Voluntary Motion: Basal Ganglia and Big Picture (Dr. Karius) TEST 3 Flashcards

1
Q

Motor Control: Basal Ganglia

A

The SCENARIO: A “bowl” of candy was passed around the room. You were free to take a piece of your favorite kind.

For you to think about:
- Even with the Cerebral Cortex and the Cerebellum, we still haven’t created a system that works well. Without the basal ganglia, you’ll end up either a) being UNABLE to INITIATE the Motion that will grab that piece of candy for you; or b) getting “STUCK” at the START of the Motion, only able to REPEAT the STARTING ACTION. Either way, you don’t get your piece of candy!

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2
Q

Basal Ganglia

A

What we understand about the Basal Ganglia:
1) They’re involved in the PLANNING and PROGRAMMING of a Movement

2) Their INPUT is particularly IMPORTANT in the INITIATION of MOVEMENT!!!

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3
Q

Anatomy of the Basal Ganglia

A
  • Actually SEVERAL NUCLEI in a (Anatomically) Loosely arranged GROUP
  • Not all participate in Motor Control, but most do..
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4
Q

Nuclei of the Basal Ganglia

A

1) SUBTHALAMIC Nucleus

2) SUBSTANTIA NIGRA
a) Pars Compacta
b) Pars Reticulata

3) PUTAMEN
4) CAUDATE NUCLEUS

  • Together, the Putamen and Caudate Nucleus are called the STRIATUM!!!*****
  • The Striatum receives INPUTS to the BASAL GANGLIA!!!!!

5) GLOBUS PALLIDUS
a) Internal (Medial) Segment
b) External (Lateral) Segment

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5
Q

The Nigrostriatal Dopaminergic System

A

FROM:
- Substantia Nigra Pars Compacta

TO:
- Nuclei of STRIATUM (Putamen and Caudate Nucleus)

EFFECTS:

  • D1 Receptors (+)
  • D2 Receptors (-)

Release DOPAMINE!!!!*

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6
Q

The Intrastriatal Cholinergic System

A
  • Between the Nuclei of the STRIATUM (Putamen and Caudate Nucleus)

EFFECTS:
- Excitatory!!!

Release ACETYLCHOLINE!!!!!*

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7
Q

The Striatonigral GABA-ergic Pathway

A

FROM:
- STRIATUM

TO:
- SUBSTANTIA NIGRA PARS RETICULATA and GLOBUS PALLIDUS INTERNAL SEGMENT

  • **” DIRECT PATHWAY”**
  • Leads to INITIATION OF MOVEMENT!!!!!!!!!!
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8
Q

Basal Ganglia Mechanism

A

1) Information LEAVES the Basal Ganglia via the SNPR and the GPi
2) The SNPR and GPi Project to the THALAMUS, releasing GABA within the Thalamus
3a) To CORTEX via Thalamus!!!!!
3b) To BRAINSTEM and SPINAL CORD!!!!!!

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9
Q

Describe the Nuclei, Major Inputs /Outputs and Neurotransmitter systems of the Basal Ganglia

A

NUCLEI:

1) SUBSTANTIA NIGRA
a) Pars Compacta
b) Pars Reticulata

2) STRIATUM
a) Caudate
b) Putamen

3) GLOBUS PALLIDUS
a) External segment
b) Internal segment

4) SUBTHALAMIC NUCLEUS

NEUROTRANSMITTERS:

1) DOPAMINE
- Cell Bodies: Substantia Nigra Pars Compacta
- Axons travel to the STRIATUM
- D1 and D2 receptors on different neurons in striatum

2) CHOLINERGIC
- Cell Bodies: neurons of Striatum
- AXONS: synapse on OTHER Neurons in Striatum
- Excitation

3) GABA-ERGIC
- Cell Bodies: STRIATUM
- Axons travel to Globus Pallidus Internal Segment and the Substantia Nigra Pars Reticulata
- INHIBITION!!!!!!

INPUTS:
- Substantia Nigra Pars Compacta receives inputs and relays them to the Striatum.

OUTPUTS:

  • Globus Pallidus (internal segment) and Substantia Nigra Pars Reticulata send axons to the thalamus
  • When activated, they release GABA at synapses in the thalamus
  • INHIBITION of THALAMUS!!!!
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10
Q

Basal Ganglia Function

A

WHAT THEY DO:
- Control BEGINNING (An to a Lesser Extend) the END of the Movement

HOW:

  • Basal Ganglia work by INHIBITION and WITHDRAWAL of that Inhibition (To start Movement)
  • EXCESS of GABA!!!*
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11
Q

Basal Ganglia Pathway

A

1) From CORTEX via CORTICOSTRIATE TRACK (EAA)!!!!!
- The Striatum receives the INPUT from the Basal Ganglia

2) The NIGROSTRIATAL PATH:
- From SNPC
- TONICALLY ACTIVE!!!!
- DOPAMINERGIC!!!!

3) The PUTAMEN receives MOST/ALL Input relates to Motor Control!!!
a) SNPC Sends DOPAMINE to both Caudate and PUTAMEN!!!

b) Primary Motor Cortex, SMC, and Premotor Cortex send EAA to the PUTAMEN!!!!
4) The effects of DOPAMINE released in the Striatum indicates that there are TWO DISTINCT PATHWAYS WITHIN the Basal Ganglia that Control Motion!!!

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12
Q

Two Distinct Pathways within the Basal Ganglia that Control Motion

A

1) DIRECT PATHWAY
- D1 RECEPTORS
- EXCITED by DOPAMINE!!!!
* ALLOWS MOTION

2) INDIRECT PATHWAY
- D2 RECEPTORS
- INHIBITED by DOPAMINE!!!!!
* INHIBITS MOTION**

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13
Q

The Direct Pathway

A

1) From STRATIUM to the SNPR and GPi
- SNPC Dopaminergic Inputs EXCITE the STRIATAL CELLS

  • The Stratal Cells RELEASE GABA in the SNPR and GPi!!!!!
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14
Q

Activation of the Direct Pathway

A

1) SNPC releases DOPAMINE to the STRIATUM (Caudate and Putamen)
- D1 Receptors

2) The STRIATUM releases MORE GABA to the SNPR and GPI
3) The SNPR and GPi are INHIBITED and release LESS GABA to the THALAMUS!!!!!!!

By Inhibiting the SNPR and the GPi, LESS GABA is Released in the Thalamus. The Thalamus is then FREE to EXCITE the CORTEX, allowing INITIATION of MOVEMENT!!!!!!!!***

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15
Q

Indirect Pathway

A

1) Input for the SNPC is INHIBITORY to the STRATAL NEURONS that are part of the INDIRECT PATHWAY due to the D2 Receptors
2) To ACTIVATE the Indirect Pathway, we must use INPUT from the Cortex and the Intrastriatal Pathway!!!!!!!!!
3) The Striatal Neurons SYNAPSE on the GPe (GABA), by activating the Stratal Neurons, we release MORE GABA in the GPe. Activity in the GPe is DECREASED!!!
4) The Neurons of the GPe Synapse in the SUBTHALAMIC NUCLEUS. Since the GPe Neurons are LESS ACTIVE, there is LESS INHIBITION of the SUBTHALAMIC NUCLEUS!!!!!!!!
5) Neurons from the SUBTHALAMIC Nucleus Synapse in the SNPR. Since they are ACTIVE (Less INHIBITED), MORE EAA are released in the SNPR!!!!!!!

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16
Q

Activation of the Indirect Pathway

A

1) STRIATUM releases MORE GABA to the GPe
2) GPe is has DECREASED ACTIVITY and releases LESS GABA to the SUBTHALAMIC NUCLEUS
3) The SUBTHALAMIC NUCLEUS is LESS INHIBITED therefore MORE EAA is RELEASED to the SNPR and GPi!!!!!!!
4) The SNPR and GPi are ACTIVATED which releases MORE GABA to the THALAMUS

With ACTIVATION of the INDIRECT PATHWAY, there is MORE EXCITATION of the SNPR and GPi and MORE GABA is released in the THALAMUS. The Thalamus is then INHIBITED, DECREASING EXCITATION of the Cortex, SUPPRESSING THE INITIATION OF MOVEMENT!!!!!!!!!!!!!!!!!!!***

17
Q

Compare and contrast the Direct and Indirect pathways, including circuitry and function

A

DIRECT PATHWAY:

  • To activate: SNPC sends dopamine to striatum •Dopamine binds to D1 receptors
  • Striatal neurons are excited
  • Axons release GABA in GPi & SNPR
  • When ACTIVE – ALLOW MOTION

INDIRECT PATHWAY:

  • To activate: Cortical inputs release EAA
  • Striatal neuronsof indirect path are excited
  • Axons synpase in GPe. (more GABA)
  • GPe axons travel to subthalamic nucleus (GABA)
  • Axons from subthalamic n. travel to GPi and SNPR (EAA)
  • When ACTIVE – INHIBIT MOTION
18
Q

Parkinsons Disease

A
  • The SNPC is ABOLISHED!!!!
    1) The Direct Pathway becomes DIFFICULT to ACTIVATE

2) The Indirect Pathway becomes OVERACTIVE (Due to Loss of INHIBITION)

We see an INABILITY to INITIATE MOTION!!!

19
Q

Voluntary Motion: Association Cortex

A

Two Major Areas of Function:
1) Planning of COMPLEX Motor Actions

2) CARRYING OUT of “THOUGHT” Processes

20
Q

Prefrontal Cortex

Planning of Complex Motor Actions
PART 1!!!!!!

A

Planning of COMPLEX Motor Actions:
1) Interacts with PARIETO-TEMPORAL- OCCIPITAL ASSOCIATION AREA and all Levels of MOTOR CORTEX!!!!!!!

2) Planning of a Complex Motor Act requires (to variable degrees) the FRONTAL Association Area, the Supplementary Motor Cortex, the Premotor Cortex, and the Cerebrocerebellum!!!!
3) Interactions between FRONTAL, PREMOTOR, SMC, and the BASAL GANGLIA (Dopamine) determine IF the Motion will OCCUR!!
4) Once the Motion is Planned, Sequenced, and “Approved”, the appropriate Columns in the Primary Motor Cortex are ACTIVATED!!!!!!
5) Action Potential then travel down the axons of the PYRAMIDAL (Betz) Cells and activate the ALPHA- MOTONEURONS that Innervate the Muscles NEEDED to COMPLETE THE MOTION!!!!

21
Q

Prefrontal Cortex

Planning of Complex Motor Actions
PART 1!!!!!!

A

6) But the Muscle Spindle could be a problem here, it will OPPOSE EVERY MOTION we make (Because Every Motion STRETCHES One or More Muscles) UNLESS we do something about it!!!
7) The Brain “Solves” this problem by using the GAMMA- MOTONEURONS to “TRICK” the Muscle Spindle into believing the the Muscle is NOT CHANGING LENGTH!!!
8) To Make MOTION OCCUR, if the BRAIN ACTIVATES the ALPHA-Motoneuron for Spindles in the CONTRACTION (AGONIST) Muscle (Alpha-Gama Coactivation)
9) To Make Motion occur, if the Brain INHIBITS the GAMMA-Motoneuron for Spindles in the STRETCHING (ANTAGONIST) Muscle
10) Once the Motion has STARTED, the SPINOCEREBELLUM is called upon to make sure the MOTION IS CORRECT!!!!!!!