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NS II > Neurotransmitters and Receptors > Flashcards

Neurotransmitters and Receptors Flashcards

1
Q

What are the 10 major sites of drug action in the CNS?

A
  1. Action potential transmission
  2. Neurotransmitter (NT) synthesis
  3. NT storage
  4. NT Metabolism (also occurs after re-uptake)
  5. NT Release
  6. NT Reuptake
  7. NT Synaptic degradation
  8. Post-synaptic receptor
  9. Post-synaptic neuron ion conductance
  10. Retrograde signaling

Note: DSA Fig 21-5

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2
Q

What type of post-synaptic potential, excitatory or inhibitory (EPSP or IPSP) occurs with (1) influx of Na+/Ca2+ and (2) efflux of K-/influx of Cl-?

A

EPSP and IPSP, respectively

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3
Q

Describe the second messenger mehcanisms of Galpha-s.

A

Activates adenylyl cyclase –> cAMP formation –> activation of ion channels and protein kinase A

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4
Q

Describe the second messenger mechanisms of Galpha-i

A

Deactivates adenylyl cyclase –> reduced cAMP –> deactivation of ion channels and PKA

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5
Q

Describe the second messenger mechanisms of Galpha-q

A

Activates phospholipase C –> catalyzes conversion of phosphotidylinositol (4,5) biphosphate (PIP2) –> Diacyl glycerol (DAG) and Inositol (1,4,5) Triphosphate (IP3)

DAG - activates membrane localized protein kinase C
IP3 - binds ER receptors –> Ca+2 release
- Ca+2 also activates PKC

Note: also effects ion conductance

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6
Q

What types of receptors does glutamate bind?

A

Ionotropic (AMPA and NMDA) and Metabotropic (mGluR; 2 locations)

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7
Q

Describe the ionotropic receptors which glutamate binds.

A

Non-NMDA (AMPA) = generates a short-lasting EPSP (Na+ influx)

NMDA = Coincidence Receptor = normally blocked by Mg2+, allows Ca2+ influx if unblocked
Multiple EPSP in a short temporal span –> removal of Mg2+ and generation of longer-lasting EPSP

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8
Q

Describe the metabotropic receptors which glutamate binds?

A

Post-synaptic - Galpha-q; Decreases K+ conductance

Pre-synaptic - Galpha-i; Decreases Ca2+ conductance (Inhibitory to vesicular fusion)

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9
Q

Describe the synthesis, storage, release, and inactivation of glutamate.

A

Synthesis - glucose is the precursor

Storage - Vesicular; ATP-dependent transport

Release - Neural impulse

Inactivation - absorbed by synaptic glial cells and metabolized to glutamine, then transported to glutamatergic neurons

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10
Q

Describe the role glutamate may play in migraines, seizures, apoptotic neuronal death, and stroke.

A

Migraines - excessive release –> cx.al spreading depression –> migraine aura

Seizures - excessive depolarization of glutamatergic focus –> region of glutamatergic neurons depolarize –> paroxysmal discharge (i.e. seizure)

Neuron Apoptosis - excessive influx of Ca2+

Stroke - cell death is more rapid in glutamatergic areas because of the above mentioned process, which can lead to cell lysis and more glutamate release; prolonged seizure may also cause cell death

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11
Q

What types of receptors does GABA bind?

A

Ionotropic (GABA-A) and Metabotropic (GABA-B; 2 locations)

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12
Q

Name and describe the function of the ionotropic GABA receptor

A

GABA-A = allows Cl- influx at the axonal hillock –> hyperpolarization and IPSP

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13
Q

Name and describe the function of the metabotropic receptors GABA binds.

A

GABA-B

Post-synaptic = increases K+ conductance
Pre-synaptic = decreases Ca2+ conductance (Inhibitory)
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14
Q

Name two NMDA receptor antagonists

A

Phencyclidine (PCP) and Ketamine

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15
Q

Describe the synthesis, storage, release, and inactivation of GABA

A

Synthesis - glucose and pyruvate are precursors

Storage - synaptic vesicle

Release - neural impulse

Inactivation - reuptake by presynaptic neurons; uptake by glial cells

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16
Q

Describe how GABA-mimetics may be useful for the Tx of convulsions, anxiety, and alcohol withdrawal. Name GABA-mimetics relevant to this discussion

A

GABA inhibition balances the excitatory effects of glutamate; dysfxn.al GABA –> hyperexcited state

Benzodiazepines, barbituates, and alcohol are all GABA mimetics.

Convulsions - Barbituates
Anxiety - Benzodiazepines (end in azolam or azepam)

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17
Q

What types of receptors does acetycholine bind?

A

Ionotropic (Nicotinic; 2 types; 3 locations) and Metabotropic (Muscarinic; 5 types)

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18
Q

Describe the types and functions of the Nicotinic Receptors.

A

There are Nm and Nn receptors. All are excitatory via increasing cation (Na/K) conductance.

Nm - NMJ
Nn - post-ganglionic in the autonomic ganglia and post-synaptic in CNS

19
Q

What is the location and mechanism of action for the M1 receptor?

A

CNS

MOA - Galpha-q results in decreases K conductance (Excitatory)

20
Q

What are the locations and MOA of the M2 receptor?

A

Systemically on smooth muscle (vessels excluded), the heart (M2>M3), and CNS

MOA - Galpha-i –> activation of K channels (inhibitory)

21
Q

What are the locations and MOA of the M3 receptor?

A

Smooth muscle (bladder/vessels), endothelium (NO synthase), and exocrine glands (sweat, lacrimal, etc.)

MOA - Galpha-q

22
Q

What are the locations and MOA of the M4 receptor?

A

CNS

MOA - Galpha-i –> activation of K channels (inhibitory)

23
Q

What are the locations and MOA of the M5 receptor?

A

CNS

MOA - Galpha-q; not much else known

24
Q

Describe synthesis. storage, release, and inactivation of acetycholine.

A

Synthesis - from choline and Acetyl-CoA in presynaptic terminal

Storage - VAT pumps into vesicles

Release - neural impulse

Inactivation - acetylcholinesterase

25
Q

What types of receptors does dopamine bind?

A

Metabotropic only (5 types)

26
Q

Which dopamine receptor subtypes are found in the CNS, and what is their MOA?

A

D1 - Galpha-s (excitatory)
D2 - Galpha-i
post-synaptic increases K conductance (inhibitory)
pre-synaptic decreases Ca conductance (inhibitory)

27
Q

Describe the synthesis, storage, release, and inactivation of dopamine.

A

Synthesis - presynaptic terminal from tyrosine by tyrosine hydroxylase

Storage - enters synaptic vesicles through VMAT

Release - neural impulse

Inactivation - reuptake through DAT

28
Q

Describe how dopamine participates in addictive behavior?

A

Drugs such as cocaine and amphetamines prevent reuptake and increase release of dopamine, respectively. The subjective effects of drugs are felt in the reward pathway, which involves the ventral tegmental dopaminergic neurons.

29
Q

What types of receptors does norepinephrine bind?

A

metabotropic only (5 types of adrenergic)

30
Q

Describe the location and MOA of alpha 1 receptors?

A

Blood vessel, intestinal, and urinary (except detrusor) smooth muscle (contraction) and the CNS

MOA - Galpha-q –> deacreased K+ conductance (excitatory)

31
Q

Describe the location and MOA of alpha 2 receptors?

A

Presynaptic receptor for retrograde signaling, also post-synaptic

MOA - Galpha-i –> (inhibitory)
Pre-synaptic - decreases Ca conductance
Post-synaptic increases K conductance

32
Q

Describe the location and MOA of Beta 1 receptors?

A

Cerebral Cx, Heart, JG cells (renin)

MOA - Galpha-s –> decreases K conductance (stimulatory)

33
Q

Describe the location and MOA of Beta 2 receptors?

A

Pancreas (+ insulin), liver (gluconeogenesis and glycogenolysis), visceral smooth msucle (relaxation; includes detrusor), vascular smooth muscle (relaxation), skeletal muscle (glycogenolysis)

34
Q

Describe the location and MOA of Beta 3 receptors?

A

Adipose tissue (lipolysis)

35
Q

What types of receptors does serotonin (5HT) bind?

A

Ionotropic (5HT-3) and Metabotropic (15 types; know 5HT-1, 2A, and 4)

36
Q

Describe the MOA of 5HT-3

A

Non-selective cation channel (Excitatory)

37
Q

Describe the MOA of 5HT-1, 5HT-2A, and 5HT-4

A

5HT-1 = Galpha-i –> increased K conductance (Inhibitory)

5HT-2A = Galpha-q –> decreases K conductance (excitatory)

5HT-4 = Galpha-s –> decreased K conductance (excitatory)

38
Q

What is the role of 5HT receptors in depression?

A

Decreased function is associated with depression

39
Q

Describe the synthesis, storage, release, and inactivation of serotonin?

A

Synthesis - presynaptic terminal from typtophan by tryptophan hydroxylase

Storage - vesicular

Release - neural impulse

Inactivation - reuptake through SERT (inhibited by many anti-depressants; FLUOXETINE)

40
Q

Describe the synthesis, storage, and release of neuropeptides (NP)

A

Synthesis - cell body and packaged in to dense-core vesicles (contain proteolytic enzyme which cleave pre-pro-peptides)

Storage - Co-packaged with traditional NT.s (Ex: neuropeptide Y with NE)

Release - neural impulse; result of co-packaging

Inactivation - Unknown

41
Q

How does glutamate contribute to Alzheimer’s Disease and what drug can be used to prevent this?

A

Glutamate mediates excitotoxicity

Memantine is an NMDA receptor antagonist used to treat dementiain Alzheimer’s

42
Q

What is the basis for acetycholinesterase inhibitors in alzheimer disease? Describe the benefits.

A

Ach production is reduced due to reduced choline acetyltransferase. Benefits are mild and don’t impact long-term outcome.

43
Q

Describe the role of dopamine in parkinson disease and schizophrenic psychosis.

A

Parkinson Disease - loss of substantia nigra pars compacta; many dopaminergic neurons

Schizophrenia - overactivity of dopamine; block with D2 antagonistsm (typical anti-psychotics)

44
Q

What is the target of atypical anti-psychotics?

A

agonists of 5HT-2A

NS II (7 decks)

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