Block B Lecture 1: Receptors and the ANS Flashcards

1
Q

What 2 systems make up the nervous system?

A

The central nervous system (CNS)
Peripheral Nervous System (PNS)
(Lecture 1, Slide 4)

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2
Q

What 3 branches make up the peripheral nervous system?

A

Sensory
Autonomic
Somatic
(Lecture 1, Slide 4)

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3
Q

What are afferent neurons and what branch of the peripheral nervous system are they found in?

A

They are found in the sensory branch of the peripheral nervous system and are neurons that transmit messages from the sense organs to the CNS
(Lecture 1, Slide 4)

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4
Q

What are efferent neurons?

A

Neurons that transmit messages from the brain to the peripheral nervous system so an action can be performed
(Lecture 1, Slide 4)

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5
Q

What 2 branches make up the autonomic nervous system (ANS)?

A

Sympathetic nervous system
Parasympathetic nervous system
(Lecture 1, Slide 5)

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6
Q

What are ganglia?

A

Clusters of nerve cells (neurons) located outside the CNS
(Lecture 1, Slide 5)

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7
Q

What is the purpose of ganglia in the ANS?

A

They serve as relay points for the transmission of signals between the CNS and target organs or tissues that the ANS supplies with neurons
(Lecture 1, Slide 5)

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8
Q

What is the function of the sympathetic branch of the ANS?

A

It is an “emergency” system that regulates the “fight-or-flight” response
(Lecture 1, Slide 6)

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9
Q

Under what conditions does the actions of the parasympathetic system predominate?

A

Under non-stressful conditions during the in-between times of “rest-and-repair”
(Lecture 1, Slide 7)

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10
Q

What are 3 physical changes in the body that the parasympathetic branch of the ANS can make?

A

Slows heartbeat
Promotes digestion
Triggers gland secretion
(Lecture 1, Slide 7)

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11
Q

What type of receptors are the ones found in the ANS (except nicotinic)?

A

G-protein coupled receptors (GPCRs)
(Lecture 1, Slide 9)

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12
Q

What type of receptor is a nicotinic receptor?

A

A ligand-gated ion channel receptor
(Lecture 1, Slide 9)

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13
Q

What is the purpose of receptors in the ANS?

A

The mediate the action of released transmitters such as acetylcholine, noradrenaline and adrenaline
(Lecture 1, Slide 9)

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14
Q

How long does it take G-protein coupled receptors to react?

A

Seconds
(Lecture 1, Slide 10)

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15
Q

Where are nicotinic receptors found?

A

In the ganglia
(Lecture 1, Slide 11)

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16
Q

What are the 2 agonists for nicotinic receptors?

A

Acetylcholine and nicotine
(Lecture 1, Slide 11)

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17
Q

How many subtypes of muscarinic receptors are there?

A

5
(Lecture 1, Slide 11)

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18
Q

What G protein are the M1, M3 and M5 subtypes of muscarinic receptors coupled to?

A

Gq
(Lecture 1, Slide 11)

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19
Q

What 2 G proteins can the M2 and M4 subtypes of muscarinic receptor able to be coupled with?

A

Gi and Go
(Lecture 1, Slide 11)

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20
Q

What are the 3 agonists for muscarinic receptors?

A

Acetylcholine, muscarine and bethanechol
(Lecture 1, Slide 11)

21
Q

What are the 2 subtypes of α-adrenoreceptors?

A

α1 and α2
(Lecture 1, Slide 12)

22
Q

What G protein are α1 adrenoreceptors coupled to?

A

Gq
(Lecture 1, Slide 12)

23
Q

What 2 G-proteins can α2 be coupled to?

A

Either Gi or Go
(Lecture 1, Slide 12)

24
Q

What are the 2 agonists for α and ß-adrenoreceptors?

A

Noradrenaline and adrenaline
(Lecture 1, Slide 12)

25
Q

What are the 3 subtypes of ß-adrenoreceptors?

A

ß1, ß2 and ß3 receptors
(Lecture 1, Slide 12)

26
Q

What G-protein are the 3 subtypes of ß-adrenoreceptors coupled to?

A

Gs
(Lecture 1, Slide 12)

27
Q

What second messenger is associated with Gq G-protein?

A

PLC (Phospholipase C)
(Lecture 1, Slide 11)

28
Q

What second messenger is associated with Gi, Go and Gs G-proteins?

A

cAMP
(Lecture 1, Slides 11 and 12)

29
Q

What are secondary messengers?

A

Molecules that transmit signals within a cell in response of the binding of a signalling molecule to its receptor
(Lecture 1, Slide 13)

30
Q

How do ß1-adrenoreceptors activate protein kinase A?

A

Noradrenaline binds to the receptor, which activates the receptor and the Gs protein it is coupled to. Gs stimulates adenylate cyclase which catalyses the conversion of ATP to cAMP. cAMP then activates protein kinase A
(Lecture 1, Slide 13)

31
Q

How does protein kinase A increase the force of contraction in the heart after they are activated by ß1 adrenoreceptors?

A

Protein kinase A increases calcium ion (Ca2+) influx by phosphorylating various proteins which leads to increased heart contraction as calcium is an important regulator of muscle contraction
(Lecture 1, Slide 13)

32
Q

What 3 things does an increased force of contraction in the heart lead to?

A

An increased stroke volume (amount of blood ejected from the heart with each contraction)
A temporary rise in blood pressure (to aid in delivering oxygen and nutrients to the body)
An enhanced exercise response
(contraction is increased to meet the bodies increased demand for oxygen and nutrients during exercise)
(Lecture 1, Slide 13)

33
Q

How do α1-adrenoreceptors activate phospholipase C (PLC) enzyme?

A

Noradrenaline or adrenaline binds to the α1-adrenoreceptor activating it and the Gq protein it is coupled with. The activated Gq protein then stimulates phospholipase C (PLC)
(Lecture 1, Slide 13)

34
Q

How does phospholipase C (PLC) activated by α1-adrenoreceptors lead to vascular smooth muscle contraction and therefore vasoconstriction?

A

PLC catalyses the breakdown of phosphatidylinositol 4,5-bisphosphate (PIP2) into inositol triphosphate (IP3) and diacylglycerol (DAG). IP3 then acts on intracellular calcium stores leading to the release of calcium ions (Ca2+) which are important regulates of muscle contraction
(Lecture 1, Slide 15)

35
Q

How is the ANS “a balanced system”?

A

Through sympathetic and parasympathetic functions opposing each other
e.g sympathetic increasing heart rate and parasympathetic decreasing it etc.
(Lecture 1, Slide 18)

36
Q

State 2 examples of the sympathetic and parasympathetic systems having opposing functions.

A

ß1 and ß2 receptors (sympathetic) causing increased heart rate while muscarinic 2 receptors (parasympathetic) lowering heart rate
α1 and α2 adrenoreceptors (sympathetic) causing vasoconstriction in skin skeletal muscle pulmonary and coronary circulation arteries while muscarinic receptors (parasympathetic) cause vasodilation in the same areas
(Lecture 1, Slide 20)

37
Q

What are sympathomimetics?

A

Drugs that mimic the actins of noradrenaline and adrenaline
(Lecture 1, Slide 23)

38
Q

What are α1-adrenoreceptor agonists used to treat?

A

Blocked nose / sinus
(Lecture 1, Slide 23)

39
Q

What kind of drugs are α2 agonists?

A

Centrally acting hypotensive drugs
(Lecture 1, Slide 23)

40
Q

What are ß1-adrenoreceptor agonists sometimes used to stimulate?

A

The force of heart contraction
(Lecture 1, Slide 23)

41
Q

What do ß2-adrenoreceptor agonists cause and what are they used to treat?

A

They cause bronchial dilation and are used to treat asthma
(Lecture 1, Slide 23)

42
Q

How do α1 adrenoreceptor agonists treat congestion?

A

Congestion is caused by vasodilation of nasal blood vessels leading to a narrow nasal pathway.
α1 adrenoreceptor agonists cause vasoconstriction of nasal blood vessels leading to a broad nasal pathway and therefore decongestion
(Lecture 1, Slide 24)

43
Q

What is a brand name of a salbutamol inhaler called?

A

Ventolin
(Lecture 1, Slide 26)

44
Q

Why is salbutamol inhalers being ß2-adrenoreceptor selective good?

A

As it avoids ß1 effects on the heart
(Lecture 1, Slide 27)

45
Q

Why is salbutamol delivered via the lung through an inhaler?

A

As there are some ß2 receptors in the heart
(Lecture 1, Slide 27)

46
Q

Is salbutamol a full or partial agonist?

A

Partial
(Lecture 1, Slide 27)

47
Q

IIs salbutamol short or long acting?

A

Short
(Lecture 1, Slide 27)

48
Q

What do α1-adrenoreceptor blockers (antagonists) reduce?

A

Arteriolar and venous tone
(Lecture 1, Slide 28)

49
Q

What do ß1-adrenoreceptor blockers (antagonists) reduce?

A

Rate and force of contraction of the heart with a lesser effect on blood vessels and bronchioles (as they are mainly controlled by ß2s)
(Lecture 1, Slide 28)