Autonomic Nervous System Flashcards

1
Q

What are the different parts of the nervous system? What are they used for?

A

nervous system splits into the central nervous system and the peripheral nervous systems
- central nervous system = brain and spinal cord

peripheral nervous system splits into the somatic and autonomic nervous systems

  • somatic = voluntary muscle movement = skeletal
  • autonomic = subconscious/involuntary control systems

autonomic nerves system splits into the parasympathetic and sympathetic nervous systems

  • sympathetic = fight, flight or fright
  • parasympathetic = rest and digest or feed and breed
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2
Q

What is the central nervous system made up of? What do they control/regulate?

A

medulla = brain
- regulates heart rate (cardioaccelerator centre), blood vessel constriction (vasomotor centre), respiration, GI activity

pons
- regulates respiration, pupils

spinal cord
- regulates defecation/urination

hypothalamus

  • sympathetic = lateral and posterior hypothalamus
  • parasympathetic = medial and anterior hypothalamus
  • regulates heart rate, blood pressure, temperature, water/electrolyte balance, hormonal activity
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3
Q

What is the difference between the somatic and autonomic nervous system?
effectors?
what muscles do they act on?
neurotransmitter released? pre vs post-ganglionic nerve fibres?

A

somatic

  • motor neurone targets are muscles or glands
  • acts on the skeletal muscle
  • does not have a post-ganglionic neutron = nerve extends to the skeletal muscle
  • neutrons are always stimulatory = release acetylcholine

autonomic

  • motor neurone targets are muscles or glands
  • acts on the cardiac muscle, smooth muscle and glands
  • pre-ganglionic neurone is thin and myelinated. post-ganglionic neurone is outside the CNS and non-myelinated
  • pre-ganglionic neurons release acetylcholine. post-ganglionic neurons release acetylcholine or noradrenaline ( can be stimulatory or inhibitory)
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4
Q

What is the different between the ganglions of the sympathetic and parasympathetic nervous systems?
length?
neurotransmitters?
receptors for transmitters?

A

parasympathetic

  • long pre-ganglionic neuron and releases acetylcholine
  • short post-ganglionic neuron and releases acetylcholine

sympathetic

  • short pre-ganglionic neuron and releases acetylcholine
  • long post-ganglionic neuron and releases noradrenaline/norepinephrine

ach receptors = nicotinic or muscarinic
ne receptors = alpha adrenergic or beta adrenergic

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5
Q

What are the seven processes in neurotransmitter action? How is it released?

A

neurotransmitter molecules are synthesised from precursors under the influence of enzymes

neurotransmitter molecules are stored in vesicles

neurotransmitter molecules that leak from vesicles are destroyed by enzymes

action potential causes the vesicles to fuse with the presynaptic membrane and release neurotransmitter molecules into the synpase
- calcium stimulates neurotransmitter molecules fusion and release

released neurotransmitter molecules bind with auto receptors on the presynaptic membrane
= inhibits release

released neurotransmitter molecules bind to receptors on the post synaptic membrane

released neurotransmitter molecules are deactivated either by re-uptake or enzyme degradation

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6
Q

What are the different mechanisms of drugs to prevent neurotransmitter action/release?
- antagonist

A

drugs can block the synthesis of neurotransmitter molecules

drugs can cause neurotransmitter molecules to leak out of the vesicles and be destroyed by enzymes

drug blocks release of neurotransmitter molecules from terminal buttons

drug activates autoreceptors on the pre-synpatic membrane to bind with neurotransmitter molecules

drugs act as a receptor blocker on the post-synaptic membrane
- blocks effects of neurotransmitter molecules

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7
Q

What are the different mechanisms of drugs to increase neurotransmitter action/release?
- agonist

A

drugs can increase the synthesis of neurotransmitter molecules
- increase the amount of precursors

drugs can destroy enzymes that would degrade leaked neurotransmitter molecules from vesicles

drug increase the release of neurotransmitter molecules from terminal buttons

drug binds to autoreceptors on the pre-synpatic membrane to block their inhibitory effect

drugs bind to the post-synaptic receptors and activate/increase their effect

drugs block the deactivation of neurotransmitter molecules
- blocks degradation or neuronal re-uptake of neurotransmitter molecules into the pre-synaptic membrane

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8
Q

How is noradrenaline synthesised and released from the nerve terminal?

A

tyrosine enters the nerve
tyrosine is converted into DOPA by tyrosine hydroxylase
DOPA is converted into dopamine (DA) by DOPA carboxylase
dopamine is pumped into a vesicle
dopamine is converted into noradrenaline by dopamine beta hydroxylase
action potential runs down the nerve terminal
action potential activates/opens the calcium channels
calcium influx signals the vesicle to fuse with the pre-synaptic membrane
noradrenaline is released into the synaptic cleft

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9
Q

What are the different routes of action noradrenaline/norepinephrine can take after being released from the nerve terminal?

A

noradrenaline can bind to pre-synaptic receptors/autoreceptors
- inhibits release

noradrenaline can diffuse into the blood

noradrenaline can bind to adrenergic receptors on the post synaptic membrane
- alpha or beta adrenergic receptors

noradrenaline can be metabolised
- will no longer have any action

noradrenaline can be re-uptaken into the pre-synaptic neurone and recycled q

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10
Q

What can block the re-uptake of noradrenaline into the neurone/nerve terminal? What can it result it?

A

cocaine can block the re-uptake of noradrenaline into the nerve terminal
- leads addiction = dopamine and noradrenaline can be retained in the synaptic cleft so effects are felt for longer

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11
Q

What are the drugs that can inhibit noradrenaline release?

A

metyrosine
- can inhibit the conversion of tyrosine to dopa, a step in the synthesis of NA.

reserpine
- can inhibit transport of the transmitter into the vesicles

cocaine or tricyclic antidepressant drugs
- blocks noradrenaline re-uptake into the cytoplasm after it has acted at the receptors

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12
Q

How can adrenergic transmission be terminated? What enzymes are involved in this?

A

diffusion away from receptors
re-uptake into the nerve terminal
enzymatic breakdown

enzymes
Catecholamine-O-Methyl Transferase
- break down catecholamines = noradrenaline, adrenaline and dopamine

Monoamine Oxidase

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13
Q

Where is adrenaline/epinenephrine released from? What causes adrenaline release?

A

adrenal medulla

adrenaline release is caused by noradrenaline binding to adrenergic receptors on the adrenal medulla

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14
Q

Where can adrenaline and noradrenaline bind? What type of receptors are they?

A

bind to

  • alpha adrenergic receptors
  • beta adrenergic receptors

are G protein coupled receptors

  • associated with heterotrimeric receptors = alpha, beta, gamma subunit
  • when bound to GDP they are inactive. when bound to GTP they are active
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15
Q

What is the signalling pathway for adrenaline/noradrenaline binding to beta adrenergic receptors?

A

noradrenaline binds to the beta adrenergic receptor (G protein coupled)
binding causes a conformational change in the heterotrimeric G protein associated with the membrane
- alpha G protein and GTP disassociate from the beta and gamma G protein dimer
- dissociation exposes the binding site for adenylate cyclase that was blocked by the beta and gamma subunits
alpha G protein and GTP complex bind to adenyl cyclase
binding catalyses the synthesis of cAMP from ATP
cAMP activates protein kinase A
PKA phosphorylates proteins in cardiac causing the opening of ion channels
- opens calcium channel in the heart causing cardiac contraction

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16
Q

What is the signalling pathway for adrenaline/noradrenaline binding to alpha adrenergic receptors?

A

noradrenaline binds to alpha 1 adrenergic receptors in the membrane
binding activates phospholipase C within the membrane
phospholipase C acts on phospholipids within the membrane bilayer
-converts phosphotidyl inositol-4,5- bisphosphate (PIP2) into inositol triphosphate (IP3) and diacylglycerol (DAG)
IP3 bind with IP3R on the smooth endoplasmic reticulum
- ER = store of intracellular calcium ions
binding releases calcium ions
calcium ion binds to calmodulin and activates the myosin light chain kinase
causes contraction

DAG activates protein kinase C
PKC phosphorylates proteins and causes contraction

17
Q

What is the difference between alpha 1 adrenergic receptors and alpha 2 adrenergic receptors?

A

alpha 1 receptors are on the post synaptic membrane of the cardiac muscle
- cAMP, PKA pathway and contraction

alpha 2 receptors are on the presynaptic membrane of the nerve terminal

  • bind to released noradrenaline and inhibits its effects
  • negative feedback control system

alpha 2 receptors are also on the post synaptic membrane
- promotes vasoconstriction

18
Q

What are the effects of the subunits of adrenergic receptors?
alpha 1 and 2
beta 1, 2 and 3

A

alpha 1
- constricts visceral smooth muscles

alpha 2
- constriction of smooth muscle = must be blocked to reduce hypertension and vasoconstriction

beta 1

  • increases heart rate and force of contraction
  • via GPCR, adenylate cyclase, ATP to cAMP, PKA
  • in the heart, lipocytes and brain

beta 2

  • relaxes bronchial smooth muscles = opens airways
  • in the smooth and cardiac muscle

beta 3

  • adipose tissue, liberates free fatty acids
  • in the lipocytes