Neuromuscular Junctions Flashcards
Normal function of neuromuscular junctions
- release neurotransmitters into the space
- have the neurotransmitters activate receptors
- cause muscle contraction
How Acetylcholine is released at the neuromuscular
- Choline and AcetylCoA are transfered and bound via Choline Acetyltransferase
- Packaged into Vesicles
- Vesciles bind to the membrane
- Release Acetylcholine (neurotransmitter)
How Acetylcholine is recycled at the neuromuscular junction:
- Acetylcholinesterase breaks down Acetylcholine into Acetate and Choline
- Choline is transfered into the cell via Choline Transporter proteins
- it then combines with AcetylCoA
Where and How do Acetylcholinesterase Inhibitors act:
- block the conversion of ACh to Choline and Acetate
- decrease the amount of ACh that can be formed and released at synaptic membrane
- increase and prolong the effect of released ACh
Drug of choice for Myasthenia Gravis
Where and How does Hemicholinium act:
- acts on the choline transporter
- blocks reuptake of choline to decrease the synthesis of ACh
- open channel block at all nicotinic receptors (can not be over come by an increase in ACh)
Where and How does Vesamicol act:
- blocks Choline Acetyltransferase
- prevents the creation and transportation of ACh into the vesicles
Where and How does Botulinum act:
- blocks vesicular release of ACh at the NMJ by cleaving docking proteins
- results in weakening to flaccid paralysis of skeletal muscles
- reversal takes up to 3-4 months
- Botulinum neurotoxin A (Botox) - cleaves SNAP 25
Where and How does 4-aminopyridine (4-AP) act:
- enhances the release of ACh at the synaptic cleft
- prolonges the action potential by blocking potassium channels
- allows for conduction through nerves damaged by loss of myelin
Therapeutic uses of 4-aminopyridine:
- Multiple Sclerosis
- Myasthenia Gravis
- Spinal Cord injury
Not used for these because of narrow therapeutic index and propensity of the drug to cause tremors and induce seizure
Multiple Sclerosis
- an autoimmine disease characterized by intermittent demyelination of nerve fibers in the brain
- results in progressive loss of motor coordination and muscle strength
Therapeutic uses of Botulinum Neurotoxin A
- Cosmestic
- Opthalmic
- Face and Neck Muscle Spasms
- Hyperdrosis
- Pain
Use of Botulinum Neurotoxin A in Cosmetics
- treatment of wrinkles
Opthalmic use of Botulinum Neurotoxin A
- treatment of strabismus (imbalance of the eye muscle strength that impairs ability to focus both eyes on the same target)
- treatment of bblepharospasm (spasmodic wrinking due to involuntary contraction of the eye lid muscle)
Use of Botulinum Neurotoxin A for Face and Neck Muscle Spasms
- hemifacial spasm (one sided spasm of the facial muscles)
- cervical dystonia (abnormal tonicity in the muscles)
Use of Botulinum Neurotoxin A for Hyperhidrosis
- excessive sweating on the palms, soles of the feet, axillae and face
- very long action on sweat glands (4-12 months)