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Y Physiology I > Week 04 Lect. 1 - Autonomic NTs + Sm Muscle > Flashcards

Week 04 Lect. 1 - Autonomic NTs + Sm Muscle Flashcards

1
Q

Where are the CNS origins of parasympathetic innervation?

Sympathetic?

A

Parasympathetic:

  • Cranial: CNs III, VII, IX, X (Oculom., Facial, Vestib., Vagus)
  • Sacral: S2-S4

Sympathetic

  • Thoracolumbar: Th1-Th12 + L1-L2/3
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2
Q

Where are the ganglia of the parasympathetic NS?

Of the sympathetic?

A

Parasympathetic: Near or within target organ

Sympathetic: Near spinal cord (para-/prevertebral ganglia)

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3
Q

How do the pre- and post-ganglionic axons differ in para/sympathetic NS?

A

Para: Long pre-, short post-

Symp: Short pre-, long post-

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4
Q

What is the preganglionic neurotransmitter for para- and sympathetic NS?

And receptor?

A

Both systems used acetycholine and a nicotinic acetylcholine receptor (nAChR) for pre-ganglionic transmission.

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5
Q

What is the most common post-ganglionic NT in the PsNS?

And less common ones?

And receptors w/ their general effects?

A

Transmitter: ACh (or sometimes VIP, NO)

Receptors:

  • Muscarinic ACh Receptors
    • M1,3,5 - (Gq >>> InsP3, increased [Ca2+])
    • M2,4 - (Gi/o >>> Ad. Cyclase inhibition, cAMP decrease)
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6
Q

What are the most common post-ganglionic NTs in the SympNS?

And their receptors/effects?

A

Transmitters: Norepinephrine + Acetylcholine

Receptors:

  • α1 - (Gq >>> InsP3, [Ca2++] increase)
  • α2 - (Gi/o >>> Ad. Cyclase inhibition, cAMP decrease)
  • β1-3 - (Gs >>> Ad. Cyclase activation, cAMP increase)
  • mAChRs
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7
Q

What are two examples of sympathetic co-transmitters which work with norepinephrine (NE) in the sympathetic NS?

A
  1. NE-NPY (Neuropeptide Y) - present in GI vessesl, effect on appetite, etc.
  2. NE-Somatostatin
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8
Q

How are NTs eliminated from synapses in the parasympathetic NS?

And sympathetic?

A

Para:

  • Acetylcholinesterase
  • Choline Reuptake
  • Diffusion

Sym:

  • Norepinephrine Reuptake (w/ cytoplasmic degradation)
  • Diffusion
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9
Q

How is neurotransmitter balance modulated at parasympathetic synapses?

And sympathetic?

A

Para:

  • Blocking transmitter release
  • Blocking choline reuptake
  • Blocking ACh-ase action

Symp:

  • Membrane NE Transporter Inhibition (Cocaine)
  • NE > Vesicle uptake inhibition
  • NE synthesis inhibition
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10
Q

Information from what 5 main sources is integrated into neurotransmission occuring at autonomic ganglia?

A

​presynaptic neuron reaches ggl. via nACHR

  1. Peripheral Afferent Signals
  2. Somatic Afferent Signals to CNS
  3. Interneurons
  4. misc. Efferent CNS signals
  5. Local Reflexes
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11
Q

What endocrine cells also release a common sympathetic neurotransmitter + its analogue?

What is special about these cells’ structure?

What signals this secretion and how does it occur?

A

Adrenal Medulla Cells

  • release epinephrine + norepinephrine
  • have the structure of a modified, axonless postganglionic neuron
  • thoracic sympathetic innervation signals adrenal medullary release of E + NE into the bloodstream
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12
Q

Where is epinephrine created?

How?

What regulates the relevant enzyme?

A
  • in the adrenal medulla
  • via Phenylethanolamine N-methyl Transferase (PNMT)
  • adrenal glucocorticoid hormones (cortisol, etc.) increase PNMT activity (resulting in a stress-response positive feedback loop)
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13
Q

What are 4 ways that an organ can be innervated by the two branches of the autonomic nervous system?

Specific examples of each?

A
  1. Innervation by only one division
    • vascular smooth muscle (α-1 adrenergic, vasoconstriction)
  2. Same target cells, both divisions, opposing effects
    • ​heart rate (Para = M2/4 rcptr > decrease, Symp = β1 rcptr > increase)
  3. Different target cells, both divisions, opposing effects
    • pupil diameter - para > sphincter, symp > dilator
  4. Similar response from both systems
    • salivary glands - secretion from both
      • Para > non-viscous, enzymatic
      • Sym > viscous, mucinous
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14
Q

How are smooth and skeletal muscles similar (3 ways)?

A
  1. Thin/Thick Filaments - slide together > contraction
  2. Both use an ATP Cycle to induce contraction
  3. [Ca2++]IC regulates contraction
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15
Q

What are smooth muscle cells’ unique properties?

(5)

A
  1. Small, uninucleate cells
  2. Non-striated
  3. No Z-lines - thin filaments anchor to dense bodies/membrane
  4. No T-Tubules - sarcoplasmic reticulum present, of variable importance
  5. Gap Junctions - connect cells for electrochem. comm.
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16
Q

What are the 3 mechanisms for depolarization-mediated intracellular calcium increase in smooth muscle cells?

A
  1. From neighboring cells via gap junctions
    • ​​no stable membrane potential
    • ex: elect. pacemaker cells (heart nodes, Cajal cells)
  2. Neural Stimulation
    • ​​NT release
  3. Mechanical Stimulation
    • ​​mechanoreceptors > mechanosensitive channels
17
Q

What is the name of the common mechanosensitive phenomenon for smooth muscle cell activation?

And basically how does it work?

A

Bayliss Effect

  1. Tissue is stretched
  2. Mechanosensitive channels open
  3. Depolarization occurs
  4. Contraction
18
Q

How are smooth muscle action potentials different compared to those of neurons?

3 ways

A
  1. Smaller amplitude
  2. Longer duration
  3. Different ion channels
19
Q

What are the ion channels associated with each of the different phases in a smooth muscle action potential?

A
  1. Depolarization - L-type Voltage-Gated Ca++ Channel
  2. Repolarization - Voltage-Gated Late K+ Channel
  3. Plateau - Ca++-Activated K+ Channel
  • also Ca++-induced Ca++ channels + Capacitative Ca++-Influx
20
Q

Describe the relationship btw membrane potential of and generation of force in smooth muscle.

A

membrane potential has to reach threshold for contraction

⇒ the greater the depolarization, the stronger the force of contraction

21
Q

What common, important pharmaceuticals act on smooth muscle cells, effecting their AP production?

And what common toxin does not effect smooth muscle APs?

A

Ca++ Channel Blockers - common blood pressure meds

TTX (tetrodotoxin) - only inhibits Na+ channels

22
Q

What is the mechanism for intracellular calcium increase in smooth muscles without membrane depolarization?

Briefly, how does it work?

A

Pharmacomechanical Activation

  1. Ligand binds α-1 adrenergic receptor
  2. Intracellular Gq signaling occurs (Phospholipase C > IP3)
  3. Ca++ released from SR
23
Q

What are the components of thin myofilaments in smooth muscle?

How is it different from skeletal muscle?

A
  • Smooth muscle-type actin
  • Tropomyosin
  • no troponin present in SMCs
24
Q

What are the components of thick filaments in smooth muscle cells?

A
  • Myosin Heavy Chain - complex of 2 heavy chains
  • Myosin Light Chain - 2 light chains per heavy chain
  • these are different subunits than skeletal muscle
25
How does increased intracellular Ca++ concentration induce contraction of smooth muscle?
1. Calcium binds **calmodulin** 2. Calmodulin complex activates **Myosin Light Chain Kinase (MLCK)** 3. MLCK Phosphorylates **Myosin Light Chain** 4. MLC **actin-binding sites** become available for binding
26
What are the 3 main mechanisms of termination of intracellular calcium signaling?
1. **Membrane Ca++-ATPase** - primary active transport of Ca out of cell 2. **Membrane Na+/Ca++ Antiporter** - secondary active transport of Ca out of cell 3. **SR-Ca++-ATPase** - active transport of Ca into the sarcoplasmic reticulum
27
What is the intracellular _calcium-independent_ mechanism for smooth muscle contraction? How does this effect de-activation of contraction mechanisms? How does it effect the calcium-dependent mechanism?
**-** **Rho-GTP** (activated by G12/13) activates **Rho-Kinase** which **phosphorylates myosin light chain** - Rho-kinase _inhibits_ **MLC-phosphatase**, stopping its de-activating effect - **MLCK** and **Rho-kinase** have an _additive effect_
28
What are the two messaging molecules which induce smooth muscle relaxation? What types of signaling increase the concentration of each one?
1. **cAMP** - β2-adrenergic stimulation 2. **cGMP** - NO-dependent activation
29
How does cAMP induce smooth muscle relaxation?
1. activates **Protein Kinase A** 2. PKA phosphorylates **Myosin Light Chain Kinase** 3. **MLCK-P** has _lower Ca_ _sensitivity_ than unphosphorylated MLCK and is thus inhibited
30
How does cGMP induce relaxaton of smooth muscle?
1. Activates **Myosin Light Chain Phosphatase** 2. Phosphorylates **InsP3** **Receptors** on sarcoplasmic membrane (deactivating it?) 3. Inhibits **calcium entry** into cell
31
As a review... considering all the mechanisms for smooth muscle contraction and inhibition, how would a flow chart-type diagram of these mechanisms look?
32
What are the two types of smooth muscle "units"? How are they controlled neurally? Other special features? Examples within the body?
1. **Multi-Unit** * **​​​**each cell has _its own innervation_ * contraction controlled _by ANS_ * ex: tightly regulated functions, **internal eye muscles, ductus deferens** 2. **Single Unit** * nerve innervates multiple cells _connected by gap junctions_, only _modulating_ activitiy * contract _spontaneously_ with _basal activity_ → pacemaker activity - "slow waves" * innervated by hormones * ex: **GI + vascular**
33
What are the characteristics of smooth muscle cell contraction regarding their... calcium signals? ATP requirements? Actin-myosin cycle + binding?
* **Long-lasting** intracellular Ca++ signals * **Lower ATP requirements** than skeletal muscle * **Slow actin-myosin cycles** * **Cross-bridges** between actin and myosin

Y Physiology I (17 decks)

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