ANS Flashcards
Peripheral nerves contain…
Both motor (somatic and autonomic) and sensory neurons
Somatic
More voluntary - both motor out ventral root
Autonomic
More involuntary - both motor out ventral root
Somatic vs. Autonomic - Tissues Innervation
Somatic = skeletal muscle only and innervation is primarily under voluntary control Autonomic = all other tissues except muscle fibers
Somatic vs. Autonomic - Myelination
Somatic = motor neurons generally myelinated Autonomic = Post ganglionic are generally not myelinated
Somatic vs. Autonomic - Neuronal Organization
Somatic = all neuronal synapses occur within the CNS, cell bodies of somatic motor neurons are in the ventral horn Autonomic = nerves may synapse outside the CNS, cell bodies of postganglionic autonomic neurons lie in ganglia or within tissues (entirely outside CNS)
Somatic vs. Autonomic - Synaptic Organization
Somatic = highly organized with terminal synapse (NMJ) Autonomic = forms extensive plexus with varicosities that are packed with NTs
Somatic vs. Autonomic - Response of Target Tissue to Lesion
Somatic = paralysis - loss of ability to contract (results in atrophy) Autonomic = some level of spontaneous activity independent of intact innervation
Primary differences btw Somatic and Autonomic
- Tissue Innervated
- Myelination
- Neuronal Organization
- Synaptic Organization
- Response of Target Tissue to Nerve Lesion
Sympathetic NS Reaction
F/F Pupils dilate Piloerection HR inc. Blood shunted (splanchnic redistribution) to active muscles GI function dec. Stored fuel is catabolized/mobilized
Parasympathetic NS Reaction
R/D Vegetative Function - SLUDD Salivation Lacrimation Urination Digestion Deification
Sympathetics originate from
Thoracic Region
T1-L2
Parasympathetics originate from
Cranial nerves (3, 7, 9, 10) Vagus is largest responsible Small sacral component S1-S4 = important for activity such as bladder control
Sympathetic vs. Parasympathetic and Pre/Post ganglions
Sympathetic = Short pre, long post Parasympathetic = long pre, short post Parasympathetic = very quick response
What receptors are stimulated with sympathetic nervous system
adrenergic - these are at the end point
Parasympathetic will have what receptors?
Muscarinic or cholinergic
Sympathetic Preganglionic
Ach
Binds to nicotinic receptors
Parasympathetic Preganglionic
Ach
Binds to nicotinic receptors
Sympathetic Postganglionic
Long and unmyelinated
NE
Binds to adrenergic receptors
Parasympathetic Postganglionic
Short
Ach
Binds to muscarinic receptors
4 options for how wired - where ganglion is
- Spinal Nerve (synapse on chain ganglion)
- Symp Nerve (synapse on chain ganglion)
- Collateral Gang (Passes thru chain ganglion)
- Direct (no postgang - passes thru chain ganglion)
4 options for how wired - where ganglion is - Spinal Nerve
Pre goes out ventral root and then joins up with a spinal nerve, goes through why ramus communicans, and then it will going to its ganglionic synapse (outside the CNS) to join up with a spinal nerve
4 options for how wired - where ganglion is - Symp Nerve
Pre to symp chain from ventral root
Postgang straight to heart
4 options for how wired - where ganglion is - Collateral Ganglion
Longer pre, passes thru symp chain, and then has ganglion that goes straight to viscera, cause dec in motility, and increase in constriction of sphincters
4 options for how wired - where ganglion is - Direct - NO postganglion
Will pass through symp chain and go directly to the adrenal gland to release EP
Parasympathetic NS - Simple Overview
Preganglionic N (originate from cranial or sacral) –> Ach released and binds to nicotinic receptors –> stimulate post ganglionic –> release Ach that will bind to muscarinic receptors at target tissue
Curare
inhibits the nicotinic receptors
will cause paralysisof muscles and paralysis on ganglion level
Atropine
Will inhibit muscarinic receptors - parasympathetic tone on the heart
How is Ach produced?
Acetyl CoA + Choline = with help of ChAT (choline acetyltransferase)–> Ach
ACE
Acetylcholinesterase - breaks down Ach
Target for many chemical weapons - inhibits ACE to allow for a buildup of Ach in the synapse - can use atropine to treat - symptoms would include SLUDD
7 types of Ach Receptors
2 are nicotinics (ligand gated) - Ach - ionotropic
5 are muscarinics (G protein coupled) - metabotropic
Parasympathomimetics
Stimulate PNS
Nicotine will do this
Or Muscarine in muschrooms
Botulinum Toxin
Blocks at nerve terminal and inhibits release of Ach into synapse - it is a preganglionic blocker
EP in blood at rest?
Exercise?
10 ng/L
can inc 10 to 12 fold with exercise
Catecholamine Biosynthesis
LTyrosine –> LDopa –> Dopamine –> LNoradrenanline –> Adrenaline
Rate limiting enzyme in catchlamine biosynthesis
This is where you have control of how much catcholamines you are producing
What do all catcholamines originate as
L-Tyrosine
What does L-Tyrosine get hydroxide from
Tyrosine Hydroxylase
Rate Limiting Step
Where is this reaction occuring?
right there in the axon terminal
At adrenal medulla have a lot of…
PNMT so most of of what you are producing is epinephrine (adrenaline)
In vessels you have a lot of…
DBH so producing a lot of norepinephrine (noradrenaline)
Long term regulation of catcholamine biosynthesis
TH is formed in the cell body then transported to terminal
Short term regulation
Inc TH activity in nerve terminal with adrenergic stimulation
Feedback regulation
TH inhibited by nc intracellular NE
Cofactor
BH4 important to maintain TH in a reduced, active state
Postganglionic Adrenergic Receptor Locations - Alpha 1
Arterioles, Veins –> VC
Liver –> glycogenolysis
Postganglionic Adrenergic Receptor Locations - Alpha 2
Pancreas, Intestine - Inhibition
Postganglionic Adrenergic Receptor Locations - Beta 1
Heart –> Inc HR and contractility
Postganglionic Adrenergic Receptor Locations - Beta 2
Lungs = bronchodilation
Liver = glycogenolysis
Skeletal muscle = glycogenolysis, lipolysis
Alpha adrenergic Antagonist
Phentolamine
would block symp VC of blood vessels
Beta adrenergic Anatagonist
propanolol
What happens to NE release with amphetamines
increases
Not everything from motor traffic is just one NT, one nerve
Cotransmitters
Catecholamine Removal
MAO and COMT
MAO
reuptake and deamination by post ganglionic neurons
Used as antidepressent drug - to inhibit MAO and keep more NE in synapse
Hypertensive crisis - need to monitor BP
COMT
catabolism at tissues like the liver (primarily), kidneys and smooth muscle
COMT inhibition is used in parkinsons to keep more dopamine around
U1
Takes NE back up into the axon terminal
U2
gets NE to the tissue
Pheochromocytoma
chromatin cell tumor that leads to excess secretion of catecholamines –> increased peripheral resistance and hypotension
Ways to test or see pheochromocytoma (symptoms)
Inc BP, headache, sweating, epigastric pain…
Can also test by taking urine sample and looking for metabolites in urine
Can image for tumor too
EPI vs. NE - CO
EPI = inc CO due to inc HR NE = small, transient inc in CO due to baroreceptor response - due to inc in SV and contractility
EPI and NE - VD/VC
EPI = VD of muscle and liver (Beta 2) NE = VC of vessels (alpha 1 and 2)
EPI and NE - BP
EPI = little impact on BP NE = elevated BP
EPI and NE - diastolic
EPI = dec cuz of dilation NE = inc due to constricting
EPI and NE - MAP
EPI = stays about the same NE = inc --> stimulate reflex --> vagal response --> dec HR
Which has bigger impact EPI or NE?
EPI - bigger impact with little stress on heart
Primary integration center for ANS
Hypothalamus
Any cervical lesion
Significant SNS dysfunction
Global BP dysregulation
Cervical Lesion T1-T4
Lung Dysfuntion
Airway hyper-reactivity
Cervical Lesion T6 and above
Affects SNS control of heart
Any lesion above sacrum
Lose parasympathetic innervation (pelvic N) to descending colon bladder and external genitalia - bowel/bladder control is #1 QOL issue in SCI
Autonomic Dysreflexia
Potential medical emergency in spinal cord injury
Acute increase in BP
50-70% of individuals with SCI lesions at or above T6 experience these symptoms
Without trigger vs. with trigger
Without trigger, patients will typically have the hypotension due to loss of sympathetic outflow
But with trigger (full bladder) will experience dysreflexia - the huge drop/change in BP
Beta 1
Inc HR, glycogenolysis, lipolysis, contractility
Beta 2
Brochodilation
Vasodilation
Alpha 1
Inc phosphodiesterase
Inc VC
Alpha 2
opposes actions of beta 1 and 2