General Concepts of the PNS and Neurotransmitters Flashcards Preview

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Flashcards in General Concepts of the PNS and Neurotransmitters Deck (42)
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1
Q

Synaptic transmission

A

When signaling factors (neurotransmitters) are released from one neuron and bind to the receptors of another neuron across a synaptic cleft.

2
Q

What determines how many transmitters should be released?

A

The amplitude of the action potential determines the amount of transmitters released.

3
Q

What role does Ca++ play in synaptic transmission?

A

When the presynaptic AP depolarizes the membrane, it opens the voltage-gated Ca++ channels. The influx of Ca++ causes vesicles in the axon terminal of the presynaptic neuron to empty quantum of transmitters into the synaptic cleft.

4
Q

What determines the action of a neurotransmitter?

A

Its receptors. One neurotransmitter can have different actions depending on the different receptors that bind it.

5
Q

What are the two types of cholinergic synapses?

A

Nicotinic - on neurons and skeletal muscle Muscarinic - on body tissues and CNS neurons

6
Q

What is an agonist substance? Give some examples.

A

A substance that mimics a naturally occurring signaling factor and binds to the same receptors to stimulate an action E.g. nicotine and muscarine can mimic acetyl choline

7
Q

Which neurotransmitters are released at adrenergic synapses? What are they classified as?

A

The catecholamines: norepinephrine, epinephrine, and dopamine.

8
Q

Which neurotransmitters stimulate adrenergic receptors?

A

Norepinephrine and epinephrine.

9
Q

Which catecholamine has its own receptor?

A

Dopamine.

10
Q

Describe the metabolism of ACh.

A

Choline acetyltransferase synthesizes ACh from acetyl CoA and choline in the presynaptic terminal. Acetylcholine esterase (AChE) breaks it down into choline and acetate in the synaptic cleft.

11
Q

What is the action (type of neurotransmission) of a nicotinic receptor?

A

Ionotropic transmission: it opens up a Na+/K+ channel

12
Q

What is the action (type of neurotransmission) of a muscarinic receptor?

A

Metabotropic transmission: uses G-proteins for its actions

13
Q

Compare the duration of the effects of muscarinic and nicotinic receptors.

A

Nicotinic receptors: short-term synaptic effects Muscarinic receptors: prolonged synaptic effects

14
Q

Where are nicotinic receptors located?

A

Autonomous ganglion neurons and skeletal muscles.

15
Q

Where are muscarinic receptors located?

A

Throughout the CNS and in tissues innervated by postganglionic parasympathetic and some sympathetic neurons.

16
Q

How do epinephrine and norepinephrine get removed from the synaptic cleft?

A

Reuptake or destruction by monoamine oxidase (MAO) or catechol-O-methyl transferase

17
Q

Describe the sequence of catecholamine synthesis from tyrosine.

A

Tyrosine –> L-DOPA –> Dopamine –> Norepinephrine –> Epinephrine

18
Q

What do adrenergic α1-receptors regulate?

A

Ca++ and K+ channels

19
Q

What do adrenergic β-receptors regulate?

A

Smooth muscle, the heart, and metabolism.

20
Q

What is the effect of propanolol on adrenergic receptors?

A

Blocks β-receptors to decrease heart rate.

21
Q

Rank these transmitters in terms of duration of effects (shortest to longest): neuropeptides, adrenergic, and cholinergic transmitters.

A

Cholinergic, adrenergic transmitters, and neuropeptides

22
Q

How do cocaine and amphetamine change the pathway for transmitters?

A

By blocking reuptake, which prolongs the action of the neurotransmitter.

23
Q

How can enzymes change the duration of the neuropeptide transmitter effect?

A

The slow breakdown of neuropeptides by enzymes extends the effect.

24
Q

Compare small molecule and neuropeptide transmitters in terms of synthesis and vesiculation.

A

Small molecule transmitters are synthesized and packaged in the axon terminal (with help from transported enzymes). Neuropeptide transmitters are transported as pre-peptides in vesicles from the cell body and are modified (by transported enzymes) in the axon terminal.

25
Q

What type of receptors (metabotropic or ionatropic) do neuropeptides bind to?

A

Metabotropic receptors (use second messengers)

26
Q

What makes the action and release of a neuropeptide unique compared to other neurotransmitters?

A

They are responsible for long-term changes in ion channel permeability, gene transcription, number of receptors, etc. They are typically co-released with another transmitter and at low thresholds, compared to small molecule transmitters.

27
Q

The peripheral nervous system can be further divided into which two systems?

A

Somatic motor system and the autonomic nervous system.

28
Q

Where are the cell bodies and axons of the _-motor neurons located?

A

Cell bodies are located in the ventral horn of the spinal cord. Axons are projected out to skeletal muscle.

29
Q

Where are the cell bodies and axons of the ANS located?

A

They comprise of two neurons in sequence: pre- and postganglionic neurons. The cell bodies of the preganglionic neurons are found in the intermediolateral column and projects axons to the postganglionic neurons within the autonomic ganglia. The cell bodies of the postganglionic neurons are found at the autonomic ganglia and project axons to smooth muscle, cardiac muscle, and glands.

30
Q

What system does the phrase fight, fright, or flight” typically refer to?”

A

Sympathetic nervous system (part of the ANS).

31
Q

What system does the phrase rest and digest” typically refer to?”

A

Parasympathetic nervous system (part of the ANS).

32
Q

Where are the cell bodies of preganglionic neurons in the sympathetic vs parasympathetic nervous systems?

A

Sympathetic: T1-L2 Parasympathetic: Cranial cells in brain stem, sacral cells of S2-4

33
Q

Compare the innervation of tissues by the somatic motor system and the ANS.

A

Motor neurons have axon branches that innervate single muscle fibers. Postganglionic neurons have axons with varicosities that synapse onto different tissue cells.

34
Q

What is the advantage to innervation by a somatic motor neuron as opposed to autonomic nervous system neuron?

A

More specificity.

35
Q

Which transmitter is used in all preganglionic neurons? Which receptor does it bind to at the ganglia synapse?

A

Acetyl choline (ACh), which binds to nicotinic receptors.

36
Q

Compare the postganglionic axons in the two parts of the ANS in terms of length, target tissue, and action.

A

Sympathetic: long axons project to organs and extremities (blood vessels, sweat glands, etc.); increases HR and BP Parasympathetic: short axons project to organs; lowers HR, promotes GI peristalsis

37
Q

Which parts of the brain directly control the ANS?

A

Hypothalamus through the brain stem directly controls the ANS.

38
Q

What role does the limbic system play in controlling the ANS?

A

It governs the hypothalamus and brain stem.

39
Q

Describe the sequence of events that lead to the release of transmitters into the synapse.

A

1) Presynaptic action potential depolarizes the membrane. 2) Presynaptic voltage-gated Ca++ channels open 3) Ca++ influx triggers vesicles to release transmitters into synaptic cleft

40
Q

If a medicine inhibits acetylcholine esterase, what impact would there be on the innervation of muscle and the activity of sympathetic and parasympathetic systems?

A

Increase ACh levels and produces extreme ANS responses: contraction of skeletal muscle, release of epinephrine from adrenal medulla, stimulation of both the sympathetic and parasympathetic systems.

41
Q

If a medicine specifically activated nicotinic receptors, what would be the impact on the motor and autonomic activities?

A

Similar to an increase in ACh, it would produce extreme ANS responses: contraction of skeletal muscle, release of epinephrine from adrenal medulla, stimulation of both the sympathetic and parasympathetic systems.

42
Q

If a medicine specifically blocked muscarinic receptors, what would be the impact on the motor and autonomic activities?

A

May have some upstream effects on somatic motor neurons, but no direct effect.

It would impair all parasympathetic and some sympathetic neuronal activity: inhibiting HR deceleration, sweating, digestion, blood vessel dilation, etc.