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NEUR3310 Neuroscience > Lecture 4: NEUROMODULATORS > Flashcards

Lecture 4: NEUROMODULATORS Flashcards

1
Q

Define Neuromodulation

A

A change in the state of a neuron or a group of neurons that alters its response to a subsequent stimulation

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2
Q

Neuromodulators commonly act on

A

the release of neurotransmitters from
the axon terminals/presynaptic neuron and/or postsynaptic receptors

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3
Q

2 type of Neuromodulation… techniques..

A

A: Point-to-point neurotransmission

vs

B: Neuromodulation and volumetric neurotransmission

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4
Q

A: Point-to-point neurotransmission

vs

B: Neuromodulation and volumteric neurotransmission

A

A:

  1. INHIBITORY
    Presynaptic neuron = depolarisation
    ….
    Postsynaptic neuron = hyperpolarisation

or
2. EXCITATORY Presynaptic neuron = depolarisation
….
Postsynaptic neuron = depolarisation

B: Look at slide 3

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5
Q

Most neuromodulators bind to….. and therefore….

A

Most neuromodulators bind to ‘GPCRs’ and therefore …

-act on a slower timescale relative to neurotransmitters that bind to ionotropic receptors

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6
Q

Most neuromodulators bind to GPCRs and therefore act on a slower timescale relative to neurotransmitters that bind to ionotropic receptors

Well known examples include 5

A
  1. acetylcholine,
  2. dopamine,
  3. serotonin,
  4. cannabinoids,
  5. nitric oxide
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7
Q

what do neurotransmitters and neuromodulators bind to? 2

A
  1. Many neurotransmitters and neuromodulators bind to ‘GPCRs’
  2. Some neurotransmitters and neuromodulators bind to:
    “ ion channels (ionotropic) and GPCRs (metabotropic)”
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8
Q

NEUROMODULATORS:

EXPLAIN RECEPTORS AND STRUCTURAL FEATURES

CLASS A: rhodopsin family

A

Receptors:
1. LARGEST GROUP
2. RECEPTORS: for most AMINE NEUROTRANSMITTERS, many NEUROPEPTIDES, PURINES, PROSTANOIDS, CANNABINOIDS, etc.

STRUCTURAL FEATURES:
1. Short extracellular (N-terminal) tail
2. LIGAND binds to TRANSMEMBRANE HELICES (AMINES) OR to EXTRACELLULAR LOOPS (PEPTIDES)

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9
Q

NEUROMODULATORS:

EXPLAIN RECEPTORS AND STRUCTURAL FEATURES

CLASS B: secretin/glucagon receptor family.

A

RECEPTORS: for PEPTIDE HORMONES, including SECRETIN, GLUCAGON, CALCITONIN

STRUCTURAL FEATURES:
1. Intermediate Extracellular tail incorporating ligand-binding domian

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10
Q

NEUROMODULATORS:

EXPLAIN RECEPTORS AND STRUCTURAL FEATURES

CLASS C: metabotropic glutamate receptor/calcium sensor family

A

Receptors:
1. SMALL GROUP.
2. METABROTROPIC GLUTAMATE RECEPTORS
3. GABA (b) receptors
4. Ca+2 SENSING RECEPTORS

STRUCTURAL FEATURES:
1. LONG extracellular tail incorporating ligand-binding Domain

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11
Q

Explain the 2 Stages of Neuromodulators

A
  1. RESTING STATE
    - G proteins coupled to receptors
  2. Agonist bind to GPCR
    - G proteins coupled to receptor separate and interact/bind with their targets
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12
Q

draw and label the 2 Stages of Neuromodulators

A

slide 6

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13
Q

What are the roles and characteristics of adenosine in the brain? = 5 and explain

A
  1. Sleep Regulation and Energy Metabolism:
    Adenosine regulates sleep homeostasis and energy metabolism in neurons.
  2. Neuromodulatory Function:
    It acts as a powerful neuromodulator in cholinergic neurotransmission in the brain.
  3. Metabolite of ATP Degradation:
    Adenosine is a metabolite of intracellular ATP degradation, increasing during high periods of neuronal activity.
  4. Production Mechanism:
    ATPases in the membrane degrade released ATP to produce adenosine, which is not stored in vesicles.
  5. Receptor Binding:
    Adenosine binds to G protein-coupled receptors (GPCRs), specifically AxARs, both pre- and postsynaptically, as well as on glia.
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14
Q

How does adenosine exert its neuromodulatory effects, specifically through A1 adenosine receptors (A1ARs), on cortical pyramidal neurons? = 3

A
  1. ‘Neuromodulatory Mechanism’ :
    - A1 adenosine receptors (A1ARs) hyperpolarize cortical pyramidal neurons.
  2. ‘Effect on Potassium Channels:’
    - A1ARs increase the probability of potassium channel opening.
  3. ‘Effect on Glutamate Release’ :
    - They decrease the release of calcium-dependent glutamate by reducing the probability of calcium channel opening.
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15
Q

What is acetylcholine’s role as a neurotransmitter in the periphery? = 2

A
  1. Neuromuscular Junction:
  2. Acetylcholine (ACh) serves as the primary excitatory neurotransmitter at the neuromuscular junction in the periphery.
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16
Q

What role does acetylcholine play as a neuromodulator in the brain? = 2

A
  1. Cholinergic Neurotransmission:
  2. In the brain, acetylcholine acts as a powerful neuromodulator in cholinergic neurotransmission.
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17
Q

How does acetylcholine affect neurotransmitter release, and what factors influence its impact on neural activity? = 2

A
  1. Impact on Neurotransmitter Release:
  2. Acetylcholine tends to increase neurotransmitter release but can either promote or decrease neural activity depending on the system and the neuronal subtype it acts on.
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18
Q

What are some suggested roles of acetylcholine neuromodulation in the brain? = 3

A

Suggested Roles:

  1. Fine-tuning circuits for “uncertainty.”
  2. Reinforcing neuronal loops and cortical synaptics during learning.
  3. Fear conditioning.
19
Q

Where are acetylcholine receptors located in the brain, and what are the main types of receptors? = 4

A
  1. Location:
    Acetylcholine receptors are found both pre- and postsynaptically in the brain.
  2. Types of Receptors:
    Acetylcholine signals through
  3. muscarinic (mAChRs) and
  4. nicotinic (nAChRs) receptors.
20
Q

What are the neuromodulatory actions produced by muscarinic acetylcholine receptors (mAChRs)? = 2

A
  1. Neuromodulatory Actions:
  2. ‘mAChRs produce a range of neuromodulatory actions in the brain’
21
Q

How do presynaptic M2/M4 mAChRs affect cholinergic terminals, and what is their impact on glutamate release? = 4

A
  1. Impact on Cholinergic Terminals:
    …2. Presynaptic M2/M4 mAChRs inhibit cholinergic terminals through autoreception.
  2. Effect on Glutamate Release:
    ….4. They reduce glutamate release.
22
Q

What are the effects of M1/M5 mAChRs on dopamine release and cortical pyramidal neurons? = 4

A
  1. Dopamine Release:
    2…. M1/M5 mAChRs promote dopamine release in the striatum.
  2. Impact on Cortical Pyramidal Neurons:
    4….. They increase the excitability of cortical pyramidal neurons.
23
Q

What are the characteristics and distribution of nicotinic acetylcholine receptors (nAChRs) in the brain? = 4

A
  1. Characteristics:
    2….. nAChRs are non-selective excitatory cation channels.
  2. Distribution:
    ….4. They are dispersed throughout the neuronal membrane, including pre- and postsynaptic regions, soma, and axons.
24
Q

What is the difference in neuromodulation speed between nicotinic acetylcholine receptors (nAChRs) and muscarinic acetylcholine receptors (mAChRs)?… 2

A
  1. Neuromodulation Speed:

2….. Neuromodulation via nAChRs is faster than that via mAChRs due to the ionotropic nature of nAChRs compared to the metabotropic nature of mAChRs.

24
Q

How does activation of nicotinic acetylcholine receptors (nAChRs) influence neurotransmitter release, and what factors contribute to its variability?

= 4

A
  1. Impact on Neurotransmitter Release:
    2…. Activation of nAChRs can increase the release of various neurotransmitters, such as glutamate, GABA, dopamine, and acetylcholine.
  2. Variability:
    4….. The effect varies depending on neuron subtype and neuronal circuit.
25
Q

How do neuropeptides differ from amino acid neurotransmitters in terms of their release sites?

A

Difference in Release Sites:

Neuropeptides are more commonly released at sites outside of the synapse compared to amino acid neurotransmitters like GABA and glutamate.

26
Q

What is the current debate surrounding the diffusion range of neuropeptides compared to amino acid neurotransmitters?

A

Debated Aspect:
It is still debated, but it is suggested that neuropeptides may travel further from their release site than amino acid neurotransmitters.

27
Q

Can you provide an example of neuropeptides traveling long distances to exert their effects?

A

Leptin, a neuropeptide released from the stomach, acts on targets in the brain, suggesting that

neuropeptides may have the ability to travel from distant sites to exert their effects.

28
Q

What type of receptors do most neuropeptides bind to, and what is the primary signaling mechanism involved? = 2

A
  1. ‘Receptor Type’:
    Most neuropeptides bind to G protein-coupled receptors (GPCRs).
  2. ‘Signaling Mechanism’:
    Neuropeptide binding to GPCRs activates multiple intracellular signaling pathways.
29
Q

Where are neuropeptide receptors typically distributed within neuronal structures?

A

Distribution:
Neuropeptide receptors are distributed throughout the neuronal structure, including pre- and postsynaptic regions, soma, and axons.

30
Q

What is the variability in neuropeptide receptor activation, and can you provide examples? = 3

A
  1. Variability:
  2. Neuropeptides may activate multiple receptors in multiple locations, as seen with Neuropeptide Y (NPY).
  3. Some neuropeptides, such as Kisspeptin, act on single receptors.
31
Q

What is a notable characteristic of neurons that release neuropeptides in addition to fast-acting amino acid transmitters?

A

Characteristic:
— Most neurons that release neuropeptides also release fast-acting amino acid transmitters, suggesting a dual mode of signaling.

32
Q

How do neuropeptides modulate presynaptic neurotransmitter release?

A

Modulation:

Neuropeptides can either INCREASE or DECREASE PRESYNAPTIC NEUROTRANSMITTER RELEASE

33
Q

What factors contribute to the specificity of neuropeptide-mediated presynaptic modulation?

A

Specificity Factors:

Neuropeptide-mediated presynaptic modulation is influenced by the peptide type, cell type, and neural circuit involved.

34
Q

What are some of the pathways through which neuropeptides modulate presynaptic neurotransmitter release?

A

Modulation Pathways:

– Neuropeptides exert presynaptic modulation through multiple pathways, including changes toION CHANNEL ACTIVATION AND ION FLOW

35
Q

How is nitric oxide (NO) produced in the brain, and what triggers its production?

A

Production Mechanism:

– NMDA receptor activation triggers the production of nitric oxide (NO)

36
Q

What is a notable characteristic of nitric oxide in terms of its release and diffusion? =3

A
  1. Release and Diffusion:
  2. Nitric oxide is not released by exocytosis;
  3. instead, it diffuses from presynaptic nerve terminals into the extracellular space and nearby cells.
37
Q

How does nitric oxide exert its effects on biological pathways? =3

A
  1. Mechanism of Action:
  2. Nitric oxide does not bind to receptors;
  3. instead, it binds to enzymes, leading to the activation of a range of biological pathways.
38
Q

What are chemokines, and what are they primarily produced and released by?

A

Definition:
Chemokines are small proteins or large peptides.

Source:
They are primarily produced and released by immune cells.

39
Q

What types of molecules are included in the category of chemokines?

A

Molecule Types:
Chemokines are a subset of cytokines, which also include interleukins, interferons, and tumor necrosis factors.

40
Q

What is a relatively new concept regarding the role of chemokines, and what does it suggest about their presence in the brain?

A
  • New Concept:
    The idea of chemokines acting as neuromodulators is relatively new.
  • Implication:
    If chemokines are involved in non-immune functions, they should be present in the intact brain.
41
Q

Where are chemokine receptors typically located, and how do chemokines enter the nervous system? = 4

A
  1. Receptor Location:
    2….. Chemokine receptors are located both pre- and postsynaptically and on glial cells.
  2. Entry into Nervous System:
    4…. Chemokines can be released by cells in the nervous system or enter through the bloodstream from peripheral release
42
Q
A
42
Q

What effects can chemokines have on neurotransmitter release, and what are some additional effects they may produce? = 4

A
  1. Neurotransmitter Modulation:
    — Some chemokines are known to modulate the release of GABA.
  2. Additional Effects:
    — Chemokines can produce either a protective effect or an apoptotic effect, or both.

NEUR3310 Neuroscience (18 decks)

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