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Flashcards in Basal Ganglia Deck (19)
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1
Q

the major source of input to the basal ganglia

A

Input to basal ganglia comes from the cortex.

2
Q

character and probable cause of Parkinson’s disease

A
  • Resting tremor, lost during intended movement.
  • increased tone
  • diff initiating movement and slowness of movement once begun
  • bradykinesia
  • Etiology: loss of dopamine neurons in substantia nigra, thus reducing effective disinhibition that striatum would normally produce in thalamus via GP. (harder to start movement)
  • Treatment: L-dopa (levodopa), crosses BBB, give with carbidopa to reduce L-dopa dosage.
3
Q

Is the output of the basal ganglia inhibitory or excitatory

A

INHIBITORY (preventing thalamic excitation of cortex)

Cells in layer V of cortex send axons to basal ganglia where they release glutamate to excite cells in caudate or putamen.
Cells in caudate or putamen send axons to GP where they release GABA to inhibit cells there.
Cells in GP send axons to thalamus where they release GABA to inhibit cells there.
-Late stages: DBS in STN or GPi

4
Q

What is the genetic cause of Huntington’s Disease and what areas of the basal ganglia are affected?

A
  • -chorea, athetosis
  • progressive disease, starting at 30-50
  • Autosomal DOMINANT
  • chromosome 4
  • Disease may be due to abnormal binding of the Huntington protein (huntingtin) in the cortex and basal ganglia. Triplet repeat (CAG)
  • Loss of striatal actions on globus pallidus; also produced by too much DA.
5
Q

How do basal ganglia exert modulation on motor performance?

A

By their massive interconnections with motor cortices.

Input from cerebral cortex, output directed to thalamus and from there back to cortex.

6
Q

The basal ganglia are impacted by ____.

Location?

A

basically all nontraumatic, metabolic disruption of motor control. Why? NT biosynthesis occurs there (80% of dopamine).

Basal ganglia are masses of cells (gray matter) at base of cerebrum, below neocortex. They are next to but do not include the thalamus. No direct connections iwth sensory syst or spinal motor apparatus. Role in MOTOR PROGRAM SELECTION.

7
Q

Name the components of the basal ganglia.

A
  1. caudate and putamen (neostriatum/striatum)
  2. globus pallidus
  3. substantia nigra (caudalmost; dopamine rich)
  4. Subthalamic nucleus
8
Q

Unilateral defects= _____ deficits

A

contralateral deficits in function (whereas cerebellum is ipsilateral).

9
Q

Describe the “direct path” from the cortex to basal ganglia and eventually back to cortex

A
  • Input from cortex. (input nuclei are caudate and putamen).
  • info flows from caudate to putamen to globus pallidus
  • info then flows from globus pallidus interna to the thalamus. So globus pallidus interna is the major OUTPUT nucleus of the basal ganglia.
  • From thalamus back to cortex.
10
Q

internal feedback loop: substantia nigra

A

SN gets projection from striatum (caud/put) and projects back to caudate and putamen (back projection made by neurons that contain/rel DA–pars compacta).
-SN pars reticulata project to thalamus (additional output pathway)

11
Q

Internal feedback loop: subthalamic nucleus

A

Subthalamic nuc receives projection from external part of GP, projects back to both the internal and external GP. “pallidal feedback loop”

12
Q

Describe the 2 populations of medium spiny neurons of the striatum.

A
  • one expresses D1 recep (coupled to excitatory Gprot)
  • other expresses D2 recep (coupled to inhibitory G prot)

Travel thru different pathways:
w/ D1 recep, project directly to GPi (main output struc of basal ganglia) (DIRECT)

w/ D2 recep, project to the GPe. The GPe projects to subthalamic nucleus (STN) and STN to GPi (INDIRECT pathway)

13
Q

Putamen (what projects to it)

A

Sensori-motor cortex projects to putamen.
Putamen to GP to VA (some VL) thalamus. Thalamic nuclei project back to motor cortex, especially supplementary motor area (SMA). (Thalamic neuron gets EPSP from dentate nuc of cerebellum OR IPSP from GP.

14
Q

Caudate projections

A

Caudate gets input from frontal assoc cortex, sends to GP, then to dorso-medial thalamus, back to assoc cortex

15
Q

Nucleus Accumbens

A

caudal juncture b/t caudate and putamen, processes info from paleo-cortex (limbic).

16
Q

Explain how basal ganglia is inhibitory.

A

Pallidal (GP) neurons fire spontaneously at high rates. Striatal neurons fire slowly, if at all. W/o cortical input, basal ganglia (GP) inhibits the thalamo-cortical input.
Signal comes down from cortex and excites the striatal neuron. Striatal neuron inhibits pallidal neuron thus DISINHIBITING the thalamo-cortical pathway. Thalamic neurons thus increase firing rate, excite cortical neurons. “Direct pathway”–>facilitates movement (indirect pathway thru GPe, leads to negative feedback)

17
Q

Inhibition at substantia nigra

A

Striatal neurons to SN produce inhibition via GABA release. SN sends DA neurons back to Striatum (excitatory).

18
Q

Inhibition at subthalamic nucleus

A

STN gets inhibitory input from GPe and projects excitation back to GPi

19
Q

Hemiballismus

A

flailing movements of the arm and leg on one side.
–>stroke in post. cerebral artery leads to damage of STN on one side–>loss of excitation by STN reduces inhibitory outflow of GP, so motor programs inappropriately initiated.