Introduction to the ANS Flashcards
1) Does the PNS or SNS dominate in the liver, and what effect will the SNS have?
2) Does the PNS or SNS dominate in the lungs, and what effect does the PNS andd SNS have + what’s it like at rest?
3) Does the PNS or SNS dominate in the eyes at rest, and why? Also what effect does the PNS or SNS have?
1) Largely sympathetic, SNS discharge will stimulate glycogenolyisis and gluconeogenesis
2) PNS dominated. There’s partial constriction so it can both constrict and dilate further.
PNS → bronchoconstriction
SNS → bronchodilation
3) PNS dominated. Because PNS causes partial constriction so that there can be further constriction or dilation from here
PNS → pupil constriction / ciliary muscle contraction
SNS → pupil dilation
What effect will the PNS or SNS have on the following effectors?….
1) Adipose
2) Kidney
3) Ureters and bladder
4) Salivary glands
5) Skin
6) Heart
7) GI
8) Blood vessels (skeletal muscle)
9) Blood vessels (skin, mucous membranes and splanchnic area)
1)
PNS - …
SNS - lipolysis
2)
PNS - …
SNS - ↑ renin secretion
3)
PNS - contraction of detrusor and relaxation of trigone and sphincter (so you pee)
SNS - relaxes detrusor and contracts trigone and sphincter (so you don’t pee, but bladder still fills)
4)
PNS - copious, watery secretions
SNS - thick viscous secretion
5)
PNS - …
SNS - piloerection, ↑ sweating
6)
PNS - ↓ HR and contractility
SNS - ↑ rate and contractility
7)
PNS - ↑ motility and tone, ↑ GI secretions
SNS - ↓ motility and tone, sphincter contraction
8)
PNS - …
SNS - vasodilation
9)
PNS - …
SNS - vasoconstriction
1) Are baroreceptors stimulating or inhibitory to the PNS / SNS?
2) PNS / SNS impact on arterioles?
3) Relationship between BP and baroreceptor firing rate?
4) Describe the arterial baroreceptor mediated normalisation of BP in reponse to a fall in BP, for example after blood loss. Also how does higher baroreceptor firing rate impact the PNS / SNS?
1)
Baroreceptors are stimulatory to the PNS and inhibitory to the SNS
2)
No PNS innervation of arterioles
SNS completely in control - controls constriction and dilation of the arterioles (remember that the SNS causes vasodilation in skeletal muscle and vasoconstriction in the skin, mucous membranes, and splanchnic areas)
3)
Baroreceptor firing rate is directly proportional to BP
4)
Lose fluid → BP falls → baroreceptor firing rate falls → so less stimulation of PNS and less inhibition of PNS → ↑ HR → normalises BP
Describe the PNS and SNS NTs and where they synapse at the pre-ganglionic and post-ganglionic areas
PNS: both pre-ganglionic and post-ganglionic, ACh is released
SNS:
- ACH pre- and NA post-ganglionic to effector organ
- ACh pre- → adrenal medulla → Adrenaline (and noradrenaline) via blood to effector organ
- ACh pre- and post-ganglionic → to sweat glands
1) Describe the PNS and SNS pre-ganglionic : post-ganglionic divergence and why its like that
2) What is the effector and NT from the somatic nervous system?
1)
- PNS is discrete and localised 1:1
- SNS is coordinated and divergent up to 1:20 because SNS post-ganglionic neurones project ut from the sympathetic trunk, so there is mass dicharge from this point
2)
Just one motor neurone innervating skeletal muscle using ACh as the NT
1) Where are nicotinic receptors found?
2) What type of receptors are nicotinic receptors, and how does it work?
3) Why are nicotinic receptors linked to their function?
4) Nicotinic receptors are blocked by?
5) Nicotinic receptors are stimulated by?
1)
- Found in ALL autonomic ganglia
2)
- Type 1 - ionotropic
- ACh binds to receptor and opens an ion channel that allows Na+ / Ca2+ influx and transmission
3)
- They are very rapid because theyre ionotropic, this rapid transmission is important at the autonomic ganglia where they’re situated
4)
- Hexamethonium
5)
- Nicotine / ACh
1) Where are muscarinic receptors found?
2) Muscarinic receptors are stimulated by…?
3) Muscarininc receptors are blocked by…?
4) What type of receptors are muscarinic receptors, and how do they work?
5) How does their speed of transmission compare to with nicotinic receptors?
1)
- Found in any tissue innervated by a post-ganglionic sympathetic fibre and on sweat glands
2)
- Muscarine / ACh
3)
- Atropine
4)
- Type 2 - g-protein coupled. Agonist binds to receptor → G-protein activated → 2nd messenger generated → activation of cell signalling
5)
- Much slower
How does the PNS impact vision?
PNS controls the lens - pupillary constriction and cilary muscle contraction - so it allows you to focus short distance
1) Where are adrenoreceptors found?
2) What type of receptors are adrenoreceptors?
3) What are the 4 subtypes of adrenoreceptors?
4) How are the adrenoreceptors involved in vasculature control?
5) What activates adrenoreceptors?
1)
- At the effector organs at the end of the SNS (synapsing with the SNS post-ganglionic nerve fibres)
2)
- G-protein coupled
3)
- Alpha-1,2
- Beta-1,2
4) Alpha-1 constricts and Beta-2 dilates, so the tone of the vasculature depends on which adrenoreceptor is being stimulated more
5) Stimulated by noradrenaline and adrenaline - produced by the adrenal medulla
Describe noradrenaline synthesis and degradation
- Tyrosine (+tyrosine hydroxylase) → DOPA
- DOPA (+DOPA decarboxylase) → dopamine
- Dopamine is packaged within a vesicle and…
- Dopamine (+dopamine-beta-hydroxylase) → NA
- Upon arrival of an action potential at the post-ganglionic nerve fibres, the vesicle now containing the NA fuses with the cell membrane
- NA diffuses across the synpatic cleft and binds the adrenoreceptors on the effector cells to have an effect
- Uptake 1 - NA back from synapse to neurone and MAO degrades it in mitochondria
- Uptake 2 - NA degraded by COMT in effector cells
Outline the subtypes of muscarinic cholinoceptors
M1 - neural: forebrain learning and memory
M2: cardiac
M3: exocrine and smooth muscle:
M4: periphery: prejunctional nerve endings (inhibitory)
M5: striatal dopamine release
