Lecture notes
NAJEEB NEURO NOTES
- Module
- Medicine
Lecture notes of 52 pages for the course medicine at UWCM (NAJEEB NEURO NOTES)
[Show more]
Seller
Follow
Content preview
Najeeb notes by Saad Ahmed QudusiIndex:
0. Najeeb NMJ
1. Introduction to CNS
2. Sensory system and ascending tracts
3. Motor system and descending tracts
4. Medulla
5. Pons
6. Midbrain
7. Cerebellum
8. Diencephalon
9. Thalamus
10. Basal nuclei
11. Oculomotor nerve palsies
12. Blood supply to the brain
1|SAQ’s Najeeb notes
, Najeeb (Extra) Neuromuscular junction
Video 1
Introduction:
• Motor neurons come off the anterior horn of the spinal cord.
• The nerve terminal (ending of the neuron) is connected to the muscle at the
neuromuscular junction. The area of muscle at the neuromuscular junction is called the
motor end plate.
• Neurotransmitters are released from the presynaptic membrane (i.e. the nerve
terminal) to transmit the impulse to the post synaptic membrane (i.e. the muscle
membrane)
The neurotransmitter machinery at the NMJ:
• Within the neuron are membrane bound vesicles loaded with acetylcholine
o The vesicles are synthesized in the cell body. These vesicles are made of special
proteins. In fact, all the proteins in the nerve ending are synthesized in the cell
body since there is no nucleus at the nerve endings.
o The acetylcholine is synthesized at the nerve terminal. However, the enzymatic
machinery concerned with ACh release and synthesis is synthesized in the cell
body.
• ACh synthesis
o The nerve ending has choline transporters (special channels which transport
choline inside the nerve ending from outside).
o The acetate for ACh comes from the mitochondria already present in the nerve
ending.
o The enzyme needed for the synthesis of ACh from acetate and choline is called
cholinacetyltransferase.
• ACh loading
o ACh is sequestered in the vesicles mentioned before via special channels in the
vesicle membrane.
The impulse:
• The wave of depolarization approaches the nerve terminal leading to massive influx of
Na+.
2|SAQ’s Najeeb notes
, • This wave of depolarisation activates depolarization sensitive calcium channels leading
to calcium influx.
• Calcium influx dependent exocytosis of ACh occurs.
o The vesicles have special calcium sensitive proteins on its surface
(synaptobrevin) and so does the membrane of the nerve terminal (syntaxin).
o These protein channels are activated when calcium is bound to them and this
allows both membranes (vesicular and nerve ending) to fuse and ACh is released.
• The ACh now diffuses from presynaptic area to the postsynaptic area.
• ACh gated cation channels (these are nicotinic channels) are present on the
postsynaptic membrane.
o These channels have to binding sites for ACh. As soon as ACh binds to these
binding sites, the channels open
o Sodium (cation) can now move in and Potassium (cation) can now move out.
o However, since the resting membrane potential of -90 mV is nearer to the
Potassium equilibrium potential, movement of potassium is not significant.
Movement of sodium does occur however since -90 mV is far removed from
sodium’s equilibrium potential
• This potential produced by sodium influx is NOT called an action potential since it isn’t
so. It’s called “end-plate potential”
o Small fluctuations in the resting potential of post synaptic membrane are
produced by a small release of ACh and these are called miniature end plate
potentials.
o The influx of sodium takes the resting membrane potential to threshold potential
(if the ACh binding is strong enough) and voltage gated channels open, sodium
influx starts and a new wave of depolarisation (action potential) ensues in the
muscle
• The ACh is degraded soon after the ACh has opened the sodium channels by
acetylcholinesterase.
o The acetate diffuses in blood and leaves
o The choline is reabsorbed into the nerve cell via the choline transporters
mentioned above.
Video 2
• The ACh vesicles which had bound to the nerve membrane to release ACh are also
recycled.
o Proteins called clathrins pull the vesicle’s membrane inward and the whole
vesicle pinches in, now without ACh.
3|SAQ’s Najeeb notes
, • CC (Patho): Myasthenia Gravis is an autoimmune disorder where the immune system
makes antibodies against the ACh receptors on the muscle which competitively inhibit
ACh binding. The miniature end plate potentials will be less in amount and it is very
difficult to generate enough sodium influx to be able to depolarize muscle cell to
threshold.
o CC (Pharma): AChE inhibitors (physostigmine, neostigmine etc.) can be given in
this condition so that ACh can accumulate in synaptic cleft which will be
beneficial since the inhibition by antibodies is COMPETITIVE and can be
countered by increasing ACh concentration.
• CC (Patho): Eaton-lambert syndrome is a condition where antibodies are produced by
the body against the presynaptic depolarisation sensitive calcium channels.
o In myasthenia gravis, the person’s condition worsens with activity since
accumulated ACh will be depleted but in ELS the person’s condition improves
with activity since repeated action potentials arrive at nerve terminal leading to
increased calcium release.
• CC (Patho): Botulinum toxin is a proteolytic enzyme which is able to enter the
cholinergic nerve ending (esp. at NMJs).
o It cleaves synaptobrevin and syntaxin which were responsible for ACh release
from vesicles into the synaptic cleft
o Neuromuscular transmission ceases. The condition in babies is called floppy baby
syndrome.
• CC (Pharma): A toxin (tubercurare) binds to post synaptic ACh sensitive Na channels to
prevent them from opening, effectively shutting down Neuromuscular transmission.
o Sometimes this drug is used with anesthesia to allow the patient’s muscle to
relax.
• CC (Pharma): Succinyl choline is a drug which repeatedly stimulate the ACh sensitive
postsynaptic Na channels.
o This causes the fast sodium channels in the muscle to transition to inactive state.
To regain their open state they must now transition to closed state first which
can only happen in repolarized state. But since our drug above has the
membrane constantly depolarised, this doesn’t happen and the fast sodium
channels are effectively trapped in inactive state so even though membrane
depolarises to threshold, the impulse is not transmitted as Na channels are
inactive.
4|SAQ’s Najeeb notes
The benefits of buying summaries with Stuvia:
Guaranteed quality through customer reviews
Stuvia customers have reviewed more than 700,000 summaries. This how you know that you are buying the best documents.
Quick and easy check-out
You can quickly pay through credit card for the summaries. There is no membership needed.
Focus on what matters
Your fellow students write the study notes themselves, which is why the documents are always reliable and up-to-date. This ensures you quickly get to the core!
Frequently asked questions
What do I get when I buy this document?
You get a PDF, available immediately after your purchase. The purchased document is accessible anytime, anywhere and indefinitely through your profile.
Satisfaction guarantee: how does it work?
Our satisfaction guarantee ensures that you always find a study document that suits you well. You fill out a form, and our customer service team takes care of the rest.
Who am I buying these notes from?
Stuvia is a marketplace, so you are not buying this document from us, but from seller nerdsnexus. Stuvia facilitates payment to the seller.
Will I be stuck with a subscription?
No, you only buy these notes for £6.57. You're not tied to anything after your purchase.
Can Stuvia be trusted?
4.6 stars on Google & Trustpilot (+1000 reviews)
72042 documents were sold in the last 30 days
Founded in 2010, the go-to place to buy revision notes and other study material for 14 years now