9. Basal Ganglia Flashcards

1
Q

basal ganglia: functions

A
  • activity of upper motor neurons
  • movement selection by:
    • reinforcing intended movements
    • suppressing unintended movements
  • movement initiation by anticipatory changes
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2
Q

basal ganglia affects which portion of descending systems (upper motor neurons)

A

motor cortex

(planning, initiating, and directing voluntary movements)

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3
Q

basal ganglia: components

A
  1. caudate
  2. putamen
  3. globus pallidus
    • external segment (GPe)
    • internal segment (GPi)
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4
Q

basa ganglia: closely related structures

A
  1. diencephalon
    • VA/VL nuclei of thalamus
    • subthalamic nucleus
  2. midbrain
    • substantia nigra
      • pars compacta (SNc)
      • pars reticulata (SNr)
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5
Q

basal ganglia: inputs

A
  • input region of BG: striatum (= caudate + putamen)
  • inputs from:
    • cerebral cortex (many regions)
    • substantia nigra pars compacta (SNc)
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6
Q

how is the basal ganglia considered part of a corticostriatal pathway?

A

almost all cerebral cortical areas (EXCEPT PRIMARY AUDITORY AND PRIMARY VISUAL CORTEXES) project to basal ganglia

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7
Q

which 2 cerebral cortical areas do NOT porject into basal ganglia?

A
  • primary auditory cortex
  • primary visual cortex
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8
Q

basal ganglia: output regions and respective targets

A

Region –> Target

  • globus pallidus internal (GPi) –> to thalamus (for relay to motor cortex)
  • Substantia nigra pars reticulata (SNr) –> to superior colliculus
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9
Q

output of basal ganglia is:

(EXCITATORY/INHIBITORY)

A

inhibitory

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10
Q

comparison of outputs from SNr and GPi

(substantia nigra reticularis and globus pallidus internus)

A
  • BOTH: have output nuclei; diff’t targets and functions

SNr:

  • projects to superior colliculus
  • controls saccadic eye movements (quick, simultaneous movement of both eyes between two or more phases of fixation in the same direction)

GPi

  • projects to VA/VL (ventral lateral, ventral anterior) complex of thalamus
  • controls body movements
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11
Q

disinhibition as it relates to SNr and GPi

A

both SNr and GPi are inhibitory to superior colliculus and VA/VL respectively

caudate and putamen connections to SNr and GPi are also inhibitory

So release from inhibition/ or disinhibition is inhibition of inhibitory input

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12
Q

Disinhibition of VA/VL by the GPi

A
  1. cortex excites striatum
  2. striatum inhibits GP
  3. GP stops inhibiting VA/VL
  4. VA/VL excites motor cortex
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13
Q

direct pathway:

through BG to GPi & VA/VL for body movements

A
  • from Striatum –> to GPi –> to VA/VL
  • Releases VA/VL from inhibition (disinhibition)
  • Pormotes activation of motor cortex –> produces movement
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14
Q

function of direct pathway

type of dopamine receptors

A

PRODUCES MOVEMENT

D1 receptors

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15
Q

function of INDIRECT pathway

type of dopamine receptors

A

inhibit movement, prevent unwanted movement

D2 receptors

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16
Q

INDIRECT pathway:

from BG to VA/VL

A
  • from Striatum to GPe –> to subthalamic nucleus to GPi to VA/VL
  • releases subthalamic n. from inhibition (disinhibition)
  • promotes inhibition of VA/VL
  • prevents activation of motor cortex
  • suppresses movement
17
Q

normal basal ganglia function and mechanism

A

to promote selective movement

  • reinforcing intended movements via DIRECT pathway
  • suppressing all other (unintended movements) via INDIRECT pathway
18
Q

substantia nigra: function and mechanism (receptors)

A

promotes movement by:

  • excitation of direct pathway via D1 receptors
  • inhibiting indirect pathway via D2 receptors
19
Q

functional organization of DIRECT and INDIRECT pathways

A
  • center: surround organization in GPi
  • cortical activation of both direct/indirect pathways
  • surround region suppresses competing (unwanted) movements
  • center region activated intended movements
20
Q

consequences of loss of direct pathway

and clinical relation

A
  • less DISINHBITION of VA/VL –> less excitation of motor cortex –> less movement
  • CC: Hypokinetic disorders - characterized by paucity and slowness of movement (e.g. parkinsons)
21
Q

CC: hypokinetic disorders

cause and description

A

caused by loss of direct pathway

characterized by paucity and slowness of movement (e.g. parkinson’s disease)

22
Q

Parkinson’s disease circuitry

A

degeneration of cells in the substantia nigra reticularis –>

less disinhibition of VA/VL via DIRECT pathway and

more inhibition of VA/VL via indirect pathway

23
Q

CC: Parkinsons disease

characterized by

A
  • tremor at rest (pill rolling)
  • difficulting initiating movement (akinesia)
  • slowness of movement (bradykinesia)
  • difficulty making postrual adjustments
  • hypertonia of neck and extremities (cog-wheel rigidity)
  • minimal facial expressions
  • walking difficulty: short steps, stooped posture, paucity of associated movements (arm swinging)
24
Q

loss of INDIRECT pathway:

consequences

A
  • less inhibition of VA/VL –> more excitation of motor cortex –> more unwanted movement
  • CC: causes HYPERKINETIC disorders
25
Q

CC: hyperkinetic disorders

in general, what are they? name 3 diseases

A

characterized by uncontrollable movements

  1. dyskinesia
  2. huntington’s disease
  3. hemiballismus
26
Q

CC: dyskinesia

A

hyperkinetic disorder in which is characterized by abnormal, uncontrolled movement

27
Q

CC: Huntington’s disease

A

hyperkinesia (uncontrollable movements) w/ choreiform (dance-like) movements

(aka huntington’s chorea)

28
Q

CC: ballismus vs. hemiballismus

A

hyperkinesia w/ wild, flinging movements of extremities

hemiballismus: ballistic movements on one side; caused by loss of contralateral subthalamic nucleus

29
Q

CC: athetoid movement

A

writhing movement

30
Q

huntington’s disease circuitry

A

degeneration of cells in striatum to GPe –> less inhibition of VA/VL via indirect pathway

31
Q

non-motor loops: what else does basal ganglia mediate?

A
  • pre-frontal loop: decision-making and planning
  • limbic loop: emotional behavior