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Neuro II - Exam 1 > CNS Neurotransmitters and Receptors (Linger) - SRS > Flashcards

CNS Neurotransmitters and Receptors (Linger) - SRS Flashcards

1
Q

What are the 4 main types of NT’s for the CNS?

A
  • AA transmitters
  • Small molecule transmitters
  • Peptides
  • Endocannabinoids
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2
Q

What are the amino acid transmitters?

Which are excitatory?

Inhibitory?

A
  1. Excitatory
    1. Glutamate
    2. Aspartate
  2. Inhibitory
    1. GABA (gamma amino butyric acid)
    2. Glycine
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3
Q

What are the small molecule transmitters?

A
  1. Acetylcholine
  2. Monoamines
  3. Histamine
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4
Q

So, monoamines are small molecule transmitters eh? What are the monamines we need to know?

A
  • Catecholamines
    • Dopamine
    • Norepinephrine
  • Serotonin (5-hydroxytryptamine, 5-HT)
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5
Q

What are the peptide NT’s?

A
  1. Opioids
  2. Tachykinins
  3. Many others
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6
Q

What are the endogenous opiod NT’s?

A
  • Enkephalins
  • Endorphins
  • Dynorphins
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7
Q

What is the tachykinin we need to know?

A

Substance P

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8
Q

What are the ten sites of drug action that allow alteration of synaptic transmission?

A
  1. Action potential in presynaptic fiber
  2. synthesis of transmitter
  3. storage
  4. metabolism
  5. release
  6. reuptake into the nerve ending or uptake into a glial cell
  7. degradation
  8. receptor for the neurotransmitter
  9. receptor-induced increase or decrease in ionic conductance
  10. retrograde signaling.
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9
Q

What are teh three basic criteria that define classical NT’s?

A
  • Localization - NT must be localized to the presynaptic terminal
  • Release - The transmitter must be released from the presynaptic terminal in a calcium-dependent manner, concomitantly with presynaptic nerve activity
  • Synaptic mimicry -
    • Exogenous application of the transmitter should mimic the action of presynaptic nerve stimulation
    • Pharmacological agonists and antagonists should mimic and block the transmitter action, respectively
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10
Q

What NT’s are not synthesized or stored in the presynaptic terminal?

A

Retrograde messengers - e.g. endocannabinoids

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11
Q

What are five examples of NT’s that activate ionotropic receptors from this DSA?

A
  1. Glutamate
  2. GABA
  3. Acetylcholine
  4. Glycine
  5. Serotonin
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12
Q

Metabotropic receptors indirectly modulate ion channels. What type of receptor are they?

A

GPCRs

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13
Q

What is the major functional effect of metabotropic receptors?

A

signal amplification, which can be excitatory or inhibitory depending on the G protein activated and the downstream effector protein

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14
Q

What are some of the key second messengers and signaling effectors mediated by metabotropic receptors?

A
  1. Adenylate cyclase and cyclic adenosine monophosphate (cAMP)
  2. Polyphosphoinositide products:
    1. Diacylglycerol (DAG)
    2. Inositol-triphosphate (IP3)
  3. Ion conductance (Ca++, K+, Na+, or Cl-)
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15
Q

What are some examples of NT’s that activate metabotropic receptors?

A
  1. Glutamate
  2. GABA
  3. Acetylcholine
  4. Dopamine
  5. Norepinephrine
  6. Serotonin
  7. Histamine
  8. Neuropeptides
  9. Endocannabinoids
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16
Q

Glutamate receptors include ionotropic and metabotropic. What are the types of ionotropic receptors?

A
  • Non-NMDA
  • NMDA
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17
Q

What are the non-NMDA receptors glutamate hits?

A

AMPA, Kainate

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18
Q

What do AMPA receptors do?

A

Mediate the vast majority of excitatory synaptic transmission in the brain via ligand gated sodium/potassium channels. (some are also permeable to calcium)

19
Q

NMDA receptors are ligand gated sodium/calcium channels that are also highly calcium permeable. Overstimulation of these receptors is especially important in what conditions?

A

Ischemia and hypoxia d/t stroke mostly, where calcium influx via these receptors triggers apoptosis

20
Q

What are two non-competative agonists for the NMDA receptor that are used recreationally/illegally?

What do they do at low doses?

High doses?

A

PCP and ketamine

Low = hallucinations and delusions

high = dissociative anesthesia

21
Q

what do postsynaptic metabotropic glutamate receptors do?

A

Decreases K+ conductance; Increases IP3, DAG

22
Q

What do presynaptic metabotropic receptors for glutamate do?

A
  1. Decreases Ca++ conductance (INHIBITORY); Decreases cAMP
23
Q

how does glutamate contribute to migraines?

A

excessive glutamate release contributes to the cortical spreading depression implicated in the aura of migraine headache

24
Q

Excessively rapid or sustained firing of a relatively small group of glutamatergic neurons in one region of the brain may rapidly lead to successive excitation of ever larger numbers of glutamatergic neurons until a major region of the brain is evoked into a paroxysmal discharge.

This can cause what potential outcomes?

A
  • Seizure
  • prolonged seizures and stroke can lead to apoptosis
25
Q

What degerative disease may glutamate have a hand in?

What does this allow for as far as tx options go?

A

AD - NMDA receptor antagonist memantine is used to treat moderate to severe dementia of the AD type.

26
Q

How is the NMDA receptor a “coincidence receptor”?

A

A single synaptic input results in the generation of a short-lasting excitatory postsynaptic potential (EPSP) that is mediated entirely by AMPA receptors. (B) When multiple inputs occur simultaneously, nerve depolarization removes the Mg++ block in NMDA receptor channels and the same single synaptic input generates a longer-lasting EPSP that is mediated by both AMPA and NMDA receptors. Thus, the NMDA receptor can “sense” the activity in adjacent inputs.

27
Q

How is GABA inactivated?

A
  1. terminated by rapid reuptake by several types of plasma membrane transporters; GABA is also taken up by glial cells
28
Q

What type of receptors are GABAA?

A

Ionotropic

29
Q

What type of receptors are GABAB?

A

Metabotropic

30
Q

What are some drugs that bind to GABAA Receptors?

A

Benzodiazepines

barbituates

ETOH

31
Q

Benzodiazepines (e.g., alprazolam (Xanax), diazepam (Valium), midazolam (Versed), Clonazepam (Klonopin)) are used to treat what disorders?

4

A
  1. generalized anxiety disorder,
  2. panic disorders,
  3. sedation
  4. sleep disorders
32
Q

What are barbiturates used for? 2

A

Sedative-hypotics

antiepileptics

33
Q

Glycine works via ligand gated Cl- channels. What is a toxin that inhibits its release?

A

Tetanus toxin

34
Q

What is an antagonist of glycin?

A

strychnine

35
Q

At what receptors does glycine act as a co-agonist with glutamate?

A

NMDA

36
Q

Parkinsons involves degeneration of dopaminogenic neurons in what structure primarily?

A

The striatum

37
Q

What is a disease state that involves increased DA activity?

A

Psychosis (schizophrenia), thus D2 receptor antagonists are the classic therapy.

38
Q

Cocaine abuse has what impact on DA?

A

Blocks DA uptake

39
Q

What do amphetamines do to DA?

A

Increase release

40
Q

Ventral tegmental DA pathways mediate the subjective effects of drugs of abuse in what pathway?

A

the reward pathway

41
Q

What are the receptor types for NE?

A

All metabotropic

42
Q

What does substance P do?

A

NT for sensory afferent neurons that mediate pain

43
Q
A

Neuro II - Exam 1 (6 decks)

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