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Flashcards in Basal Ganglia Deck (55):

What are the major functions of the basal ganglia?

1. Planning and initiation of complex movements
2. Modulation of motor activity
3. Cessation of volitional movement


What are the five major components of the basal ganglion and what part of the brain circulation to they get supplied blood by?

1. Caudate- ant.
2. Putamen- Ant.
3. Globus pallidus (lateral/external and medial/internal)- ant.
4. Substantia nigra (pars compacta/pars reticulata)- posterior
5. Subthalamic nucleus- posterior


What structures make up the neostriatum?

Caudate and putamen


What two subdivisions of the basal ganglia serve similar function?

Pars reticularis and internal/medial globus pallidus do essentially the same thing


Generally, is input to the basal ganglia excitatory or inhibitory? Where does the input come from?

What is the output of the basal ganglia and is it excitatory or inhibitory?

The basal ganglia receives:
1. Excitatory signal from the cerebral cortex
2. Excitatory input from the thalamus

Output goes to:
1. Inhibitory to the thalamus


Where does the thalamus send signals after they are received from the basal ganglia?

The thalamus sends excitatory signals to the cerebral cortex and basal ganglia


What is the major receptive area of the basal ganglia?
What three major areas does it receive input from?
What receives mostly motor stimulation?
What receives mostly non-motor?

Neostriatum (caudate and putamen) which receive signal from most areas of the cerebral cortex as well as from the pars compacta, and centromedian nucleus of the thalamus.

Motor- putamen
Non-motor is mostly received by the caudate


What is the nucleus accumbens?

It is located in the ventral area of the neostriatum and receives cortical and subcortical limbic input to regulate reward behavior


What neurotransmitter is the cortical input to the basal ganglia?



What two parts of the basal ganglia project to areas outside of that basal ganglia?
What neurotransmitter do they send and is it excitatory or inhibitory?

Pars reticularis (substantia nigra)
Internal/medial globus pallidus

They send GABA and it is inhibitory to VA/VL of the thalamus


How do the signals get from the pars reticularis/medial globus pallidus to the thalamus?

The ansa lenticularis and lenticula fasciculus converge to make the thalamic fasciculus which synapses on the VA/VL of the thalamus


Which neurons of the basal ganglia produce GABA?

Pars reticularis
Medial globus pallidus


What is the only excitatory neuron in the basal ganglia and what transmitter does it send?

Subthalamic nucleus makes glutamate which is excitatory


Which components of the basal ganglia secrete dopamine and is it excitatory or inhibitory?

Pars compacta of the substantia nigra and it can be inhibitory or excitatory depending on the receptor in the neostriatum with which it acts.


What is the major receptive area of the basal ganglia?

The neostriatum (caudate and putamen)


What nuclei are the source of projections leaving the basal ganglia?

Pars reticularis and medial globus pallidus


What is the major target of signal leaving the basal ganglia?

VA/VL nucleus of the thalamus for motor activity
Dorsomedial nucleus of the thalamus for non-motor activity (limbic)


What are the two main populations of neurons in the neostriatum?

1. Medium spiny
2. Large aspiny


What projections are received by the medium spiny neurons on the neostriatum?

1. Excitatory glutaminergic from the corticostriate pathway
2. Excitatory glutaminergic from the thalamostriate pathway
3. Excitatory/inhibitory dopamine from the pars compacta (nigrastriatal)


Where do medium spiny neurons send their projections?

Both segments of the globus pallidus receive GABA inhibition from the neostriatum


Dopamine from the pars compacta excites what neuron? What neuron does it inhibit? Where are these neurons located?

Excite D1 neurons in the putamen
Inhibit D2 neurons in the putamen


What are the only cortical areas that do NOT seem to have significant projections to the neostriatum?

Primary visual cortex
Auditory cortex


D1 and D2 neurons from the putamen send what types of signals? Where do the signals go?

D1 sends GABA inhibition to the medial globus pallidus and D2 sends GABAinhibition to the lateral globus pallidus


How does the globus pallidus derive its color?

Myelinated fibers from the neostriatum that transverse it


Where do projections from the medial globus pallidus travel?
Where do projections from the lateral globus pallidus travel?

Medial- to VA/VL of the thalamus
Lateral- to the subthalamic nucleus


What is the neurotransmitter output from both segments of the globus pallidus?

Medial- GABA inhibition to thalamus
Lateral- GABA inhibition to the subthalamic nucleus


What is the major afferent to the lateral globus pallidus?
What is the major efferent from the lateral globus pallidus?

D2 neurons from the neostriatum send GABA inhibition to lateral globus pallidus

Lateral Globus pallidus sends GABA inhibition to the subthalamic nucleus


What signal is received by the medial globus pallidus?
What signal does it send?

It receives GABA inhibition from the D1 neurons of the neostriatum
It receives glutamate excitation from the subthalamic nucleus
It projects GABA inhibition to the va/VL nucleus of the thalamus


Behind what midbrain structure is the substantia nigra located?

Behind the cerebral peduncle


What neurotransmitter is released from the pars compacta?
What gives the pars compacta it's color?
Where does the pars compacta receive signal from?
What does it send signal to?

The accumulation of neuromelanin (byproduct of dopamine synthesis)
Receives projections from the neostriatum
Sends excitatory dopamine to D1 neurons in the neostriatum and inhibitory dopamine to D2 neurons in the neostriatum


What neurotransmitter is used by the pars reticularis?

GABA inhibitory
Afferents- D1 from the neostriatum and glutamate from subthalamic
Efferents- VA/VL of thalamus


Where does the subthalamic nucleus receive afferents from?
What are its efferents?

Afferents from the lateral globus pallidus (GABA inhibitory)
Efferents to the medial globus pallidus (glutamate excitatory)


What is disinhibition?
What system influences the motor cortex using disinhibition?

Disinhibition is the removal of an inhibitory signal.
In the classic loop, an intermittent inhibitory signal acts on a tonically active inhibitory neuron which synapses on an excitatory neuron
The basal ganglia regulates the motor cortex via disinhibition


What kind of output goes from the thalamus to the upper motor neurons in the motor cortex?
How is this regulated?

Excitatory input.
This is regulated because the thalamus receive tonic inhibition from the median globus pallidus.


What parts of the basal ganglia are in the direct motor pathway?
What does the direct motor pathway do to the thalamus?

The cerebral cortex excites neurons in the neostriatum. The neostriatum sends inhibitory signals to the median globus pallidus.
The median globus pallidus tonic inhibitory signal is shut off.
The thalamus is able to fire excitatory signals to the motor cortex.

The direct pathway disinhibits the thalamus allowing it to excite the motor cortex.


Describe the steps in the indirect motor pathway in the basal ganglia.

Inhibitory signals from the neostriatum are sent to the external (lateral) globus pallidus --> less inhibition is sent to the subthalamic nucleus--> more excitation is sent to the median globus pallidus--> more inhibition is sent from the median globus pallidus to the thalamus--> the thalamus sends less excitation to the motor cortex --> less motion


Which basal ganglia motor pathway increases thalamic output to the motor cortex?

The direct pathway


What signals influence the non-motor activities of the basal ganglia ?

Prefrontal cortex
Orbital frontal cortex


What are the non-motor basal ganglia loops?

Prefrontal loop and limbic loop


To what thalamic nucleus do the non-motor paths of the basal ganglia project?
Where does this thalamic nucleus project?

Dorsomedial nucleus which projects to cortical areas controlling behavior cognition, memory and emotion.


What are the main brainstem areas involved with the basal ganglia non-motor influence?

Ventral tegmentum area-dopamine rich medial to the pars compacta

Ventral striatum- neocortex area where the nucleus accumbens is located


What are the characteristics of a hyperkinetic disturbance?

Abnormal involuntary movements


What is the defining characteristic of a hypokinetic disorder?

Reduction of normal motor activity


What movements are associated with hemiballism?
A lesion to what area would cause hemiballism?
Why would such a lesion cause this?

- random involuntary unilateral flinging of limbs
-lesions to the contralateral subthalamic nucleus

-there is less excitation of the median globus pallidus by the subthalamic nucleus--> less tonic inhibition of the thalamus--> increased motor cortex stimulation--> increased movement


If we ablate the subthalamic nucleus, what motor pathway are we ruining?
Which pathway is "winning"? What effect does this have?

We would knock out the indirect pathway (which usually stops movement)
The direct pathway will "win" and the neostriatum will inhibit the median globus pallidus and that will decrease thalamic inhibition which will increase signal to the motor cortex


Why does a subthalamic nucleus injury affect movement on the opposite side of the body?

It disinhibits the ipsilateral thalamus which excites the ipsilateral motor cortex to the lesion. But when the motor neurons are descending through the corticospinal tract, they decussate in the medulla and innervate the opposite side of the body.


What is the major hypokinetic disorder associated with basal ganglia disfunction?
What causes this disorder?
What are the 5 major symptoms?

Parkinson's disease which is caused by a reduced level of dopamine in the pars compacta.
1. Bradykinesia- slow movements
2. Shuffling gait
3. Stooped posture
4. Resting tremor
5. rigidity


Parkinson's disease decreases input to what neurons in the basal ganglia?

Less input to D1 and D2 neurons in the neostriatum.

It usually excites D1 to increase inhibition of the median globus pallidus and increases movement. Because it is not getting excited in Parkinson's--> less movement
It usually inhibits D2 neurons which inhibit lateral globus pallidus


What is the overall effect on the direct and indirect circuits when you remove dopamine?

You will decrease the activity of the direct circuit and increase the activity of the indirect circuit (both reducing movement)


How does Parkinson's decrease the effect of the direct circuit?

There is less excitation of D1 neurons in the neostriatum.
Less inhibition is sent to the medial globus pallidus.
More inhibition is sent from the globus pallidus to the thalamus.
Less excitation is sent from the thalamus to the motor cortex.


How does Parkinson's disease increase the activity of the indirect basal ganglia motor circuit?

There is less inhibition on D2 neurons in the neostriatum.
More inhibition is sent to the lateral globus pallidus.
Less inhibition is sent to the subthalamic nucleus.
More excitation is sent to the medial globus pallidus.
More inhibition is sent to the thalamus.
Less excitation of the motor cortex.


Is huntingtons disease hyperkinetic or hypo kinetic?
How is it different from Parkinson's?
How does it differ from hemiballism?

Parkinson's is hypokinetic.
It is different from hemiballism because it is bilateral


What causes huntingtons disease?

What are the physical abnormalities associated with it?

Autosomal dominant genetic disorder where there is an abnormal expansion of CAG repeats on chromosome 4
1. Rigidity
2. Abnormal involuntary movements
3. Behavioral abnormality, dementia


What is the major structural change in the basal ganglia that results from huntingtons disease?

Loss of neurons in the caudate (behavioral, dementia) and putamen (movement) which atrophies the neostriatum


Which medium spiny neurons are more affected in huntingtons?
Why does this fit the symptoms?

The ones that project to the lateral globus pallidus (D2)
This reduces the indirect circuit and there is more direct circuit influence (increased movement).
Less influence of D2 on lateral globus pallidus leads to increaSed inhibition of the subthalamic nucleus, less excitation of th medial globus pallidus so there is less inhibition of the thalamus and increased movement