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Receptors and ion channels > autonomic nervous system > Flashcards

autonomic nervous system Flashcards

1
Q

ganglion neurone

A

collection of neuronal bodies found in the voluntary and autonomic branches of the peripheral nervous system (PNS).

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2
Q

Parasympathetic paths

A

Cranial nerve III controls eyes
Vagus nervous system controls glands
sacral s2-s4 controls the bladder and genitals

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3
Q

What acetylcholine affects

A

Somatic- skeletal muscle
Sympathetic-glands, adrenal medulla
Parasympathetic- salivary glands

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4
Q

Types of receptors for acetylcholine

A

Muscuerinic

Nicotonic

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5
Q

Nicotinic acetylcholine receptor

A

Ligand gated channel that has 5 sub units
Has 2 binding spots for Ach
Stimulates adrenaline secretion from adrenal medulla

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6
Q

Muscarinic Ach receptor

A

G protein coupled receptor
Causes release of calcium ions and inhibits
Causes activation of sweat glands

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7
Q

M2 receptor(cardiac)

A

Decreased cAMP
Causes inhibitory affect
Potassium ion increase and calcium ion decrease
Ca2+ decreases heart rate

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8
Q

M1 receptor(neural)

A

Activates phospholipase C increasing IP3 and DAD

Excites CNS and ganglia

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9
Q

M3 receptor

A

Activates phospholipase C and increases IP3 and DAG

Causes smooth muscle contraction and vasodilation

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10
Q

cholinergic transmission

A

Acetylcholine can be taken back to the presynaptic terminal by the transporter choline carrier
Choline can then be catalysed by choline acetyltransferase to form Ach again
This can then be transported back to the vesicle through Ach carrier choline

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11
Q

Drugs on cholinergic transmission

A

Atropine inhibits the effect of acetylcholine by complexing the acetylcholine receptor
Cholinesterase inhibitors function to decrease the breakdown of acetylcholine

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12
Q

depolarizing agents vs nondepolarizing

A

depolarizing muscle relaxants act as ACh receptor agonists, whereas nondepolarizing muscle relaxants function as competitive antagonists

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13
Q

Muscuerinic agonists

A 
Acts for parasympathetic system
Decreased heart rate
smooth muscle contraction
Sweating and salvation 
Affects CNS by causing excitation
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14
Q

Nicotine

A

stimulates ganglia and neuromuscular junction and causes a depolarising block
Depolarising block is now desensitised to anymore depolarisation
It can cause many undesirable effects

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15
Q

Ganglion blockers

A

Block muscle contractions therefore blocking skeletal muscle BY BLOCKING OF nicotine receptors
This can be dangerous because the diaphragm needs to be able to contract so therefore we need artificial ventilation to assist breathing

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16
Q

Non depolarising agents

A

Can be long term, short term or intermediate
Eventually all the drugs will need to be metabolised in the liver and released from the kidney
If these organs are impaired then they can remain in the body longer and cause more effects

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17
Q

Acetylcholine in muscle cells

A

Muscle cells cannot be repolarised so when acetylcholine binds to the receptor they cannot cause further depolarisation causing desensitisation
Phase 2 is consistently depolarised and cannot repolarise causing muscle relaxation

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18
Q

Acetylcholinesterase

A

AChe main function is to hydrolyse acetylcholine in the blood
Causes increased skeletal muscle contraction
Has short, medium and irreversible duration

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19
Q

Sympathetic and parasympathetic systems

A

Sympathetic pathway(adrenergic) uses norepinephrine neurotransmitter and parasympathetic uses acetylcholine

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20
Q

Adrenaline

A

Adrenaline can cause vasoconstriction in vascular beds

There is alpha adrenaline receptor neuroadrenaline> adrenaline>isoproternal

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21
Q

adrenoreceptors

A

Two subtypes for alpha adrenoreceptors
Three subtypes for beta adrenoreceptors
All use G proteins

22
Q

A1 adrenoreceptor

A

Activates phospholipase C increasing IP3 and DAG

Constriction of smooth muscle in blood vessel

23
Q

A2 adrenoreceptors

A

mainly expressed in the presynaptic terminal
Reduces cAMP
Inhibition of neurotransmitters
Decreased insulin secretion

24
Q

adrenoreceptor antagonist

A

Non selective can reduce blood pressure

Selective can cause hypertension

25
Q

B1 adrenoreceptors

A

Mainly expressed in the heart
Use in heart failure which is when heart activity is reduced
Increases cAMP
Increases heart rate and contraction

26
Q

B2 adrenoreceptors

A

Increases cAMP

Relaxes smooth muscle in bronchi

27
Q

B3 andrenoreceptor

A

Exercise’s are mediated by B3 receptors
Increased cAMP
B3 have many clinical usage
renin is a Chemical substance produced in the kidney and activated during exercise
Can be used to correct irregular heart contraction and chest pain

28
Q

B adrenoreceptor antagonist

A

Decrease blood pressure and sympathetic output

B adrenoreceptor causes reduction of heart rate and reduces bronchoconstriction

29
Q

Selectivity in drugs

A

Ideal drug will be selective to a certain subtype
beta 1 adrenoreceptor specific to slow heart rate
Drugs are selective not specific

30
Q

Adrenergic neurotransmission

A

Processes in the synapse of somatic nerve terminal
Localised effect on vasoconstriction)Noradrenaline
CA has 3 neurotransmitters that is secreted at adrenal medulla into the blood and cause a widespread effect

31
Q

CA

A

Adrenaline, noradrenaline and dopamine secreted as a hormone to cause widespread effect

32
Q

synthesis of CA

A

Synthesis of CA uses multiple enzymes to catalyse the reaction
First enzyme adds an hydroxyl group
Next enzyme removes of carboxyl group
Next enzyme adds a hydroxyl group on to form noradrenaline
PNMT adds another carboxyl group
The first enzyme called Tyrosine hydroxlase is red limiting step and is critical for all production of adrenaline

33
Q

Dopamine in CA

A

Dopamine is transported into the vesicle of nerve terminal by transporter
Once in the vesicle it can form noradrenaline due to the presence of DBH enzyme

34
Q

Noradrenaline in CA

A

Noradrenaline is released via exocytosis calcium is required.
Noradrenaline is released onto post synaptic adrenoreceptors
Indirectly acting sympathomimetic amine promotes the release of noradrenaline
Once noradrenaline is released into the synaptic cleft there can be re uptake and go back into the vesicle again

35
Q

CA stages

A 
synthesis
storage
release
interaction of adrenoreceptors on target organ and glands
Degradation or re-uptake
36
Q

Reuptake of noradrenaline in CA

A

Uptake occurs in the nerve terminals and is transported into the vesicles via VMAT’s

37
Q

Dales principle(outdated)

A

a given neuron contains and releases only one neurotransmitter and exerts the same functional effects at all of its termination sites.

38
Q

co transmission

A

Neurotransmission usually uses co transmission
We know that released neurotransmitters can also act on presynaptic neurones causing pre synaptic modulation
Neurotransmitter release can also vary during development and injury

39
Q

Neuromodulation

A

It is difficult to differentiate from neurotransmissions and neuromodulation
Neuromodulation is usually slower
Neuromodulation acts via second messenger system whereas neurotransmission acts via ligand gated ion channels

40
Q

NANC

Non-adrenergic and non cholinergic transmitters

A

Two types:
Ganglionic transmission:serotonin, GABA and dopamine
Post ganglionic terminal:Nitric oxide

41
Q

Presynaptic modulation

A

Usually inhibitory

Co transmitters can affect transmitter release

42
Q

post nerve terminal tissue

A

Activation of post nerve terminal tisssue cause biological response

43
Q

Homotropic auto inhibition

A

Pre synaptic auto receptor activation causes inhibition of neurotransmitter release in cholinergic and adrenergic

44
Q

hetrotropic presynaptic inhibition

A

Noradrenaline inhibits Ach in nerve terminals
rELEASE neurotransmitter x can act on another nerve terminal which can inhibit neurotransmitter Y and works in the opposite direction

45
Q

Serotonin

A

Inhibits noradrenaline release and causes vasodilation and excitatory effect on eccentric neurones

46
Q

Post synaptic medators

A

Mediators modify excitability
Mediator Y can also cause an individual effect by itself
But when and X and y act together they cause a strong effect
X and Y act on different tissues

47
Q

NPY

A

NPY enhances the function of noradrenaline by increasing calcium

48
Q

Co transmission of ATP and noradrenaline

A

Neuroadranaline and ATP are co stored in the vesicle at a ratio of 4:1
NA can also act on presynaptic a2 adrenoreceptor so GI coupled receptor can inhibit adynlayse cyclase inhibiting cAMP reducing calcium channel function reducing calcium

49
Q

ATP

A

Stored in synaptic vesicle at terminals
Allows for fast transmission in autonomic ganglia
Co transmitter with noradrenaline causes contraction in bladder

50
Q

Nitric oxide

A

Nitric oxide is synthesised from L-argine which is an amino acid
cGMP increases the vasodilation in the lungs
Sildenafil increases NO by inhibiting breakdown of cGMP(Localised effect)
Can reduce blood pressure which can cardiovascular reflex response to reduce vascocontrisction

Receptors and ion channels (8 decks)

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