Autonomic NS (SCI) challenges and research Flashcards
parasympthathetic outflow from CNS is distributed through how many cranial nerves?
4 cranial nerves: 3,7,9,10!
the efferent preganglionic neurons are located in the cranial and sacrum regions of spinal cord
which of the following is NOT a physiological response controlled by Autonomic NS? A sweating B shivering C picking up food D iris constricting E heart rate increasing
OPTION C
Autonimic NS is for involuntary movement and picking up food is the only option here that isn’t that
That is somatic or voluntary nervous system
true or false?
both excitatory and inhibtory neurotransmitters are released at nueromuscular junctions
FALSE
inhibtion occurs at the spinal cord with inhibititory relay neurons
How is smell detected?
The binding of odour molecules causes the depolarisation of the cilia via sodium ions and action potential that passes past soma to the brain. .
The binding of odour molecules activates GPCR that stimulates Adenylyl cyclase. High cAMP in the cilia cause the opening of ion channels causing depolarisation and an action potential that passes past soma to the brain.
The binding of odour molecules stimulate calcium channels that stimulate Adenylyl cyclase. High cAMP in the cilia cause the opening of ion channels causing depolarisation and an action potential that passes past soma to the brain.
OPTION B
secondary messenger systmes use GPCR
> mammals have 1000 odour recepors and can smell 10,00 smells!
how do the pre and post synaptic neurons differ in the ANS?
how do the Somatic and autonomic NS differ?
pre - myelinated so Atype fibre
post - unmyelinated so C type fibre, no salutatory conduction
somatic only has 1 efferent myelinated neuron and ends at NMJ instead of having a central ganglionic neuron
where are the efferent pre-ganglionic neurons of the SNS located? A CRANIAL B THORACIC C LUMBAR D SACRAL
OPTION B AND C
what is the key neurotransmitter associated with the SNS?
noradrenaline released from synapses can stimulate adrenal medulla to increase adrenaline release
80% of the SNS actions are due to actions of adrenaline as it can circulate 10times longer than the synaptic nora-adrenaline
what does ipsilateral mean?
cranial nerve systems are mostly ipsilateral, meaning that a cranial nerve on the right side of the head is connected to the right side of the brain.
so control of organs is ipsilateral
where do the sacral segments of the PNS innervate to?
the bladder, anus, large intestine and genitalia
how is the digestion controlled?
GIT is controlled by the ENTERIC NS
> auerbach nerve plexus and meissners nerve plexus to control peristalsis and fluid/ion regulation
PNS can stimulate the ENS increasing motility of the system
how does the SNS affect the enteric nerous systme?
doesnt directly affect it but very strong SNS stimulation inhibits it
> increase tone of the sphincters and decrease motility
and secretion
what is the key neurotransmitter associated with the PNS?
acetylcholine (Ach) and other parasympathetics
> degraded by Ach-esterase
how do ionotropic receptors work?
through ligand biding, the receptors becomes activated and undergoes a confirmation change
this opens up a pore so the ion can pas through
eg. ligand gated or voltage gated sodium channel, nicotinic receptors have
how do metabotropic receptors work?
these receptors are coupled to G-proteins so when ligand binds there is intracellular signalling which can then lead to pores opening up
e.g. action of beta adrenergic receptors and muscurinic receptors
what are the key differences in metabotropic and ionotropic receptors
ion - faster acting, uses multiple subunits, nicotinic receptor uses
meta - slower acting, only a monomeric subunit, muscurinic receptor use
Which intracellular response(s) typically occur following activation of muscarinic receptors?
A Stimulation of adenylyl cyclase and an increase in cyclic AMP
B Hydrolysis of phosphoinositides and activation of protein kinase C
C Inhibition of adenylyl cyclase and a decrease in cAMP
D Release of intracellular Ca2+ from the endoplasmic reticulum
E Phosphorylation of ryanodine receptors by protein kinase A
OPTION B + C + D
options B - protein kinase C - reduced cAMP D- release of intracellular
muscurinic receptors are metabotrophic/GPCR and typically use Galphaq or Galpha-i
A - Galpha S B - G alpha Q C - G aplha i D - this is after effects of GalphaQ E - This is excite-contract
Binding of which substance(s) to receptors on the cell surface causes an increase in cAMP in the cytoplasm?
A Acetylcholine on muscarinic receptors
B Adrenaline on beta-adrenergic receptors
C Atropine on muscarinic receptors
D Propranolol on beta-adrenergic receptors
OPTION B
β1, β2 + B3 adrenergic receptors use GalphaS
can’t be any of the mucurininic R as they don’t really use the GalphaS subunits
cant be propanolol as that is a beta-blocker so would decrease the cAMP
Which of the following manipulations or chemicals will cause an increase heart rate?
A Stimulating the vagus nerve
B Severing or damaging the vagus nerve
C The beta receptor antagonist Propranolol
D The muscarinic receptor antagonist Atropine
E The alpha adrenergic agonist Phenylephrine
OPTION B + D
B - damage vagus nerve means PNS goes down
D - atropine as it antagonizes the PNS so heart rate won’t be able to go down
cant be A as that vagus nerve is PNS
can’t be C as beta receptors are SNS if you antagonise then the SNS will decrease so HR drops
can’t be E as the alpha receptors work on the blood vessels and not the heart
Which of the following manipulations or chemicals will cause constriction of peripheral blood vessels?
(select all options that apply)
A Acetylcholine on muscarinic receptors
B Adrenaline on beta adrenergic receptor
C Atropine on muscarinic receptors
D Noradrenaline on alpha adrenergic receptor
E Propranolol on beta adrenergic receptors
OPTION D
> ONLY alpha adrenergic receptors are involved in vascular tone - type 1 constricts, type 2 contracts smooth muscle
A - muscurinic is PNS so would dilate/ rest and digest
B - beta-adrenergic dont work on blood vessel, only cardiac and JXG
C - blocking muscurinic doesn’t affect vessel tone
D - proponolol is a beta blocker so no effect on blood vessels
why can curane be dangerous?
curane can block the action of nicotinic Ach receptors // nAch antagonist// so can block action of both the SNS and PNS
curane can also block the somatic synapses in skeletal muscle which could inhibit action of muscles = paralysis
what are the 2 main challlenges to the ANS?
exercise
spinal cord injury
how does the PNS control heart rate?
the cranial nerves 9 and 10 (baroreceptors are will innervate to the SAN and AVN to decrease heart rate
they will release Ach at the postganlgionic axon terminal which activates mACH on the SAN, AVN to hyperpolarise them = less excitable so heart rate decreases
> can increase vasodilation by increasing NO
how does the SNS control heart rate?
- the T1-T4 section will increase heart rate by acting on the nodes and myocardial tissue
> Nora acts on B1 receptors of the nodes to increase depolarisation and speed of AP propagation increasing heart rate (HR)
2. the lower thoracic region T5-L2 will regulate blood vessel tone and constrict the periphery vessels > Nora acts on B2 receptors of cardiac muscle to increase contractility (increased intrac. Ca release) and on α1 AdR in smooth muscles of the the lower limbs to constrict
what is miosis and ptosis?
contriction of pupils and drooping eyelids
> these are symptoms of horners syndrome where there is a spinal cord injury above T1 so no SNS input to the eyes from the superior cervial ganglion
how do the SNS and PNS regulate exercise?
INITIALLY - parasympathetic tone will dominate but then SNS tone will take over as we keep on exercising
regular exercise will enhance vagal/PNS tone and decrease sympathetic tone vagal
> vagal inputs will help to maintain resting heart rate and exercise can enhance the vagal tone = lowering of heart rate
why does it take some time for our rate to go back down after completing exercise?
'’Heart rate recovery delay’’
due to a delay in PNS activation as sympathetic tone has to be decreased
could be due to the reason that adrenaline takes 3-4 mins to clear from the circulation
what is spinal shock?
Spinal shock is the altered physiologic state immediately after a spinal cord injury
> decreased motot, sensory and reflex function
and lead to neurogenic shock in the ANS
What is neurogenic shock? what causes it?
> irregular blood circulation, low BP, brachycardia, hypothermia // unable to keep HR, BP and temp stable
caused ‘‘sympathetic dysautoniomia’’ = loss of sympathetic innervation and increase in vagus stimlation (as a result of SCI)
> can be compensated by dendrite sprouting to resotre neuronal connectiosn
which is affected more by SCI? SNS or PNS
SCI depends on the location
more likely to affect SNS as their preganglionic neurons are in the TL region whilst PNS has cranial nerves near brainstem
anything below the injury is affected
