Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuro > basal ganglia > Flashcards

basal ganglia Flashcards

1
Q

What’s special about the basal ganglia’s connections to the motor pathway?

A
  • The basal ganglia receive no direct sensory input
    • They do not directly generate a descending spinal control pathway
    • They exert their modulation of motor performance by their massive interconnections with the motor cortices
    • Input comes from cerebral cortex and output is directed to thalamus and from there back to cortex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why are metabolic disturbances that mess with NT biosynthesis likely to manifest first in the basal ganglia?

A
  • The basal ganglia are disproportionately active in NT biosynthesis
    • 80% of the brains dopamine is in the basal ganglia, though they collectively are 0.5% of the total brain weight
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

In general, what is the major role of the basal ganglia?

A

• Motor program selection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What and where are the basal ganglia?

A
  • Bilaterally paired masses of cells, gray matter, situated below the neocortex
    • More or less surrounding the thalamus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What nuclei are the basal ganglia?

A
  • 4 of them total
    • Caudate + Putamen = striatum
    • Globus pallidus
    • Substantia nigra
    • Subthalamic nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What member of the basal ganglia is the prinicple output?

A
  • To the thalamus
    • Gpi
    • Globus pallidus interior
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Unilateral basal ganglia issues manifest how?

A

Contralateral motor issues.

*the basal ganglia on the left side of the brain interact with the left cerebral cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the major direct pathway in the basal ganglia?

A

• Input comes from the cortex
• The basal ganglia components nearest the cortex are input nuclei
○ Caudate and putamen
• From the striatum to the globus pallidus
• Information flows from the globus pallidus interna to the thalamus (VA and VL for motor portion, DM for cognitive and associattional)
• Globus pallidus interna is the major output nucleus
• The main circuit of the basal ganglia involves cortical input to the striatum, then to the globus pallidus interna, out to the thalamus and from there back to cortex
• Feedback loop to cortical function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the internal feedback loops in the basal ganglia?

A

• Those components not directly involved with cortical function (striatum, globus pallidus) are invloved mostly in internal feedback loops within the basal ganglia
• Substantia nigra receives a projection from striatum, projects back to caudate and putamen
• Back projection is made by neurons that contain and release dopamine to produce their effects
○ Pars compacta
• Cells in another protion fo the substantia nigra (pars reticulata) project to thalamus
○ Provide an additional output pathway for basal ganglia
• Subthalamic nucleus receives a projection from the external segment of the globus pallidus
• Projects back to both the external and internal segment of the globus pallidus
○ Pallidal feedback loop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the difference in response to a D1 and D2 receptor activation?

A

• Both are dopamine receptors
• Cortex projects to medium spiny neurons in the striatum
• Two populations of neurons: D1 and D2 expressing
• D1 is a Gs metabotropic receptor, which activates those neurons
• D2 is a Gi/o metabotropic receptor, inhibiting those neurons
• The D1 neurons in the striatum project directly to the Gpi
○ Direct pathway
• The D2 neurons in the striatum project to the Gpe, then to subthalamic nucleus (STN) then to Gpi
○ Indirect pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the indirect pathway thought to be doing?

A
  • Inhibiting simultaneous competing motor programs

* The brain chooses a motor program over another one, so the other one is inhibited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the input and output of the Putamen?

A

• Putamen recieves input from the sensori-motor cortex
• Output projections are to a specific subsection of the globus pallidus
• Globus pallidus in turn projects to mostly VA thalamus (some VL)
• Thalamic nuclei project back to motor cortex
○ Mostly supplementary motor area = SMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the input and output of the caudate?

A

• Receives input widely from frontal association cortex (frontal lobes)
• Sends information to it’s own subsection of the globus pallidus
• Globus pallidus transmits info to dorso-medial thalamus
• Dorso-medial thalamus projects to association cortex
○ Thus cognitive problems in basal ganglia disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

The cerebellum projects to the VA thalamus. Does this system converge with the putamen circuit?

A

• Not really, there is separation between them
• A thalamic neuron either receives an EPSP from the dentate nucleus OR IPSP from globus pallidus
○ Never both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the nucleus accumbens?

A
  • Caudal juncture between caudate and putamen is also called the nucleus accumbens
    • Processes information from paleo-cortex (near olfactory cortex)
    • Part of the limbic system
    • Subserves emotional and drive-related aspects of behavior
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

In general, what is the difference in the systems between the caudate and the putamen?

A

• The caudate and putamen might be seen as parallel systems, receiving cortical input that is directly related to:
○ the motor system (putamen) or
○ cognitive/affective process (caudate)
• Individual neurons in putamen fire in synchrony with ongoing movements
• Localized stimulation of putamen produces discrete movements
• Few caudate neurons respond during movement, nor does stimulation produce movement

17
Q

Follow the information from the VL thalamus and back.

A
  • VL thalamus
    • Supplementary motor area (cortex)
    • Putamen
    • Globus pallidus
    • Substantia nigra
    • VL thalamus
18
Q

Follow the information from the DM thalamus only and back

A 
• DM and VA thalamus together project to caudate in a different parallel pathway
	• DM thalamus only
		○ DM thalamus
		○ Cingulate anterior and medial orbito frontal cortex
		○ Nucleus accumbens
		○ Globus pallidus
		○ Substantia nigra
		○ DM thalamus
19
Q

Follow the information from the VA and DM thalamus and back

A 
• Could be one of two pathways
	• One
		○ VA and DM thalamus
		○ Dorsolateral prefrontal cortex
		○ Caudate (DL)
		○ Globus pallidus
		○ Substantia nigra
		○ VA and DM thalamus
	• Two
		○ VA and DM thalamus
		○ Lateral orbito frontal cortex
		○ Caudate (VM)
		○ Globus pallidus
		○ Substantia nigra
		○ VA and DM thalamus
20
Q

What is the major principle of cellular information processing through the basal ganglia?

A
  • DISINHIBTION

* Activation of a motor control signal is achieved by release from inhibiton, not by direct excitation

21
Q

The direct pathway is mediated by disinhibtion of thalamic neurons. Explain this.

A
  • Pallidal neurons have high frequency of resting AP (50 AP per second)
    • Pallidal neurons are thus at rest inhibiting thalamic neurons, which is trying to activate a certain area of cortex
    • Inhibition of pallidal neurons means there is a relative activaiton of thalamic neurons, increasing activation in that area of cortex
    • Disinhibiton principle, and pallidal neurons are inhibited by activating striatal neurons (GABA)
22
Q

Describe the three steps of information processing through the basal ganglia (cellular)

A
  • Cells in layer V of cerebral cortex are output cells
    • Send axons to the synapse in basal ganglia where they release glutamate to excite cells in caudate or putamen
    • Cells in caudate or putamen send axons to globus pallidus where they release GABA to inhibit cells in GP
    • Cells in GP send axons to thalamus where they release GABA to inhibit thalamic neurons
    • THUS, GP is principle output, and thus principle output is inhibitory, preventing thalamic excitation of the cortex
23
Q

What is going on in the substantia nigra?

A
  • The striatal neurons that project to the substantia nigra produce inhibition there by release of GABA
    • Substantia nigra sends dopaminergic axons back to the striatum
    • DA release in striatum appears to be largely excitatory, and largely diffuse
    • Think of it as essentially a “go ahead” signal for the general activity increase of the striatum
    • No selection for specific neurons with SN DA release
    • SN activation is not phase locked with a given motor response, but can happen before and after it
24
Q

What does the subthalamic nucleus do?

A

• Receives an inhibitory input from external (lateral) globus pallidus and projects excitation back to the internal (medial) globus pallidus
• If you blow-out the subthalamic nucleus you disinhibit the thalamus
○ Thus showing that STN stimulates globus pallidus interna normally

25
Q

What are the clinical ramifications of basal ganglia dysfunction in Parkinsons?

A

• Characterized by resting tremor
○ 3-6 Hz
○ Lost during intended movement
• Increased tone due to simultaneous activation of flexors and extensors
• Difficulty in initiating movements
• Slowness of movement once begun
• Shaking movements of head
• Shaky, tremulous speech
• Tremors increase in emotional stress, decrease with intended movement
• Bradykinesia
• No extraneous movements while walking
• Very little change in facial expression
• Inability to perform two complex movements simultaneously
• Difficulty in performing a sequence of complex movements
• Difficulty making predictive motor output based on past performance or instructions

26
Q

What is the etiology of Parkinsons?

A
  • Loss of dopamine neurons in substantia nigra
    • DA is excitatory to some striatal neurons and thus there is reduction of the effective disinhibtion that striatum would normally produce in thalamus by way of globus pallidus
    • Motor acts become harder to get started because of this
    • Activity of substantia nigra is not obviously linked directly to movement, but they appear to be continously active
    • DA likely acts hormonally with little selection of certain neurons
27
Q

What is the treatment of Parkinsons?

A

• L-dopa (levodopa)
• BBB permeant and diminishes symptoms
• Given in combo with carbidopa to block degradative pathways to decrease necessary dose
• Through progression of disease more L-dopa needed to produce long-term results
• On/off moments for the patient
• At the latest stages implanted electrodes into subthalamic nucleus or Gpi will allow for disinhibiton of thalamus and thus allow for initiation of movement
○ Deep brain stimulation
• Acts like the well medicated state, but can last longer (throughout the day)
• Ideal candidate here is patient that benefits from drugs but is advanced to have a dependence on a certain plasma concentration

28
Q

What’s the difference between athetosis and chorea?

A

• Chorea - dance
○ Continuous rapid movements of face, tongue or limbs
• Athetosis - slow, writhing, ceaseless movements of hand, sometimes lips, tongue, neck, foot

29
Q

What are the clinical ramifications of basal ganglia dysfunction in huntington?

A

• Adult onset form of the disease is at age 30-50
• Choreic movements
• Progressive and culminates in dementia
• Initial stages involve motor effects like those of parkinsons, hypokinesia or immobility
• Also early symptoms of change of affect or cognition
○ Mood degradation and loss of computational and memory skills

30
Q

What is the inheritability of Huntington?

A
  • Autosomal dominant
    • Short arm of chromosome 4
    • Codes for a large protein with unknown function
    • Involves triplet repeat, CAG (glutamine)
    • Excess of 40 repeats is threshold
31
Q

Which neurons are affected in huntington?

A

• Specific sets of cholinergic striatal neurons
• GABA-ergic medium spiny output neurons
○ Both degenerate
○ May involve glutamate excitotoxicity, possiblty through excessive intracellular Calcium build-up
○ Mimic this with over-treatment of patient with L-dopa causing dyskinesias

32
Q

Define the relationship of acetylcholine and DA in the basal ganglia.

A
  • They are in balance
    • They have opposting effects on the function of the basal ganglia
    • Anti-cholinergic treatment exacerbates the choreic movements in huntingtons disease
    • Reflects balance between direct and indirect basal ganglia pathways
    • Too much indirect, paucity of movement - parkinsons
    • Too much direct, hyperkinetic - huntington
33
Q

What disease of the basal ganglia is more common in the elderly because it’s caused by a stroke in the posterior cerebral artery distribution?

A
  • Hemiballismus
    • Flailing movements of the arm and leg on one side
    • Small ganglionic branch artery is blocked and subthalamic nucleus is damaged on one side
    • Loss of excitation by the subthalamic nucleus reduces inhibitory outflow of globus pallidus
    • Motor programs are inappropriately initiated through the disinhibited thalamus
34
Q

Basal ganglia - caused motor dysfunctions are characterized how?

A
  • Various abnormalities in the organization of motor output
    • Parkinsons - becomes difficult ot initiate movement or to perform sequential complex movements (paucity of movement)
    • Huntingtons chorea and hemi-ballismus - excess, inappropriate movements
    • No sensory deficits nor loss of muscular strength

Neuro (59 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions