ANS Flashcards by Emma Hrvacic

ANS

divided in sympathetic and parasymapthetic + enteric nervous system (GIT)

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preganglionic

lightly myelinated slow conducting, thin, type B
conduction speed = 100 m/s

originates from the intermediolateral area of the grey horn from spinal regions:
T1 - T 12
L1 - L2

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postganglionic

unmyelinated slow conducting, very thin, type C
conduction speed = 1 m/s

ganglion is collection of cell bodies outside of CNS.

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denervation of autonomic nervous system

denervation hypersensitivity as up-regulation of NAChR receptors occurs and there is an exaggerated response to exogenous agonists.

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primary organs ANS

viscera of thoracic and abdominal cavities
cutaneous blood vessels
sweat glands
piloerector muscles

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SNS

originates in ventral/anterior horn and travels uninterrupted.
myelinated fast conducting type A alpha motor neurons. conducting 1000 m/s

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denervation of SNS

flaccid paralysis and atrophy due to lack of innervation and activity at the muscle site

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organisation of sympathetic nervous system

preganglionic originate at the intermediolateral area of grey horn. exit via the ventral roots and enter the sympathetic trunk via white ramus communicans.

synapse in the sympathetic trunk at the same spinal level and can then ascend or descend by entering para vertebral ganglion or passing to collateral ganglia.

postganglionic leave sympathetic trunk via gray ramus.

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somatic neurons

monosynaptic
NT = ACh
receptor = Nicotinic 1 type

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sympathetic neurons

cardiac tissue, smooth muscle and gland cells:
NT = NE
receptor = alpha and beta receptors

sweat glands:
NT = ACh
receptor = Muscarinic

Renal tissue:
NT = dopamine
receptor = dopamine 1

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all preganglionic neurons

NT = ACh
receptor = Nicotinic type 2

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parasympathetic neurons

NT = ACh
receptor = muscarinic receptor

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block N1 type receptor

pancuronium is selective N1 type agonist and is used for general anaesthesia

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block N2 type receptor

trimethaphan is selective N2 type agonist and blocks both arms of the ANS, used for treatment of hypertensive crisis

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endocrine ANS neuron

adrenal meduall activation releases:
20% NE
80% epinephrine

NE endocrine release adds to effect of sympathetic stimulation on alpha and beta receptors

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adrenal medulla enzyme

phenyl ethanolamine N methyl transferase converts NE into —–> epinephrine

epinephrine effects

epinephrine stimulates beta receptor to a greater extent.
epinephrine causes weak constriction of blood vessels.
epinephrine is 5 - 10 times more effective in stimulating metabolism.

vascular tone and denervation of the ANS

initially: marked increase in blood flow as vascular tone is lost

following days to weeks: vascular tone returns towards normal because of progressive increase in intrinsic tone of vascular muscle.

following test doses of NE: the response of vessels to NE (constriction) can increase 3 to 4 fold due to upregulation of receptors at denervation site.

organs with only sympathetic innervation

kidneys, liver, arterioles and veins, piloerection and sweating

beta1 adrenergic receptors only

heart + kidneys

alpha receptors only

eyes, endocrine pancreas, exocrine pancreas, sex organs

both alpha and beta receptors

arteries and veins, salivary glands, stomach, urinary bladder

alpha 1 receptor activation

always contraction in its target areas

vascular smooth muscle of skin, splanchnic region, sphincters of the GIT and urinary tract, radial muscle of the iris.

NE binds to alpha 1 receptor triggering a conformational change in the GqPCR at the membrane. the alpha q subunit is inactive when bound to GDP.

conformational change of GPCR causes alpha q subunit to bind to GTP and be released into the cytosol.

alpha q bound to GTP interacts with phospholipase C triggering the activation of PIP2.

PIP2 allows the liberation of diacyclgycerol and IP3.
IP3 activates calcium release from ER/SR.
diacyglycerol in the presence of calcium will activate protein kinase C.

protein kinase C has a major role in phosphorylating various proteins in the cell.

beta receptors

beta1 receptor activation in SA node causes heart rate increase and increase in contractility of the heart, renin secretion in the kidney.

NE binds to beta receptor causing a conformation change in GsPCR at the membrane.

alpha s subunit is inactive when bound to GDP and becomes active and released when conformational change occurs and bound to GTP.

alpha s bound to GTP will phosphorylate adenyl cyclase.

phosphorylated adenyl cyclase converts ATP to cAMP (second messenger).

cAMP activates protein kinases and induces downstream changes.

nicotinic AChR

ligand gated with ion channel (for potassium out, sodium in) as part of the receptor itself. always excitatory

muscarinic AChR

GPCR. binding to muscarinic receptor causes conformational change in membrane proteins which in turn affects release longer lasting effects and can be both excitatory or inhibitory excitatory: (smooth muscle of digestive tract) causes contraction when potassium channels close and sodium channels open allowing depolarisation ``` inhibitory: (slow heart rate) causes relaxation (produces slower heart rate) when potassium channels open i.e. hyperpolarisation. ```

non adrenergic non cholinergic @ sympathetic axon

3 phases of response: (contraction) 1. ATP binds to P2X purinoceptor (ligand gated cation channel) and causes calcium and sodium to enter the cell causing depolarisation and activation of another voltage gated calcium channel causing rapid phase of contraction 2. NE binds to alpha 1 adrenoceptor and Gq/PLC/IP3 cascade results in calcium release from ER/SR causing second phase of contraction 3. neuropeptide Y binds to Y1 receptor and causes slowest calcium increase producing the slowest phase of contraction.

non adrenergic non cholinergic @parasympathetic axon

the parasympathetic axon releases: ACh NO VIP (vasoactive intestinal peptide) 2 phases of response: (relaxation) 1. NO is released by the neuron into smooth muscle cell. ACh is also released by the neuron which acts on M3 receptors on endothelial cell to produce NO also which will diffuse into smooth muscle cell. both sources of NO activate guanylyl cyclase and raise cGMP in smooth muscle cell contributing to the first phase of relaxation. 2. neuropeptide VIP binds to receptors on smooth muscle cell causing an decrease in calcium also which contributes to the second (delayed) phase of relaxation.

vasoactive intestinal peptide

is released along with ACh by sympathetic nerves to sweat glands and by parasympathetic nerves to enteric nervous system.

cGMP inducing smooth muscle relaxtion

3 mechanisms: 1. inhibits calcium entry into the cell and decreases intracellular calcium concentrations 2. activated potassium channels which leads to hyperpolarisation and relaxation. 3. stimulates cGMP dependent protein kinase which activates myosin light chain phosphatase (an enzyme that dephosphorylates myosin light chains)

peripheral nervous system

function: communication between CNS and rest of body includes the ANS + SNS 31 spinal nerves carry info to and from spinal cord 12 cranial nerves carry info to and from the brain

enteric nervous system

includes the myenteric and submucosal plexuses in the wall of GIT myenteric plexus regulates motility submucosal plexus regulates ion + water transport and secretion

functions of the ANS

1. Maintenance of homeostasis (blood pressure) 2. integration of stress response 3. integration of visceral function (food digestion)

overactive bladder case study

parasympathetic antagonist (muscarinic cholinergic antagonist) specifically M3 which mediates bladder contractions are useful. sympathetic agonist at alpha 2 receptors to inhibit bladder contraction would have a small effect. sympathetic alpha 1 agonist would inhibit urination but the urge to urinate would still be present.