Flashcards in MR 10 Deck (15)
Describe the key features of the sympathetic nervous system
Aka thoracolumbar division
Short myelinated pre ganglionic fibres
Long unmyelinated post ganglionic fibres
Secrete ACh onto nAchR at ganglion
Release NA onto adrenoreceptors receptors post synapse
- except sweat glands which is ACh released.
What type of receptor is the nAchR ?
This is a ligand gated ion channel, capable of fast transmission.
Give 3 example of non-adrenergic non-cholinergic neurotransmitters.
5-HT, ATP, NO.
What is different about stimulation of the adrenal glands?
Sympathetic innervation, however the post ganglionic neurone is just a chromaffin cell instead of a neurone as such.
On stimulation, it secretes adrenaline into the blood stream.
What is the effect in the heart of parasympathetic stimulation of M2 receptors?
Slow down the heart by affecting the SAN and AVN.
m2 is coupled to Gi - this causes a decrease in PKA and cAMP causing inhibiton.
The BY subunit can also increase the permeability of K+ too causing efflux of the ions hence being inhibitory.
What is the action of M3 activation via the Parasympathetic system in the lungs and GI system
m3 coupled to Gq - causes increase in IP3 via PLC and hence bronchoconstriction in the lungs and in the GI system, it causes increased motility and secretions.
Sympathetic innervation of the heart leads to positive inotropic and chronotropic effect. Which receptor is involved here?
This is the B1 receptor.
This is couple to Gs which causes an increase in PKA and cAMP.
Why are B2 agonists used to relieve an acute asthma attack?
They are B2 agonists - when acting in the lungs they cause bronchodilation.
How is ACh synthesised, name the enzyme and products and also the degradation products.
Acetyl CoA + choline = ACh + CoA. (Via choline acetyltransferase).
When ACh is degraded by Achesterase:
ACh --> acetate + choline.
Name a gas that can bind to AchE. Is this reversible or irreversibly?
Describe the pathway, including enzymes, of the synthesis of noradrenaline
Tyrosine -->> DOPA via Tyrosine hydroxylase
DOPA -->> Dopamine via DOPA decarboxylase
Dopamine -->> Noradrenaline via Dopamine Beta-hydroxylase.
What is Uptake 1 and Uptake 2
Mechanisms of lower noradrenaline concentration in the synaptic cleft.
Uptake 1 - NA taken back into secreting terminal and can either be degraded via MAOor repackaged into vesicles ready for another release.
Anything not taken back into the releasing terminal is then removed via uptake 2.
How do indirectly acting sympathomimetic drugs act?
They are a substrate for uptake 1. They get taken into a neurone and then they cause the NA to leak from vesicles that they are stored in. The displaced NA then leaks into the synaptic cleft - this is not by Ca2+ mediated exocytosis but by a different mechanism.
What is the mechanism of action of increasing contractility in the heart muscle?
NA acting on B1 receptors cause cAMP increase, which phosphorylate VOCC allowing a greater influx of calcium which then increases the contractility.