Synapses and neurotransmission

Why this matters

Almost every drug a dentist gives or meets acts at a synapse: midazolam on GABA-A, nitrous oxide and ketamine on glutamate receptors, botulinum toxin on the SNARE proteins, antimuscarinics on the salivary gland, pyridostigmine on acetylcholinesterase. Toothache itself is synaptic — substance P and CGRP at the pulpal terminal, NMDA-driven amplification in the brainstem. About 5.3% of root-treated teeth still hurt six months later, and more than half of those are not the tooth.

The big picture

A chemical synapse is a controlled leak: transmitter stored in packets, released only when calcium floods a nanodomain, read by a receptor that decides the sign of the message. That design costs half a millisecond and buys everything else — gain, inhibition, memory and a hundred drug targets. The postsynaptic cell then adds every input up and one small patch of axon casts the only vote that matters.

The 15 cards in this lesson

1. 01What a synapse has to solve
2. 02Chemical versus electrical
3. 03The synapse, labelled
4. 04Calcium is the trigger
5. 05Release, step by step
6. 06The quantum: Katz and the miniature potential
7. 07Ionotropic versus metabotropic
8. 08EPSPs, IPSPs and summation
9. 09Where the decision to fire is made
10. 10Clearing the cleft
11. 11The neuromuscular junction
12. 12CGRP, substance P and the inflamed pulp
13. 13Muscarinic receptors and the dry mouth
14. 14Bliss and Lomo: how a synapse learns
15. 15Clinical alert — in the lesson

You have got it when

You can trace an action potential to a postsynaptic response naming calcium entry, the sensor and the SNARE step, and say what fills the 0.5 ms delay. You can explain why inhibition is defined against threshold, not against rest, and why a depolarising chloride current still inhibits. Given a toxin, an antibody or an antimuscarinic drug, you can predict which step fails and what the patient looks like.