Bg

Front 1

What is the main function of the basal ganglia?

Back 1

Initiating and terminating movement

Front 2

What is the main NT of the BG?

Back 2

GABA

Front 3

What is the main NT of the cerebellum?

Back 3

GABA

Front 4

What is the transition zone between the brainstem and the cortex?

Back 4

Basal Ganglia

Front 5

Where do the caudate and the putamen come together?

Back 5

Nucleus accumbens

Front 6

What phenomenon does the nucleus accumbens have to do with?

Back 6

Addiction

Front 7

What structures comprise the BG?

Back 7

1. Caudate
2. Putamen
3. Globis pallidus
4. STN
5. Substantia nigra

Front 8

What does the putamen receive input from? Where does it project?

Back 8

1. Motor and Somatosensory Cortex
2. M1, M2 and premotor areas

Front 9

What type of function is the putamen involved with in regards to the BG?

Back 9

Motor Function

Front 10

What does the caudate receive input from? Where does it project?

Back 10

1. Association cortex
2. Prefrontal cortex

Front 11

What type of function is the caudate involved with in regards to the BG?

Back 11

Cognitive function

Front 12

What are the three input nuclei of the BG?

Back 12

1. Caudate
2. Putamen
3. Nucleus accumbens

Front 13

Where do the glutaminergic inputs to the caudate come from?

Back 13

Association cortex

Front 14

Where do the glutaminergic inputs to the putamen come from?

Back 14

Primary motor and sensory corticies

Front 15

Where do the dopaminergic inputs to the striatum come from?

Back 15

SNpc

Front 16

What type of inputs(NT) are sent to the caudate, putamen and striatum?

Back 16

1. Gluatminergic
2. Gluatminergic
3. Dopaminergic

Front 17

What are the processing nuclei of the BG(4)?

Back 17

1. GPe
2. SNpc
3. Subthalamic nucleus
4. Ventral tegmental area

Front 18

What are the output nuclei of the BG(3)?

Back 18

1. GPi
2. SNpr
3. Ventral pallidum

Front 19

What do the GPi and SNpr output to(2)? What are the two paths they can take to get there?

Back 19

1. VA & VL
2. Ansa lenticularis (digs a tunnel underneath) & lenticular fasciculus (runs across)

Front 20

What part of the SN produces dopamine?

Back 20

Pars compacta

Front 21

What part of the SN is non-dopaminergic and what does it function like?

Back 21

1. Pars reticulata
2. GPi (Both output nuclei)

Front 22

The direct BG pathway has been paired with what?

Back 22

The direct pathway releases or enables behavior to occur by releasing the thalamus from tonic inhibition from the inner segment of the globus pallidus

Front 23

The indirect BG pathway has been paired with what?

Back 23

This circuit decreases the probability of unwanted behaviors being released and more generally inhibits the release of any behavior.

Front 24

How does the indirect pathway work?

Back 24

Corticostriatal input excites cells of the neostriatum. Activity of the striatal GABAergic neurons projecting to GPe increases. Activity in the tonically active GPe decreases, decreasing the amount of inhibition on the subthalamus. This increases the activity of the glutaminergic neurons of the subthalamus, resulting in excitation of both segments of the globus pallidus. This increase in activity increases the inhibitory outflow from GPi to the thalamus, suppressing thalamic output, decreasing behaviors.

Front 25

How does the direct pathway work?

Back 25

Corticostriatal input excites cells of the neostriatum. Activity of the GABAergic neurons projecting to the GPi increases. Activity in the tonically active GPi decreases, causing the disinhibition (inhibiting the inhibitor) of neurons in thalamic nuclei (specifically VA, VL, and CM). These thalamic nuclei then project back to specific areas of cortex, premotor areas 6 and 5. Such a scheme reinforces activity originating in cortex by running through a loop. In addition, it decreases the probability of other unwanted behaviors via lateral inhibition in the neostriatum. Topographical excitation of striatal elements inhibits neighbor elements via axon collaterals of the striatum making inhibitory contacts on its neighbors. Finally, direct projections from the neostriatum to the SNr disinhibit structures normally inhibited by the SNr (e.g., VA and VL of thalamus, the superior colliculus).

Front 26

Which pathway is totally GABAnergic?

Back 26

Direct pathway

Front 27

Which pathway involves glutaminergic neurons?

Back 27

Indirect pathway

Front 28

What are the three modulators of the striatum?

Back 28

1. Dopamine
2. Serotonin
3. Norepinephrine

Front 29

What determines whether your response is excitatory or inhibitory in the BG?

Back 29

The receptor, not the NT

Front 30

What dopamine receptors are inhibitory and excitatory in the striatum?

Back 30

1. D1 - excitatory
2. D2 - inhibitory

Front 31

What are continuous rapid movements associated with Huntington's disease?

Back 31

Chorea

Front 32

What is typically the cause of chorea?

Back 32

Problems associated with the caudate

Front 33

Are chorea movements hyperactive or hypoactive movements?

Back 33

Hyperactive

Front 34

What are twisting movements that are associated with chorea? Where is the problem when associated with chorea? Without chorea?

Back 34

1. Athetosis
2. Striatum with chorea
3. Globis pallidus without chorea

Front 35

What are flinging movements called? What is destroyed with this condition? What usually causes this?

Back 35

1. Ballismus
2. One side of the STN
3. PCA stroke

Front 36

What causes Parkinson's?

Back 36

Lesion of the SNpc or projection

Front 37

What causes Huntington's?

Back 37

Lesion of the striatal projections

Front 38

In hemiballismus, what is destroyed? What effect does this have on the thalamus?

Back 38

1. STN
2. Since the STN causes the GPi to inhibit the thalamus, the thalamus is now disinhibited.

Front 39

What happens in Parkinson's disease?

Back 39

The output of the GPi is too much causing too much inhibition of the thalamus.

Front 40

Is rigidity velocity dependent or velocity independent? What is it a malfunction of?

Back 40

1. Velocity independent
2. Basal ganglia

Front 41

Is spasticity velocity dependent or velocity independent? What is it a malfunction of?

Back 41

1. Velocity dependent
2. Upper motor neurons

Front 42

Describe the deep tendon reflex pathway.

Back 42

1. Stretch of the tendon causes a signal in the muscle spindle
2. Muscle spindle sends a signal to the spinal cord
3. After a monosynaptic exchange to an alpha neuron the muscle fires

Front 43

What happens with an upper motor neuron lesion in terms of relexes? Why?

Back 43

The reflexes are hyperactive because the gamma neuron is disinhibited causing the muscle spindle to set the muscle tone too taut.

Front 44

What is considered the rostral part of the sympathetic nervous system?

Back 44

Zona inserta

Front 45

The Fields of Forel have to go around what? What two fasciculi are they divided into? What do they become?

Back 45

1. Zona inserta
2. H1 - Thalamic & H2 - Lenticular
3. H

Front 46

What makes up the H Fasciculus?

Back 46

H1, H2 and ansa lenticularis

Front 47

People with dystonia need stimulation where? People with Parkinson's?

Back 47

1. GPi
2. Vim