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SBM Neuro > 10-15 NeuroPHARM: Transmitters and Receptors > Flashcards

10-15 NeuroPHARM: Transmitters and Receptors Flashcards

1
Q

NMDA receptors:
MOA?
Modulators?

A

NDMA receptor MOA:

Modulators: glutamate

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2
Q

Match the following items:

  • -excitation
  • -inhibition
  • -inward Ca2+
  • -inward Cl-
  • -inward Na+
  • -depolarization
  • -hyperpolarization
A

DEPOLARization ——> EXCITation w/ inward Na+ and Ca2+ flow

HYPERpolarization ——>INHIBition w/ inward Cl- flow

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3
Q

What’s the AP threshold? RMP?

A

AP thresh = -40mV

RMP = ~ -70mV

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4
Q

What do neurotransmitters modulate?

A

the AP threshold

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5
Q

EPSP and IPSP

A

excitatory post-synaptic potential and inhib…

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6
Q

Which of these statements is false?

1) Ionotropic receptors involve direct opening of ion channels
2) G-protein coupled receptors can be both ionotropic and metabotropic
3) Secondary messengers are required for signaling through metabotropic receptors
4) Na+ and K+ commonly pass through ion channel receptors to alter membrane potential

A

2 G-protein coupled receptors are ONLY metabotropic

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7
Q

Name the different classes of neurotransmitter

A

Amino acids (e.g. GABA, glutamate)
ACh
Monoamines (Dopa, NE, serotonin)
Others (e.g. histamine, cannabinoids, adenosine, opioids, endorphins…)

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8
Q

Which Amino Acid neurotransmitters are inhibitory? Excitatory?

A

Inhib are NEUTRAL amino acids: GABA, glycine

Excit are ACIDIC amino acids: glutamate, aspartate

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9
Q

What is the major excitatory NT in CNS?

A

glutamate

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10
Q 
Glutamate:
effect?
where made?
binds what receptors?
excess?
deficiency?
A 
—EXCITATORY
—secreted by pyramidal cells
—binds both ionotropic (main=AMPA also NMDA, Kainate) and metabo receptors
—excess = excitotoxicity
—deficiency may lead to schizophrenia
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11
Q

Tell me about the ionotropic glutamate receptors

A

-Na+ selective channel
——NMDA, main one, allows in Ca2+, too
-needs glycine as co-agonist
-must be depolarized to work (blocked by Mg2+ @ RMP)
-antagonists: PCP, ketamine
-crit for synaptic plasticity, network assoc., memory

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12
Q

metab glutamate receptors?

A

signal via GPCR —> ∆s intracellular Ca2+ or adenyl cyclase —> cAMP

  • also memory
  • Agonists of Group II ? tx anx & schizo
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13
Q

GABA (gamma-aminobutyric acid):

  • inhib or excitatory?
  • where made?
  • binds what receptors?
  • role?
  • drugs affecting?
  • clinical action?
A
  • INHIBITORY
  • made by interneurons from glutamate via glutamic acid decarboxylase (GAD)
  • GABA(A), GABA(B) and GABA(C)
  • benzos, barbiturates, EtOH, general anesthetics
  • anxiolytic, musc relax, anesthesia, anti-sz, sedation
  • *may be excitatory in utero/in neonates
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14
Q

GABA(A)

  • type?
  • subunits?
  • drugs?
A

—ionotropic (ligand gated ion channel)
—GABA—>α-subunit—>Cl- influx—>hyperpol—> inhib
—barbiturates bind β-sub
—benzos bind between α-γ

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15
Q

GABA(B)

  • type?
  • drugs?
A

—metabotrop —> causes nearby Ca2+ channel closure and K+ opening (K+ efflux)—>hyperpol—> inhib
—baclofen is selective GABA(B) agonist; antiplasticity tx in ALS and MS

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16
Q

GABA(C)

  • type?
  • drugs?
A

AKA GABA(A-ρ_ receptor (only have one subunit-ρ)
—Ionotropic —> Opens Cl- Channels (inhib)
—High expression in retina, spinal cord and pituitary
—**Not modulated by benzos, barbiturates, or baclofen

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17
Q 
Acetylcholine is:
...mainly excit or inhib?
...neurotransmitter for?
...bound by what receptors?
...enzymes involved include?
A

—mainly EXCITatory
—neurotrans for NMJ, parasmyp, CNS
—bound by Nicotinic (ionotrop w/ Na+) and muscarinic M1-M5 receptors (GPCR, metab)
—made by ChAT (decr in AD); degraded by AChE

18
Q

nicotinic receptors

A

—Ionotropic Opens Na+ —> depolarization (EPSP)
—CNS and periphery in mammals
o Agonists: nicotine (addictive, anxiolytic, analgesic, increases alertness); epibatidine*, & choline

*analgesic frog poison

19
Q

Muscarinic Receptors

A 
M1, M3, M4, M5: CNS
M2: Heart
M3: smooth muscle
Antagonists: Atropine (M1-5; mydriatic; ACLS); Scopolamine (M1; motion sickness, salivation)
Agonists: Muscarine (M1-M2), carbachol
(M1-5), Pilocarpine (M3; glaucoma)
20
Q

Name some AChE inhibitors

A

for dementia/AD: donepezil (Aricept), tacrine, galantamine, rivastigmine
**pesticides, nerve gases

21
Q

What are the subclasses of monoamines?

A

catecholamines: dopamine, NE, epi
tryptamines: 5-HT, melatonin
histamine

22
Q 
Dopamine:
—inhib or excite?
—made from/in?
—activates which/what receptors?
—involved in?
—degraded by?
A

Dopamine:
—D1&5: EXCITE; D2,3,4: INHIB
—made from/by/in L-tyrosine in VTA and sub nigra
—activates D1-D5 metabo. GPCRs
—involved in behavior, cognition, motor activity, motivation, reward, addiction
—degraded by COMT and MAO

23
Q

Dopamine receptor families w/ mech?

A

—D1 Family (D1, D5) increases adenylyl cyclase —> excitat.

—D2 Family (D2, D3, D4) increases PDE and —> inhibit.

24
Q

Dopamine receptor pathways?

A

1) Nigrostriatal (Subs. Nigra—>striatum)—>Parkinson’s
2) Mesolimbic (VTA—>N.accumbens, amygdala)—> Schizophrenia, Addiction
3) Mesocortical (VTA—>[?PF]Cortex)—>Schizophrenia
4) Tuberoinfundibular (Hypothalamus—>pituitary) = steroid effects

25
Q

Dopaminergic drugs for Parkinson’s?

A

L-Dopa
COMT inhibs
DOPA decarboxylase inhibs
DA agonists

26
Q

Methylphenidate MOA?

A

dopamine reuptake inhibitor

27
Q

Amphetamines

A

Induces DA release

28
Q

Cocaine

A

prevent DA reuptake

29
Q

Antipsychotics (e.g. clozaril)

A

D2 Receptor Antagonists

30
Q 
Norepi
—made from/in?
—activates what receptors?
—involved in?
—degraded by?
—reuptake by?
A

—Made from L-Tyrosine via Dopamine in Locus Coeruleus,Caudal Raphe Nucleus
—Activates Metabotropic (α/β adrenergic receptors) —> ∆s intracellular cAMP
—Involved in arousal, attention, focus.
**Disorders:depression,ADHD,phobias,pain **Main NT in symp sys
—Degraded by MAO and COMT
—Reuptake by NET (NE Transporter)

31
Q

clonidine: MOA, type and indications

A

—α2 agonist
—works both pre-and post-synaptically
—Neuropathic pain, opioid detoxification, ADHD, Tourette’s

32
Q 
5-HT (Serotonin)
—made from/in?
—activates what receptors?
—metab or iono?
—involved in?
—degraded by?
—reuptake by?
A 
—made from L-tyrptophan
—activates 5-HT(1-7) receptors
—5-HT1&2: metab; 5-HT3 iono, excitatory
—involved in anger, aggression, mood, sleep, sexuality, appetite, pain
—degraded by MAO
—reuptake by SERT
33
Q

TCA MOA?

A

tricyclics block serotonin transporter (SERT)

34
Q

sumatriptan MOA

A

5-HT(1B)

35
Q

ondansetron MOA

A

5-HT(3)

36
Q

psychedilc MOA (LSD, ecstacy, peyote)

A

5-HT(2A)

37
Q

Histamine
—receptors
—neuro effects?

A

H1-4

H1 —> imp for arousal (?JXC: drowsiness with anti-histamines)

38
Q

Purinergic receptors:

  • -types?
  • -subunits?
  • -drugs?
A

types = P1 & P2

P1 - Adenosine receptor, modulate cAMP, blocked by caffeine
—A1: decr HR
—A2A: conorary vasodilation, decr DA
—A2B: bronchoconstriction
—A3: smm constric; card musc relax

P2 = ADP, ATP receptors, IONOtropic
—P2x: mod synap transmiss (nociception/pain)
——effect on muscle contract (heart SMM of vas def)
—P2y: metabo (GCPR)

39
Q

Cannabinoids
—receptors
—neuro effects?
—agonists?

A

metabotropic GCPR
—CB1: inhib GABA (inhibiting the inhibition of DA)
——anandamine: endogenous CB1 agonist that attenuates pain, present in chocolate
——∆9-tetrahydrocannabinal; cannabidiol (anti-psychotic)

—CB2: immune system

40
Q 
Opiods
—receptors
—neuro effects?
—Drugs?
—endogenous agoninsts?
A

Opioid receptors are metabotropic
—Mu, Delta, Kappa, nociceptin
—Effect depends on receptor and opioid
—Endogen.: endorphins, enkephalins, dynorphins (may be inv w/ drug abuse, antidepressant activity and chronic pain)

SBM Neuro (29 decks)

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