Voluntary motion: Basal ganglia

Question 1

What is the function of basal ganglia when it comes to voluntary motion?

Answer 1

Involved in planning and programming of movement
Initiation of movement

Control beginning and end (to a lesser extent) of movement

Question 2

In general terms, how does the basal ganglia control voluntary motion?

Answer 2

Inhibition
Withdrawal of inhibition

“excess of GABA”

Question 3

Describe the Nigrostriatal pathway.

Answer 3

From: SNPC
To: Striatum (Putamen + Caudate)

Tonically active
Dopaminergic

Question 4

Describe the Direct pathway.

Answer 4

Uses D1 receptors

SNPC to Striatum = Excitatory by dopamine - Allows motion

Striatum —> SNPR and GPi —> Thalamus
Releases GABA both times (inhibitory)

Question 5

Describe the Indirect pathway.

Answer 5

Uses D2 receptors

SNPC to striatum = Inhibited by dopamine
Excited by EAA/Ach
Inhibits motion when active

Striatum —> GPe (GABA)
GPe —> Subthalamic nucleus (GABA)

Subthalamic nucleus —> SNPR & GPi (EAA)

SNPR & GPi —> Thalamus (GABA)

Question 6

Describe the striatonigal GABA-ergic pathway.

Answer 6

From: Striatum
To: SNPR/GPi

Release of GABA from presynaptic terminal - inhibition

Question 7

The direct and indirect pathways have opposing jobs: what are they?

Answer 7

When active, the direct pathway ALLOWS motion.

When active, the indirect pathway OPPOSES motion.

Question 8

Walk me through how motion occurs through the actions of the direct and indirect pathway.

Answer 8

Cortical influence increases SNPC activity. This releases Dopamine into the Striatum. This activated the direct pathway and inhibits the indirect pathway.

Direct path:
Dopamine from SNPC binds to D1 receptor in striatum —> increases AP in Striatum —> Releases GABA in SNPR/GPi —> hyperpolarization —> decreases release of GABA at thalamus —> decreases inhibition of thalamus —> axons to cortex —> increased release of EAA —> allows motion to occur

Indirect path:
Dopamine binds to D2 receptor —> decreases AP in striatum —> decreases GABA at GPe —> increases GPe activity —> increases GABA inhibition at Subthalamic nucleus —> hyperpolarization at STN —> decreases EAA at SNPR/GPi leading to decreased activity —> decreases release of GABA at thalamus

Question 9

In Parkinson’s Disease, how are the direct and indirect pathways affected?

Answer 9

SNPC input is abolished.

Direct pathway becomes difficult to activate

Indirect pathway becomes overactive due to loss of inhibition

Inability to initiate motion.

Question 10

What do we have to activate in order to inhibit motion?

Answer 10

The indirect pathway

Question 11

Describe the intrastrial cholinergic system.

Answer 11

Between nuclei of striatum

Excitatory
It seems to excite the indirect pathway.

Question 12

How would you activate the indirect pathway?

Answer 12

Intrastriatal cholinergic pathway

EAA inputs from the cortex

Question 13

Name the functions of the prefrontal cortex in regards to voluntary motion.

Answer 13

Planning of complex motor action

Carrying out of thought processes

Question 14

What parts of the brain are required for planning of complex motor actions?

Answer 14

Interaction between parieto-temporal-occipital (PTO) + all levels of motor cortex + cerebellum

Frontal association area
Supplementary motor cortex
Cerebrocerebellum

Question 15

Once the motion is planned, sequenced, and approved, what happens?

Answer 15

The appropriate columns in the PMC are activated.

APs travel down the axons of pyramidal cells and activate the alpha-motoneurons that innervates muscles needed to complete motion

Question 16

What else does the brain activate along with alpha-motoneurons?

Answer 16

Gamma-motoneurons in the AGONIST muscle

Known as alpha-gamma coactivation

Question 17

What happens in the antagonist muscle when the agonist is contracting?

Answer 17

Alpha and gamma motor neurons are inhibited.

Question 18

Once motion starts, what is called upon to make sure the motion is correct?

Answer 18

Spinocerebellum