Neuronal signaling (4) Flashcards

(29 cards)

1
Q

Why must neurotransmitters be removed from the synapse?

A

If neurotransmitters remain active, they could clog the synapse and prevent new signals from being transmitted.

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2
Q

What are the two main mechanisms that terminate synaptic messages?

A
  1. Reuptake by transporters
  2. Enzymatic degradation
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3
Q

What is reuptake?

A

The process where neurotransmitters are drawn back into the presynaptic terminal by transporter mechanisms after being released.

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4
Q

What is enzymatic degradation in the synapse?

A

The breakdown of neurotransmitters by enzymes in the synapse; e.g., acetylcholine is broken down by acetylcholinesterase.

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5
Q

What happens to neurotransmitter molecules and vesicles after deactivation?

A

They are recycled: neurotransmitters or their breakdown products are drawn back into the terminal, and vesicles are reused to create new vesicles.

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6
Q

What roles do glial cells play in synaptic transmission?

A

Glial cells, especially astrocytes, release chemical transmitters, contain neurotransmitter receptors, conduct signals, and influence neuron-to-neuron synaptic transmission.

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7
Q

What are gap junctions?

A

Narrow spaces between adjacent cells bridged by connexins, connecting the cytoplasm of two cells and allowing electrical signals and small molecules to pass directly.

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8
Q

What is the function of gap junctions in the brain?

A

They synchronize the activity of like cells (e.g., inhibitory interneurons or astrocytes) and enable rapid electrical communication via electrical synapses.

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9
Q

Where do gap junctions occur on astrocytes?

A

At the end of astrocytic processes, where they contact adjacent astrocytes’ processes.

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10
Q

Why are glial cells and gap junctions important in modern neuroscience?

A

They play major roles in brain function, including synaptic coordination, rapid communication, and regulation of neuronal activity, challenging the traditional neuron-centric view.

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11
Q

What are the four major classes of neurotransmitters?

A
  1. Amino acids (small-molecule)
  2. Monoamines (small-molecule)
  3. Acetylcholine (small-molecule, in its own class)
  4. Neuropeptides (large-molecule)

Unconventional small-molecule neurotransmitters are sometimes treated separately.

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12
Q

Name the four most widely studied amino acid neurotransmitters.

A

Glutamate, aspartate, glycine, GABA

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13
Q

Which amino acid neurotransmitter is the most prevalent excitatory neurotransmitter in the mammalian CNS?

A

Glutamate

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14
Q

Which amino acid neurotransmitter is the most prevalent inhibitory neurotransmitter?

A

GABA (but it can be excitatory at some synapses)

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15
Q

What are monoamine neurotransmitters, and how are they synthesized?

A

Small-molecule neurotransmitters synthesized from a single amino acid. They include dopamine, norepinephrine, epinephrine (catecholamines from tyrosine) and serotonin (indolamine from tryptophan).

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16
Q

What are the differences between catecholamines and indolamines?

A

Catecholamines (dopamine, norepinephrine, epinephrine) are synthesized from tyrosine. Indolamines (serotonin) are synthesized from tryptophan.

17
Q

What neurons are called noradrenergic, adrenergic, and cholinergic?

A
  • Noradrenergic: release norepinephrine
  • Adrenergic: release epinephrine
  • Cholinergic: release acetylcholine
18
Q

How is acetylcholine synthesized and deactivated?

A

Synthesized by adding an acetyl group to choline. Deactivated by acetylcholinesterase.

19
Q

What are unconventional neurotransmitters?

A

Neurotransmitters with unusual mechanisms, such as soluble-gas neurotransmitters (nitric oxide, carbon monoxide) and endocannabinoids (like anandamide).

20
Q

How do soluble-gas neurotransmitters function?

A

Produced in the cytoplasm, diffuse through cell membranes, act quickly to stimulate second messengers, then are rapidly deactivated. They can act retrogradely from postsynaptic to presynaptic neurons.

21
Q

What are endocannabinoids, and how are they released?

A

Neurotransmitters similar to THC, synthesized from fatty compounds in the cell membrane, released from dendrites and cell bodies, mainly inhibiting presynaptic neurons.

22
Q

How are neuropeptides categorized?

A
  1. Pituitary peptides (first identified as pituitary hormones)
  2. Hypothalamic peptides (first identified as hypothalamus hormones)
  3. Brain–gut peptides (first discovered in the gut)
  4. Opioid peptides (similar to opium compounds)
  5. Miscellaneous peptides (not in other categories)
23
Q

What is the general function difference between small-molecule neurotransmitters and neuropeptides?

A
  • Small-molecule neurotransmitters: rapid, brief, localized signals
  • Neuropeptides: slow, long-lasting, diffuse signals
24
Q

What are the two fundamental effects drugs can have on synaptic transmission?

A
  • Agonists: facilitate the effects of a neurotransmitter
  • Antagonists: inhibit the effects of a neurotransmitter
25
What are the seven general steps common to most neurotransmitters in synaptic transmission?
1. Synthesis of the neurotransmitter 2. Storage in vesicles 3. Breakdown of leaked neurotransmitter in the cytoplasm 4. Exocytosis (release) 5. Inhibitory feedback via autoreceptors 6. Activation of postsynaptic receptors 7. Deactivation
26
How do agonistic and antagonistic drugs influence synaptic transmission?
- Agonists can bind to and activate postsynaptic receptors. - Antagonists (receptor blockers) bind to postsynaptic receptors without activating them, blocking the normal neurotransmitter.
27
What is atropine, and how does it act as a drug?
- Main active ingredient of belladonna - Receptor blocker (antagonist) of muscarinic receptors - Pupillary dilation via ANS; high doses disrupt memory via CNS
28
What is curare, and how does it affect synaptic transmission?
- Nicotinic receptor antagonist - Blocks transmission at neuromuscular junctions, causing paralysis - Used in small doses in surgery to prevent muscle contraction
29
What is Botox, and how does it affect neurotransmission?
- Nicotinic antagonist - Blocks release of acetylcholine at neuromuscular junctions - Toxic in large doses, but used medically (tremor reduction) and cosmetically (wrinkle reduction) in small doses