OCAT 2: Pain

1. β-Bungarotoxin of the pain world. Think about it…
3. Long-term potentiation/depression? Forming memories? Plasticity? What kind of detection makes neurons do that?
12. Although not in the standard definition, pain is not a purely quantifiable, biological phenomenon, but rather this as well.
13. If you eat spicy food for long enough, the pain will go away. That’s because TRPV1 can do this very easily.
16. Some of these noxious sensors are the good ol’ ones we know and love.
18. Too much glutamate from cancer? Well you might end up with an excess of this bone-breaking guy.
20. Glutamate doesn’t only play around with ions, but also with a well known G of ours… changed his name recently.
21. This stimulatory signalling molecule is essentially cousins to the inhibitory one.
22. 3rd wheeler of the synapse, useful for breaking-down the stimulatory type.
23. Information traveling towards the control centers of the body.

2. TOXIC tales was quite an EXCITING lecture… Now let’s put a neurological spin on it!
4. Can GABA-B cause influx of chloride post-synaptically?
5. What concept allows researchers to determine chronic pain from reflexes?
6. Long pokey stick; tickles mices’ feet.
7. The modern view of pain and its multiple variables are described by this word.
8. QUICK! I need to heighten my ability to detect heat! Oh gosh, what’s something that did that again?
9. Remember how you didn’t necessarily need a stimulus to get a response (constitutive), now imagine that for pain.
10. Who said iNOS could only make NO. It can also regulate the creation of this peptide (with the help of serotonin).
11. Ionotropic, co-incidence detector for glutamate.
14. Sensors of noxious stimuli, the quantifiable type.
15. It’s been so long, shouldn’t the pain receptors shut-off by now?
17. TRPV1 is essentially a glorified electric tunnel, what did we call these before?
19. I can work in both directions and I normally slow down the firing rate. Who am I?