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PRITE Ninja 2022 > Receptors, Neurotransmitters, and Signal Transduction > Flashcards

Receptors, Neurotransmitters, and Signal Transduction Flashcards

1
Q

Receptors are made up of protein chains that span a membrane and thus have what three parts?

A

Extracellular
Transmembrane
Intracellular

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2
Q

The neurotransmitter (NRT) binding site is generally on the ___ portion of the receptor.

A

Transmembrane

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3
Q

How are receptors categorized?

A

By the number of times the protein chain loops within the membrane

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4
Q

What are the two major receptor categories?

A
  1. Ionotropic receptors
  2. Metabotropic receptors
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5
Q

How many receptors combine to form an ionotropic receptor? The individual receptors that combine are what type?

A

5; 4 transmembrane region types

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6
Q

What happens at an ionotropic receptor?

A

NRT binds –> Na influx (excitation) or Cl influx (inhibition) through the receptor channel; note this is a fast response

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7
Q

List examples of ionotropic receptors

A

NMDA
Nicotinic (ACh)
5HT-3
GABA-A

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8
Q

List 3 types of metabotropic receptors.

A
  1. G-Protein Coupled Receptors
  2. Receptor Tyrosine Kinases
  3. Nuclear Receptors
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9
Q

GPCRs often have ___ (#) transmembrane regions and use a second messenger system. Explain.

A

7; NRT binds on external site; receptor transforms; activates 3 G-Proteins; activates an enzyme; creates a second messenger (usually cAMP or IP3); activates a protein kinase; phosphorylates (activates) a transcription factor; binds to an inactive gene to activate it; RNA transcribes and makes proteins

This is a slow response.

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10
Q

While ionotropic receptors are involved in changes in cell excitability GPCRs have what direct effect?

A

Gene transcription, resulting in widespread changes in the cell

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11
Q

When can GPCRs have a fast response (instead of the usual slow response leading to gene transcription)?

A

When they change membrane permeability to ions

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12
Q

Which receptors constitute 80% of all known receptors in the body?

A

GPCRs

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13
Q

List 4 examples of GPCRs.

A
  1. ACh
  2. Catecholamines (NE, Epi, DA)
  3. Peptides
  4. 5HT
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14
Q

What are Receptor Tyrosine Kinases?

A

Receptors that are mainly influenced by growth factors and neutrophic factors, which are involved in axon generation, migration, neural plasticity, and regulation of apoptosis

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15
Q

How do receptor tyrosine kinases work?

A

BDNF or another neutrophic factor binds to two inactive monomers -> dimerization -> phosphorylation of cytoplasmic tyrosine -> activation of enzymes -> genetic transcription -> synaptic plasticity

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16
Q

List the basic action of the following receptors:
1. Ionotropic
2. GPCRs
3. Receptor TK
4. Nuclear Receptors

A
  1. Excitability
  2. Genetic transcription (can also lead to excitability)
  3. Synaptic Plasticity
  4. Genetic transcription
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17
Q

How do nuclear receptors work?

A

Lipophilic ligands (hormones) pass through the membrane and bind to floating intracellular receptors; receptor-ligand complex enters the nuclear, binds to hormone-specific regions of DNA, and leads to gene transcription

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18
Q

What are autoreceptors?

A

Inhibitory pre-synaptic GPCRs specific to NRT release

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19
Q

What are somatodendritic autoreceptors and what do they do?

A

Located on cell bodies and dendrites, these regulate the presynaptic neuron’s firing rate; generally inhibitory (open K channels, reduce cAMP)

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20
Q

As an example of somatodendritic autoreceptors, what do 5HT-1A autoreceptors do?

A

Decrease 5HT firing rate/amount

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21
Q

What do nerve terminal autoreceptors do? Give an examples.

A

Decrease the amount of NRT released by closing Ca channels; alpha-2 adrenergic receptors inhibit NE release (clonidine’s MOA)

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22
Q

What are heteroreceptors?

A

Presynaptic GPCRs - non-specific, not always inhibitory

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23
Q

Give 2 examples of heteroreceptors.

A

5HT presynaptic heteroreceptor on DA neuron decreases firing rate/amount of DA released (atypical antipsychotics MOA)

NE alpha-1 presynaptic heteroreceptor on 5HT neuron increases 5HT firing

24
Q

Describe the process of desensitization of a GPCR.

A

A GPCR with chronic agonist activation can be desensitized. In this process, the receptor gets overphosphorylated –> arrestin proteins bind –> blockade of G-protein cascade –> receptor reset

25
Q

Describe the process of GPCR down-regulation.

A

After prolonged desensitization, the GPCR is internalized and degraded, leading to less GPCRs, decreased production of GPCRs on the genetic level.

26
Q

Give an example of GPCR down-regulation as it relates to SSRIs.

A

SSRIs chronically activate 5HT-1A autoreceptors, causing downregulation, where the autoreceptors are degraded and less are produced. This results in less 5HT-1A autoreceptors, more 5HT, and improvement in depression due to changes at the genetic level

27
Q

Given an example of GPCR upregulation related to antipsychotics.

A

Chronic antagonism of GPCRs (like antipsychotics on DA neurons) leads to more receptors on the membrane and increased sensitivity to NRT

28
Q

Discuss TD as a consequence of upregulation.

A

Chronic D2 blockade leads to making more D2 receptors (in areas responsible for movement); leads to increased sensitivity to DA

29
Q

Unlike EPS, why do anticholinergic medications make TD worse?

A

Anticholinergics decrease ACh and increase DA. EPS is caused by too little DA, so adding DA improves the condition. TD is caused by hypersensitivity to DA from adding too many receptors. Increasing DA with anticholinergics worsens TD.

30
Q

___ allow the presynaptic genome to communicate with the postsynaptic genome.

A

Neurotransmitters

31
Q

List 5 criteria that define NRTs.

A
  1. Synthesized and released from neurons
  2. Released from nerve terminals in a chemically or pharmacologically identifiable form
  3. Interact with postsynaptic receptors and bring out same effects as are seen with stimulation of the presynaptic neuron (not sure what this means?)
  4. Interaction with the postsynaptic receptor displays a specific pharmacology
  5. Actions are terminated by active processes
32
Q

What are the three dimensions of neurotransmission?

A
  1. Space
  2. Time
  3. Function
33
Q

Discuss the “space” dimension of neurotransmission.

A
  • Signals can be local or distant
  • Addressed anatomically: presynaptic electrical signal -> postsynaptic chemical messenger via direct communication
  • Addressed chemically: NRT diffuses across far distances, binding to receptors based on affinity/compatibility
34
Q

Discuss the “time” dimension of neurotransmission.

A
  • Fast vs. slow-onset signals
  • Fast: ion channel receptors change membrane permeability/excitability (eg, NMDA, GABA, glutamate)
  • Slow: second messengers change genetic transmission (eg, monoamine like NE, DA, 5HT)
35
Q

Discuss the “function” dimension of neurotransmission.

A
  • Presynaptic electrical impulse -> opens calcium channels -> anchors synaptic vesicles containing NRT to membrane -> spills NRT into synaptic cleft
36
Q

Compare monoamine NRTs to neuropeptide NRTs with respect to function.

A

Monoamine NRTs are packed with enzymes which make more NRT and have transports for NRT reuptake.

Neuropeptide NRTs do not have reuptake transmitter. Here, a chemical NRT binds a receptor and starts a chemical cascade (second messenger) or is converted to an electrical signal (ion)

37
Q

List 9 categories of NRTs.

A
  1. Amines
  2. Cholinergic
  3. Amino acids
  4. Primary peptides
  5. Circulating hormones
  6. Hypothalamic-releasing hormones
  7. Gut hormones
  8. Opioid peptides
  9. Gases
38
Q

Monoamines are derived from aromatic amino acids like tyrosine, tryptophan, and phenylalanine. They are packed into vesicles by ____ for release and have reuptake transporters. List 6 examples.

A

VMAT;

5HT, DA, NE, E, melatonin, histamine

39
Q

List 1 example of cholinergic NRT.

A

ACh

40
Q

List 4 examples of amino acid NRTs.

A

GABA, glycine, glutamate, aspartate

41
Q

List 6 examples of primary peptide NRTs.

A

ACTH, GH, oxytocin, vasopressin, TSH, Prl

42
Q

List 8 examples of circulating hormone NRTs.

A

Angiotensin
Glucagon
Insulin
Calcitonin
Estrogen
Androgen
Progestin
Thyroid hormone

43
Q

List 3 examples of hypothalamic-releasing hormone NRTs.

A

CRH
GnRH
Somatostatin

44
Q

List 5 examples of gut hormone NRTs.

A

CCK, gastrin, motilin, secretin, VIP

45
Q

List 2 example of opioid peptide NRTs.

A

Endorphins, enkephalins

46
Q

List 2 example of gas NRTs.

A

NO
CO

47
Q

What are co-transmitters?

A

Neurons with >1 NRT release both simultaneously for combined or interactive effects

48
Q

What are allosteric interactions?

A

Each receptor has a primary NRT. Allosteric interaction is the effect of a 2nd NRT (or medication) on that receptor.

49
Q

Give 2 examples of allosteric interactions (alcohol; SSRIs)

A

Alcohol: positive allosteric effects on GABA receptor (increases GABA’s action on Cl channels)

SSRIs: negative allosteric effects on 5HT reuptake transporter

50
Q

What are the 4 components of the agonist spectrum of NRT effects?

A
  1. Full agonist
    2 Partial agonist
  2. Antagonist
  3. Inverse agonist
51
Q

What is a full agonist?

A

Drug or NRT that strongly opens ion channels or has 2nd messengers which lead to the greatest effect on gene transcription

52
Q

What is a partial agonist?

A

Weaker effect on ion channels or second messenger symptoms; acts as a weak agonist alone.

53
Q

How do a full and partial agonist interact?

A

In the presence of a full agonist, a partial agonist competes and dilutes the full agonist’s ability (acting antagonistically)

54
Q

What is an antagonist?

A

Has no intrinsic activity of its own; when bound alone, the receptor is in a resting state (channels are neither open nor closed). In the presence of an agonist, an antagonist works to return the membrane to its resting state.

55
Q

What is an inverse agonist?

A

Does the opposite of agonists; most channels have some intrinsic flux of NRTs, but an inverse agonist stops even that.

56
Q

What happens when an antagonist is in the presence of an inverse agnoist?

A

The antagonist would return the channel to its resting state intrinsic activity

PRITE Ninja 2022 (1 decks)

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