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B&B Week 2 Flashcards > Lecture 19: Basal Ganglia: Anatomy and Pharmacology > Flashcards

Lecture 19: Basal Ganglia: Anatomy and Pharmacology Flashcards

1
Q

Definition of basal ganglia

A

collection of subcortical nuclei (gray matter) deep within the brain

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2
Q

What does the basal ganglia do?

A 
It modulates
	-movement
	-cognition
	-behavior (emotional changes)
Still an area of active research
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3
Q

What are the anatomical components of the basal ganglia?

A

i. striatum (caudate and putamen)
ii. The pallidum (globus pallidus interna(medial) and externa (lateral))
iii. . Substantia nigra = pars compact and reticularis
iv. Subthalamic nucleus

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4
Q

Striatum

A

name gotten from the striation of fibers that separate the caudate and the putamen

i. caudate and 
ii. putamen
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5
Q

How are the anatomical components of basal ganglia organized?

A

From superior/anterior to inferior/posterior
Caudate
Putamen
Pallidum
Subthalamic nucleus
Substantia nigra (black colored in real life)
You really only see the subthalamic nucleus and the substantia nigra via coronal section

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6
Q

Where is the basal ganglia located?

A

Lateral to the thalamus

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7
Q

The pallidum

A

globus pallidus interna (medial) and externa (lateral

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8
Q

Substantia nigra

A

i. pars compacta: dopaminergic
ii. pars reticularis: GABAnergic
Easy to identify because it is black in gross section

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9
Q

Subthalamic nucleus:

A

helps modulate the interaction between the globus pallidus externa and interna
-lies ventromedial to the pallidum and above the substantia nigra
When activated, it inhibits GPi/SNr

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10
Q

How is basal ganglia organized in functionally?

A

a. input nuclei: caudate and putamen
b. output nuclei: Substantia nigra pars reticularis (SNr), Globus pallidus interna (GPi)
c. intrinsic nuclei: globus pallidus externa, substantia nigra pars compacta (SNc), Subthalamic nucleus (STN)

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11
Q

What sends input into the basal ganglia, specifically to caudate/putamen?

A
  • M1
  • Premotor cortex
  • Supplementary motor areas
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12
Q

What sends output out of the basal ganglia?

A

Globus Pallidus interna and Substantia Nigra Pars Reticularis
Sends axons to VA and VL of thalamus, which eventually gets to the cortex

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13
Q

Lenticular nucleus

A

putamen and globus pallidus

-components of basal ganglia form numerous functional circuits or loops

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14
Q

Attenuation

A

reduce the force, effect, or value of

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15
Q

What is the Direct pathway? What nuclei are involved?

A

a. Initiates movement
b. Helps you learn of POSTIVIE outcomes associated with specific behaviors
- carried out by neurons in Globus Pallidus interna and Substantia Nigra Pars Reticularis (SNr)
- GPi/SNr normally inhibit neurons in the thalamus
- when cortex sends signal to striatum, striatum INHIBITS GPi/SNr, thereby DISinhibiting the neurons in thalamus
- the thalamus neurons then sends excitatory signal to cortex and increases cortical activity
- excitation of striatum leads to excitation of motor, premotor and supplementary motor areas
- SNc also participates by facilitating activation of striatum once striatum is activated by cortex

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16
Q

How does excitation of striatum lead to excitation of M1, premotor and supplementary areas? And does excitation of the striatum ALWAYS lead to excitation of cortex?

A

Excitation of striatum, which inhibits GPi/SNr, which DISinhibits (activates) VA/VL of thalamus, which activates M1
However, just keep in mind that excitation of striatum can lead to both direct and indirect pathways (or also to cortex inhibition as well)

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17
Q

What is the Indirect pathway? What nuclei are involved?

A

i. Terminates movement
ii. Helps you learn of NEGATIVE outcomes associated with specific behaviors
- increases basal ganglia (inhibitory) output
- excitatory signal reaches cortex, inhibits GPe and disinhibits subthalamic nuclei
- subthalamic nuclei excites GPi/SNr which inhibits thalamus
- DECREASED cortical activity

18
Q

What is the role of Substantia Nigra Pars Compacta (SNc)

A

SNc is technically an inhibitor of the indirect pathway since it activates the direct pathway
SNc dopaminergic neurons always lead to cortical stimulation
Decreased SNc = DECREASED cortical stimulation
(decreased dopamine = decreased cortical stimulation)

19
Q

What are the principal neurotransmitters for pars reticularis and pars compacta?

A

GABA from SNr (that’s why it inhibits thalamus)

Dopamine from SNc

20
Q

What is Parkinson’s Disease?

A

Slow, progressive brain degeneration related to the accumulation of the protein alpha-synuclein into the cytoplasmic aggregates called Lewy bodies

- one of the most common basal ganglia diseases
- most common form of disease is idiopathic
21
Q

What is most common MOA of PD?

A

Loss of dopaminergic function from SNc

22
Q

What are the key histological features of Parkinson’s?

A

Lewy bodies created by alpha-synuclein accumulation

23
Q

How do patients who take MPTP (N-methyl-4-phenyl 1,2,3,6-tetrahydropyridine) get Parkinson’s? What is the treatment?

A

MPTP is oxidized into MPP+ by Mao-B (which normally metabolizes dopamine)
-uptake of MPP+ degenerates the dopaminergic neurons…MPP+ in mitochondria in neurons inhibit oxphosph and depletes energy stores, excess oxygen radicals, neuron death
Treatment: MAO-B inhibition

24
Q

What are the motor features of Parkinson’s?

A

Cardinal motor signs:
a. Bradykinesia: slow initiation of voluntary movements
b. Rigidity: increased muscle tone (resistance to passive movement)
c. Resting tremor: “pill-rolling” (fingers move like they are rolling a pill)
d. Stooped and unstable posture
Diagnosis requires 2 out of 4 cardinal motor signs

25
Q

What are the non-motor features of Parkinson’s?

A
  • Depression
  • constipation
  • urinary symptoms
  • sleep disorders
  • hyposmia
26
Q

What does loss of dopamine in striatum mean?

A

Reduced signaling in direct pathway
Increased signaling in indirect pathway (since SNc was what “inhibited” the indirect pathway)
Less motor cortical activity

27
Q

What is Huntington’s Disease (in relation to basal ganglia)?

A

Selective loss of medium spiny GABAergic neurons of striatum (SNr) whose output is through indirect pathway
What is MOA of HD?
MOA is loss of inhibition to GPe. GPe then is allowed to continue inhibiting Subthalamic nuclei. Inhibition of subthalamic nuclei leads to LESS excitation of GPi/SNr. Less GPi/SNr output means greater (or too much) motor cortical activity

28
Q

What are symptoms of Huntington’s Disease?

A

-chorea (brief, jerk-like movements)
-athetosis (slow, writhing movements)
-mental decline (executive dysfunction, slowness, memory decline)
-personality changes (irritable, anxious, depressed)
In contrast to PD, HD is a disease of excess uncontrolled movements

29
Q

What are genetics of HD?

A

CAG repeat length

-what happens to kids when dad is over age of 35

30
Q

From a big picture, what does injury to brainstem/cerebellum do? Injury to pyramidal system? Injury to basal ganglia?

A

I. Injury to brainstem/cerebellum = ataxia
II. Injury to pyramidal (corticospinal tract) system = weakness, spasticity, hyperreflexia
III. Injury to basal ganglia (extra-pyramidal) = bradykinesia/hypokinesia; rigidity; postural instability OR hyperkinetic abnormal movements (chorea, tremor, in HD)

31
Q

What is NOT a symptom of PD?

A

Muscle weakness

32
Q

Hypokinesia

A

decreased bodily movment

  • associated with basal ganglia diseases
  • SAME THING AS BRADYKINESIA
33
Q

What are all the neurotransmitters in basal ganglia?

A

a. Glutamate = excitatory
b. GABA = inhibitory = gamma-aminobutyric acid
c. Acetylcholine
M1 receptor = excitatory
M4 receptor = inhibitory
Allows you to pick one pathway over the other
d. Dopamine
D1 receptor = excitatory
D2 receptor = inhibitory
Allows you to pick one pathway over the other

34
Q

What is the rate limiting step is the biosynthesis of dopamine?

A

Rate limiting step = L—tyrosine  L-DOPa

Enzyme = tyrosine hydroxylase

35
Q

What is a catecholamine?

A

A derivative of tyrosine

Example: dopamine

36
Q

What are options of treating Parkinson’s?

A

i. Dopamine Agonist (an artificially synthesized molecule that does the same shit as dopamine)
ii. Mao-B and COMT inhibitor (to decrease dopamine breakdown)
iii. Levodopa (L-dopa agonist) and carbidopa/benserazide
iv. direct brain stimulation

37
Q

What is the treatment for HD?

A

Dopamine blockade can decrease chorea

  • but nothing can stop progression of disease
  • antipsychotics given to handle mood disorders
38
Q

What are the side effects of Levodopa?

A

Side effects include nausea, dizziness and hallucinations

39
Q

How is levodopa administered and how does it get to the CNS?

A

Levodopa is actively transported across the gut and the blood barrier and converted into dopamine in the CNS

40
Q

What is carbidopa and why is it necessary to be given in conjunction with levodopa?

A

It is a Dopa decarboxylase (DDC) inhibitors
-prevents the peripheral breakdown of levodopa so it is always given in conjunction with levodopa to decrease side effects

41
Q

pathology of substantia nigra pars compacta leads to

A

Parkinson’s

Because lack of dopamine leads to increased basal ganglia output and decreased motor cortical activity

42
Q

pathology of striatum leads to

A

Huntington’s

Because lack of GABA inhibition of GPe leads to excess inhibition of GPi/SNr and increased abnormal motor activity

B&B Week 2 Flashcards (14 decks)

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