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APP Part 2 > Basal Ganglia > Flashcards

Basal Ganglia Flashcards

1
Q

Medium Spiny Neuron

A
  • Dendrites are studded with spines, many projections, 95% of basal ganglia.
  • Modal “balanced” state membrane potential (-78 to -60mV) **These are targeted in Huntington’s**
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2
Q

OBJ 7: Functional role of the basal ganglia. (3)

A
  • collection of subcortical structures that control movement. Regulate activities of motor cortical areas– allows voluntary movements to be performed smoothly, AND surpasses unwanted movements.
  • allow us to do repetitive motions automatically (walking, chewing gum, typing)
  • also contribute to higher level cognitive processing
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3
Q

OBJ 1: Where are the 2 places that basal ganglia receive input from?

A
  1. Cortex– via descending pathway – excitatory via glutamate
  2. SNc – via ascending pathway – excitatory via dopamine (*Dopaminergic projections*)
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4
Q

Basal ganglia connections

A

SNpc release dopa and cholinergic interneurons and Glu from cortex all influence the basal ganglia.

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5
Q

OBJ 4: What does the striatum signal?

A

Striatum only sends INHIBITORY signals (GABA) to:

  • GPe (indirect pathway)
  • GPi/SNr (direct pathway)
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6
Q

OBJ 4: What does the thalamus signal?

A

Sends EXCITATORY signals via glutamate to the CORTEX thereby completing the loop of the basal ganglia.

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7
Q

What is the INDIRECT pathway from the striatum?(Remember: Stripes indirectly excite SIR Thalamus)

A

INDIRECT = Striato-pallidal pathway

** Striatum inhibits GPe **

Normally, GPe inhibits STN, and prevents this: STN→ excites GPi/SNr→ inhibit THALAMUS.

key: INHIBITION of GPe (by striatum) allows EXCITATION of STN, and then GPi/SNr, which INHIBIT thalamus.

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8
Q

Clinical manifestation of Tourette’s syndrome (3)

A
  • Neurological disorder characterized by childhood onset
  • Motor and vocal “tics”
  • Comorbidity with OCD, ADHD, depression
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9
Q

OBJ 4: What does the subthalamic nucleus signal?

A

STN is unique in the basal ganglia because it is the only structure to send EXCITATORY signals via glutamate to:

  • GPi/SNr
  • GPe
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10
Q

Treatments for Huntington’s

A

No treatment to slow or treat progression of Huntington’s. Can only treat depression, irritability, and paranoia symptoms with SSRI’s (Fluoxetine, carbamazepine).

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11
Q

Inhibitory NT GABA has 3 receptors:

A

GABAA – ligand gated ion ch permeable to cations (Cl-)

GABAB – GPCR’s, metabotropic (?), opens K+ or Ca2+ channels to dampen the membrane potential.

GABAC – in retina

** All are inhibitory, dampens the membrane potential**

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12
Q

OBJ 4: What is the role of the cortex in stimulation of the basal ganglia?

A

Cortex sends EXCITATORY signals (glutamate) to the STRIATUM

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13
Q

Dorsal striatum

A
  • Convergence of multiple inputs.
  • receives inputs via Glu, Dopa, and Ach
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14
Q

striatum RECEIVES _____ inputs from cortex, and SENDS output to ______ .

A
  • topographic descending.
  • Globus Pallidus and SNiagra.
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15
Q

What are aspiny interneurons?

2 types? (location, NT, target, action)

A

5% of striatum, DO NOT project outward, entirety of neuron is within striatum, but may influence MSNs that send info out from striatum. Two types:

  1. Cholinergic interneurons
  2. GABAnergic interneurons (Fast-spiking and Low-threshold-spiking)
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16
Q

Clinical manifestations of basal ganglia disease

A
  • Tremor
  • Changes in posture and muscle tone
  • Poverty of movement without paralysis
  • Hyperkinetic involuntary movements
  • Obsessive compulsive disorders

… all tend to involve uncoordinated movement

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17
Q

Cortical Basal Ganglia Loops

A
  • Involved in associative, limbic mvmt, sensory, motor loops.
  • a problem in a motor loop may be caused by a defect, Huntington’s, or eye movement???
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18
Q

What causes Tourette’s syndrome? treatment?

A
  • “Hyper-dopaminergic” neurons
  • dopamine receptor antagonists
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19
Q

Clinical manifestations of Parkinson’s disease (Motor symptoms)

A
  • Muscle rigidity
  • Bradykinesia (slowness of movement)
  • Resting tremor (goes away during voluntary movement)
  • hyperkinetic INVOLUNTARY mvmts (like reflexes)
  • Poor postural balance leading to disturbances in gait and falling episodes
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20
Q

Dopaminergic Modulation: Dopa is more of a neuromodulator than a NT, because ______

A
  • b/c doesn’t have its own receptor, instead binds to GPCRs generally. (What the heck are D1 and D2 receptors then???)
  • Send inputs to striatum (+/-) and thalamus (-).
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21
Q

General Basal Ganglia Pathway goes from ____ to basal ganglia via _____

A
  • Cortex to basal ganglia, via striatum.
  • striatum RECIEVES topographic descending inputs from cortex, and SENDS input to GP and SN.
  • All inputs go to the thalamus and feedback on cortex. It’s a loop!
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22
Q

Direct vs Indirect pathway

A
  • SMA/MC to putamen to GPi directly, or indirectly to GPe and eventually reach the GPi.
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23
Q

What is “down-state”?

A

Resting state of the medium spiny neuron of striatum– at resting membrane potential.

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24
Q

What are the firing patterns of the 2 types of GABAergic interneurons of striatum, in comparison to MSNs?

A
  • Fast-spiking GABAergic interneurons – have a much greater frequency of action potential firing than MSNs (which have a consistent steady firing pattern).
  • Low threshold spiking GABAergic interneurons – don’t need as much depolarization as the MSNs in order to reach threshold and fire an AP.
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25
Q

Potential causes of Parkinson’s (3)

A

More than 95% are idiopathic. Some genetic ties.

Some chronic pesticide exposure may be correlated, due to mitochondria dysfunction

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26
Q

All addictions (cocaine, amphetamines, nicotine, alcohol) all share common mechanism of ….

A

elevating dopamine in Ventral Striatum/Limbic Loops – probably hyperactive reward pathways.

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27
Q

Excitatory NT Glutatmate has 3 receptor:

A
  • NMDA R (Na, Ca, K channels will be open)
  • mGLURs (GPCRs - open channels to depolarize membrane potential- dampens memb potential, decreases probability of opening Ca channels)
  • kainate receptors
28
Q

Glutamate and its receptors

A

*Major excitatory NT

NMDA and Non-NMDA receptors (AMPA, Kainate): Ionotropic non-selective ion channels that mediate influx of cations like Na+ and Ca++

Metabotropic receptors: coupled to intracellular excitatory pathways

29
Q

The central event in Huntington’s disease, aka ___, is the loss of _____. Which pathway is affected?

A
  • aka Chorea
  • Loss of striatal medium spiny projection neurons **
  • Indirect pathway affected more **
  • Interneurons and neighboring neurons unaffected.
30
Q

OBJ 4: What is the DIRECT pathway from the striatum?

A

DIRECT = Striato-nigral pathway

Striatum → inhibits GPi/SNr

Normally, GPi/SNr → inhibits Thalamus

INHIBITION of GPi/SNr by the striatum removes inhibition and allows EXCITATION of Thalamus.

31
Q

3 nonsurgical treatment for Parkinson’s. *Can’t treat with dopamine bc ____

A
  • dopamine doesn’t cross BBB
    1) L-dopa + Carbidopa (AADC inhibitor)
    2) MAO-B inhibitor
    3) Dopamine receptor agonists
32
Q

Clinical manifestations of Parkinson’s disease (non-motor symptoms)

A

(senses and intellect are spared until later in disease?)

  • Cognitive impairment, hallucination, mood/sleep disorders, OCD
  • Constipation/Erectile dysfunction
  • Altered pain sensation
33
Q

Parkinsonism

A

Many types of diseases. Substantial death of cells in SNpc. Theory: there is unbalanced activity of direct and indirect pathway to develop PD.

34
Q

What are tonically active neurons (TAN)? (location, NT, target, action)

A
  • TANS, cholinergic interneurons of striatum, modulate MSNs using acetylcholine (Ach binds to muscarinic M1 receptors on MSNs)
  • large cell bodies, typical firing pattern and are tonically active WITHOUT cortical innervation. Even if you remove cortex, TAN cells continue to fire APs.
35
Q

MAO-B inhibitor

A
  • Used to treat Parkinson’s disease.
  • Prevents degradation of dopamine in the synapse by MAO-B.
  • CONS: but modest affects, works early in disease
36
Q

Why is the general basal ganglia pathway considered a loop?

A

bc pathway starts from cortex/thalamus, and all inputs go to the thalamus and feedback on cortex. It’s a loop!

37
Q

hyperactive reward pathways are characterized by ___

A

elevated dopamine levels in Ventral Striatum or Limbic Loops

38
Q

Globus Pallidus

A
  • Receive inputs from striatum
  • majority are projection neurons, some interneurons
  • uses GABA and targets thalamus
39
Q

GABA and its receptors

A

Major inhibitory NT

  • GABA-A receptors: ligand-gated ion channels selective for Cl-, thus hyperpolarize cells
  • GABA-B receptors: GPCRs that acivate 2nd messenger cascades of cAMP
40
Q

What causes Huntington’s disease?

A
  • HERITABLE fatal neurodegenerative disease, caused by abnormal number of CAG repeats in DNA (38-100 repeats in HD, normally 9-34).
  • Huntingtin and other genes is involved.
41
Q

What are medium spiny neurons (MSN)?

2 types? (location, NT, target, action)

A

95% striatal neurons. Project out of striatum to communicate with other parts of basal ganglia. 2 types:

  1. Striato-pallidal (Striatum –> GP)
  2. Striato-nigral (Striatum –> SN)
42
Q

Dopaminergic neurons

A
  • Found in the pars compacta of Substantia Nigra.
  • firing pattern is regulated by SALIENCE – determines if a sensory input is important to integrate or not.
  • Known to be associated with rewards pathway
  • Stimulate the direct pathway and inhibit the indirect pathway
  • destruction of these neurons in parkinson’s.
43
Q

Dopamine and its receptors

A

Dopamine modulates the opening and closing properties of other types of ion channels (K+, Na+, Ca++).

  • D1 receptor: GPCR coupled to G-s-alpha subunit and INCREASE cAMP to stimulate adenylyl cyclase. Present in the DIRECT pathway.
  • D2 receptor: GPCR coupled to G-i-alpha subunit and DECREASE cAMP to inhibit adenylyl cyclase. Present in the INDIRECT pathway.
44
Q

OBJ 4: What does the globus pallidus signal?

A

Globus pallidus only sends INHIBITORY signals (GABA).

  • GPi/SNr– inhibits THALAMUS
  • GPe– inhibits STN and GPi/SNr
45
Q

OBJ 4: What do inputs to the basal ganglia tell them (in general terms)?

A
  1. release of wanted movements (excitatory via glutamate) OR…
  2. inhibition of unwanted movements (inhibitory via GABA)
46
Q

manifestation of hemiballismus:

A

Hyperkinetic disease – uncontrolled flinging movements of contralateral arm or leg.

47
Q

symptoms of Huntington’s

A
  • uncontrolled head movement, twitchiness
  • Grimacing movements of face, lips, tongue
  • Gesticulating mvmt of limbs
  • Jerking movements of lower limbs
  • Paranoia, depression, irritability

Like Parkinson’s, symptoms appear later in life

48
Q

Central event of Parkinson’s disease - neurons and pathways involved.

A

** Degeneration and death of dopaminergic neurons in the Substantia Nigra (SNc) of the midbrain**

  • dopa neurons stimulate direct and INHIBIT indirect pathway, so in Parkinson’s direct pathway doesn’t get stimulated and INDIRECT pathway is chronically OVERSTIMULATED (lack of inhibition).
  • GPe inhibited→ STN excited→ leading to excitation of GPi/SNr→ inhibition of thalamus.
49
Q

OBJ 1: What is the basal ganglia composed of? (4 major structures + their substructures)

A
  1. Striatum - gateway of info processing from cortex + thalamus. Contains Caudate Nucleus, Putamen, Nucleus Accubens.
  2. Globus Pallidus - external and internal (GPe, GPi)
  3. Subthalamic Nucleus (STN)
  4. Substantia Niagra - Pars Compacta, Pars Reticulata (SNc, SNr)
50
Q

← ↑ → ↓ ↔ ∴ ∵ ∼ ≈ ° % ÷ × ± − + ½ ¼ ¾ ⁰ ¹ ³ ⁴ ⁵ ⁶ ⁿ ⁺ ⁻ ∧ ₀ ₁ ₂ ₃ ⊕ ⊗ ∑ Θ ƒ ∫ ‖ | ⊥ ∠ α β γ δ ε γ η θ π ∆ ∞ σ κ λ µ ∨ ℵ ∞ ∆

A

← ↑ → ↓ ↔ ∴ ∵ ∼ ≈ ° % ÷ × ± − + ½ ¼ ¾ ⁰ ¹ ³ ⁴ ⁵ ⁶ ⁿ ⁺ ⁻ ∧ ₀ ₁ ₂ ₃ ⊕ ⊗ ∑ Θ ƒ ∫ ‖ | ⊥ ∠ α β γ δ ε γ η θ π ∆ ∞ σ κ λ µ ∨ ℵ ∞ ∆

51
Q

Carbidopa and levodopa

A
  • used to treat Parkinson’s Disease
  • L-dopa CAN crosses BBB, converted to dopamine in the brain by AADC (Tyr→ L-dopa → dopamine).
  • Carbidopa is a AADC inhibitor, CAN’T cross BBB, prevents L from being broken down/converted outside the brain.
52
Q

Surgical therapies for Parkinson’s (2)

A

– Ablation of thalamus, GP (UNILATERAL), or STN (BILATERAL)– may improve tremors, rigidity, slowness.

– Deep brain stimulation– Implant electrodes to stimulate dopaminergic neurons. Targets STN or GPi bilaterally. Less invasive, reversible, and adjustable.

53
Q

Internal capsule separates the ____ and _____.

A

putamen and caudate nucleus.

54
Q

Action Selection involves ___ neurons bringing input to ___ (area).

A

Tonically active Ach Neuron (TAN) inputs to striatum

55
Q

What is hemiballismus? 3 causes?

A
  • Hyperkinetic disease
  • unilateral lesion of the subthalamic nucleus causes decresed output from Globus Pallidus.
  • Often caused by stroke, tumor, or infections
56
Q

____ and _____ Loops within the Globus Pallidus all implicated in Parkinson’s disease

A

Motor and oculomotor loops

57
Q

Subthalamic Nucleus

A
  • Project to globus pallidus
  • uses Glu so it is excitatory.
  • autonomous firing pattern (5-50Hz).
  • It is driven by the cortex.
58
Q

Demographics of Parkinson’s patients

A
  • 1-1.5 million Americans, more Caucasians.
  • Onset in the elderly
  • Some genetic correlation
  • No conclusive diagnosis
59
Q

D1 vs. D2 receptors

A

D1 Receptor: couples to Gs – increase AC activity, increase cAMP

D2 Receptor: couples to Gi – decrease AC activity, decrease cAMP

60
Q

Parts of the Striatum

A

Caudate nucleus (medial) Putamen (lateral).

They send inputs to other parts of the basal ganglia only.

61
Q

Substantia Nigra

A
  • Distinctive black color
  • pars compacta uses dopamine and express melatonin
  • firing patterns regulated by “salience”
  • it degenerates in Parkinson’s
62
Q

Basal ganglia Injuries/Diseases

A

Tourette’s Syndrome

Parkinson’s Disease

Huntington’s

63
Q

Basal ganglia (caudate and putamen) neurons:

A
  • Medium spiny neurons (95%) – projecting neurons
  • Aspiny Interneurons (5%) – cholinergic and GABA-ergic, non-projecting, influence projecting neurons.
64
Q

Dopamine receptor agonists

A
  • Used to treat Parkinson’s disease.
  • PRO: No enzymatic activity required! targets receptor subtypes.
  • CONS: doesn’t work + side effects: dyskinesia, orthostatic hypotention, nausea, hallucinations/confusion
65
Q

Obsessive-compulsive disorder

A
  • likely associated with loops of basal ganglia
  • things that give us pleasure (shopping, gambling) but when it’s at the level of compulsiveness probably something wrong with the basal ganglia.
66
Q

What is “up-state”??

A
  • active state of the MSN of striatum, when it is depolarized and firing action potentials.
  • a MSN reaches the up-state (gets excited) via glutamatergic innervation from the cortex.

APP Part 2 (9 decks)

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