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121 > Module 2D (Pt3) > Flashcards

Module 2D (Pt3) Flashcards

1
Q

What are the junctional transmission steps

A
  1. Storage and release of the transmitter
    1. Post junctional potential
    2. Initiation of post junctional activity
    3. Destruction or dissipation of the transmitter
    4. Non electrogenic functions
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2
Q

Storage and release of the transmitter

A

the neurotransmitter is packed into synaptic vesicles in the axon

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3
Q

Post junctional potential

A

the transmitter crosses the synaptic cleft, interacts with a receptor and evokes a response from the post synaptic neuron

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4
Q

Initiation of post junctional activity

A

summation of responses caused by the transmitter(s) results in a change in the post synaptic neuron

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5
Q

Destruction or dissipation of the transmitter

A

enzymes, reuptake pumps, or simple diffusion limit the transmitters signal

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6
Q

Non electrogenic functions

A

continual quantal release is a homeostatic control for maintaining receptor, enzyme and pump levels

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7
Q

What are receptors

A
  • Biological molecules (often proteins) that are selective in their ligand-binding characteristics and modifiable when a ligand is bound so as to produce a functional change
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8
Q

What is a receptor site for a drug (ligand)

A
  • Is the specific binding region of the receptor
    • Has a high and selective affinity for the drug molecule
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9
Q

What initiates the action of the drug

A
  • The interaction of a drug and its receptor
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10
Q

Receptor

A

a molecule to which a drug binds to bring about a change in a biological system

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11
Q

Receptor site

A

specific region of the receptor molecule to which a drug binds to

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12
Q

Effector

A

component of the system that accomplishes the biological effect

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13
Q

Spare receptor

A

receptor that doesn’t bind agonist when drug concentration is sufficient to produce max effect Kd> EC50

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14
Q

Agonist:

A

a drug that activates its receptor

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15
Q

Antagonist

A

a drug that binds without activating its receptor and prevents activation by agonist
-(competitive, irreversible, physiologic, chemical, inverse)

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16
Q

What causes regulation in receptors

A
  • Number, location, interaction with effectors
    • Desensitization, tachyphylaxis (become down regulated if over used)
    • Internalization
    • Substrate depletion
    • Down or up regulation
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17
Q

What are ionotropic receptors

A
  • Ligand-gated ion channels
    • Rapid response (microseconds)
    • Often more then 1 subunit (oligomeric
    • Examples are nAChR (Ach receptor, Na channel)
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18
Q

What are metabotropic receptors

A
  • G protein coupled receptors
    • Slower, modulatory response (milliseconds/ seconds)
    • Single 7 helix subunit
    • Example is mAChR (Ach receptor)
    • BAR (norepinephrine receptor)
19
Q

Cholinergic transmission steps

A

i) Acetylcholine synthesis
ii)Choline transport and storage
iii)Release of Ach by SNAREs: CAMPs and SNAPs
iv)Ach degradation

20
Q

Acetylcholine synthesis

A
  • Occurs through choline acetyltransferase (ChAT)
    i) ChAT transfers an acetyl group from acetyl-CoA onto choline
    ii) Acetyl- CoA synthesized by pyruvate dehydrogenase in mitochondria
    iii) Choline is brought into the axon terminal by active transport
21
Q

Choline transport and storage

A
  • Occurs through the enzymes choline transporter (CHT1) and vesicular Ach transporter (VAChT)
    i) CHT1 brings choline into the axon
    • ATP- dependent (active transport), rate limiting
    • Inhibited by hemicholiunium (not used clinically rather for research)
      ii) CAChT brings Ach into synaptic vesicles
    • Atp dependent
    • Inhibited by vesamicol
    • 1,000- 50,000 Ach/ vesicle
    • About 300,000 vesicles in an axon
22
Q

Release of Ach by SNAREs: VAMPs and SNAPs

A

i) When an axon terminal depolarizes
- Voltage gates Ca channels open
- Ca allows for interactinos between Vesicle-associated Membrane proteins (VAMPs) and synaptosome associated proteins (SNAPs) on the vesicles and membrane
- Membrane fusion occurs, allowing Ach (and co trasnmitters) to exit the cell by exocytosis
- Ach release is inhibited by botulinum toxin
ii) 2 ACh pools
- The readily releasable pool
- The reserve pool

23
Q

Ach degradation

A
  • Occurs through acetylcholinesterase (AChE)
    i) Ach Is broken down quickly in the synaptic cleft
    • AChE hydrolyzes Ach into acetate and choline, both are recycled
    • Ach is present in the synapse or neuromuscular junction for < 1 millisecond
    • Inhibition of AChE is therapeutically important (and potentially toxic) effect of many drugs
24
Q

If you were to give someone botulism toxin would you be promoting or inhibiting the sympathetic nervous system

A
  • Net effect is blocking ach so your promoting sympathetic nervous system as you are inhibiting the parasympathetic
    - Look at the end effector
25
Q

How many homologous subunits are in nicotinic acetylcholine receptor

A
  • 5 homologous subunit form Na+/K+ pore
    • Subdivided based on location and their ability to bind a bungarotoxin
26
Q

What are m nAChR

A

Muscle receptor

27
Q

Where are Neuronal type nAChR:

A
  • Exist in peripheral ganglia, adrenal medulla, and brain as homopentamers and heteropentamers (Nn)
28
Q

What do peripheral Nn

A

Depolarization and firing of post ganglionic neurons, secretion of catecholamines

29
Q

What are muscarinic acetylcholine receptors

A
  • Get name from muscimol, from mushrooms (mimics and activates the effects of the parasympathetic nervous system)
    • 5 distinct subtype (1-5)
    • All GPCRs with different roles
30
Q

What are the Gq coupled GPCRs

A
  • M1,3,5
    Important in smooth muscle fibers (in gut, eye…)
31
Q

What are the Gi coupled GPCRs

A
  • M2,4
    • I stands for inhibitory
    • Does three things all at the same time
    • Found mainly on muscles of heart (heart slows down)
32
Q

Cholinergic actions in the body (Skeletal muscle, Autonomic ganglia, autonomic effector cells, Prejunctional sites, extra neuronal sites)

A
  1. Skeletal muscle
    • Ach released from motor nerve-> nAChR open-> skeletal muscle-> contraction
      2. Autonomic ganglia
    • Ach released from pre-ganglionic nerve-> nAChR open -> EPSP in post ganglionic nerve
      3. Autonomic effector cells
    • Ach released from post-ganglionic PNS nerve -> mAChR activated -> electrical activity is modulated
    • Heart SA and AV nodes: increase K, hyperpolarization –> slowed heart rate
    • Smooth muscle: Increase Na, Ca –> partial depolarization contraction via Ca
      4. Prejunctional sites
    • Negative feedback via M2 and M4
      5. Extra neuronal sites
33
Q

What are cholinomimetics also called

A
  • Parasympathomimetic
34
Q

What are cholinomimetics clinically useful

A
  • Glaucoma
    • Loss of normal function in bowel and bladder
    • Smoking cessation
35
Q

Muscarinic toxicity

A
  • Miosis, bronchoconstriction, excessive GI activity, sweating, vasodilation, slowing of heart rate followed by reflex tachycardia (vagus nerve kicks in)
36
Q

Explain nicotinic toxicity

A
  • Fasciculations and paralysis, stimulation (convulsions) and then depression, addiction
37
Q

What happens when AChE is inhibited

A
  • DUMBBELSS
    • Diarrhea, urination, miosis, bronchoconstriction, bradycardia, excitation (skeletal muscle and CNS), lacrimation, salivation, sweating
38
Q

What are muscarinic antagonists clinically useful in

A
  • Scopolamine: nausea
    • Atropine: treating miosis, reducing airway secretion, reducing diarrhea and gastric secretions (in the past), treating AChE intoxication
    • Ipratropium: bronchodilation in asthma
    • Oxybutynin: bladder spasm
39
Q

Toxicity in muscarinic antagonists

A
  • Hyperthermia (through inhibition of sweating), dry mouth, tachycardia, arrhythmia, acute angle glaucoma, urinary retention, constipation, blurred vision, flushing (redness), sedation, delirium and hallucinations
40
Q

What are nicotinic antagonists useful in (clinically)

A
  • Hypertensions (hexamethonium)
41
Q

Are nicotinic antagonists used clinically often

A

Rarely used clinically

42
Q

Toxicity of nicotinic antagonists

A
  • Venous pooling and postural hypotension
    • Dry mouth, blurred vision
    • Constipation
    • Sexual dysfunction
43
Q

look at extending concepts

A

121 (16 decks)

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