggregate into a variety of assemblies, some of which impair synapses and neuronal dendrites, either directly or through the engagement of glial loops. Build-up of pathogenic Aｧ assemblies could result from increased production or aggregation or from deficient clearance mechanisms. ApoE4 and tau promote Aｧ-induced neuronal injury and also have independent adverse effects. Microglia could be beneficial or harmful, depending on which of their signaling cascades and functions are engaged. This multifactorial scenario leads to progressive disintegration of neural circuits, isolation and loss of neurons, network failure, and neurological decline.

7b......
Drug targets involved in Aｧ production and assembly. Aｧ production depends on sequential proteolytic cleavage of APP by ｧ-secretase (marked 1), also known as ｧ-site APP-cleaving enzyme 1 (BACE1), and the multiprotein -secretase complex (2) (88). -Secretase targets include the enzyme's active site, substrate docking site, and ATP-binding site (2a to 2c) and its predilection for -versus -cleavage (2d) or for generating Aｧ42 versus Aｧ40 (2e). The pathogenicity of released Aｧ peptides depends on self-assembly (3). APP cleavage by -secretases (ADAM family metalloproteases) prevents Aｧ production (4). Caspase cleavage of the APP intracellular domain (AICD) generates a C31 fragment (5) that may participate in Aｧ-induced toxicity or act independently.

7c..........
Plaques and tangles in Alzheimer's disease. Amyloid plaques contain the A peptide, which is produced from the amyloid precursor protein (APP). Cleavage of APP at one point (not shown) generates a carboxy-terminal fragment. This is then severed by the ypsilon-secretase complex (which consists of at least four proteins10 — presenilin-1, APH-1, PEN-2 and nicastrin), producing A-beta. Tangles are produced from hyperphosphorylated tau protein, possibly by means of the enzyme glycogen synthase kinase-3 (GSK-3). GSK-3 also regulates phosphorylation of beta-catenin (which can bind presenilin-1). Phiel et al.1 find that GSK-3 might also regulate — either directly or indirectly — the cleavage of APP carboxy-terminal fragments. They show that lithium and kenpaullone (two GSK-3 inhibitors), as well as small interfering RNAs that prevent GSK-3 expression, inhibit A-beta production. So, GSK-3 inhibitors might interfere with the generation of both amyloid plaques and tangles in Alzheimer's disease The precise roles of the two forms of GSK-3, alpha and beta, are unknown.

Front 121

do transgenic mice that mimic changes seen in AD patients have similar cognitive deficits?

Back 121

no

Front 122

vulnerable neurons in AD (6)

Back 122

HAM BEN

Basal forebrain cholinergic system (nucleus basalis)

Monoaminergic system

Hippocampus (CA1 and CA2 pyramidal cells)

Amygdala

Entorhinal cortex

Neocortex

Front 123

drugs approved for treatment of AD

Back 123

Don Galluped the River to get the Tac in his Memory......AD

Mild to moderate AD: cholinesterase inhibitors

Donepezil
Galantamine
Rivastigmine
Tacrine

Moderate to severe AD: NMDA receptor antagonist

Memantine

-acetylcholinesterase (AChE) inhibitors
(donepezil (Aricept), rivastigmine (Exelon) and Reminyl (Razadyne)
All prevent the breakdown of acetylcholine, to keep ACh levels high
despite the loss of Ach producing cells
-non-competitive low affinity N-methyl-D-aspartate (NMDA) receptor antagonist
Memantine (Namenda)
Memantine protect cells against excess glutamate (and toxicity)
by partially blocking NMDA receptors.