Page Contents
OVERVIEW
This page is dedicated to compiling Step 1 study notes for the topic of cholinergic signaling. This page is likely disorganized as it was made in haste.
MUSCARINIC CHOLINERGIC RECEPTORS
How do they work?
- M1 and M3 muscarinic receptors utilize the inositol triphosphate pathway to increase intracellular calcium concentrations, which in turn activates protein kinase C.
- M2 muscarinic receptors act via the cAMP second messenger system. Upon activation they decrease intracellular cAMP concentrations.
Where are they?
- Face: facial flushing occurs when this signaling is antagonized in the face.
- Eyes: pupillary dilation occurs when this signaling is antagonized here.
- Bladder: antagonism stops urge incontinence by decreasing smooth muscle contractions.
NICOTINIC CHOLINERGIC RECEPTORS
How do they work?
Nicotinic cholinergic rejectors are a ligand gated ion channel receptor (inotropic receptor). When acetylcholine binds this receptor the ion channels will open. The net effect is multifold:
- Calcium and sodium influx
- Potassium outflow
The end result is is the generation of an end-plate potential.
Where are they?
- Neuromuscular junction
- Central nervous system: on postganglionic neurons of autonomic ganglia.
ANTI-CHOLINERGIC STATE
Causes:
Jimsonweed,
Symptoms:
- Hot as a hare: increased body temperature
- Dry as a bone: dry mouth
- Red as a beet: flushing (msucarinic)
- Blind as a bat: mydriasis/acute angle glaucoma (muscarinic)
- Mad as a hatter: hallucinations
- Tachycardia:
Treatment:
- Physostigimine: cholinesterase inhibitor. Increases amount of acetylcholine around.
INCREASED CHOLINERGIC STATE:
Causes:
- Organophsphates (inhibit cholinesterase inhibitors): pesticides,
Symptoms: DUMBELS acronym
- Diarrhea
- Urination
- Bronchospasm/bradycardia
- Excitation of skeletal muscles and CNS
- Lacrimation
- Sweating/Salivation
Page Updated: 04.22.2017