Table 1.

Drugs used

Drug	Actions/Receptors Targeted	Dose, µM	Source
nAChR agonists
ACh	Endogenous transmitter	20–100	Sigma-Aldrich
Nicotine*	Agonist at all nAChRs except α9-containing channels where it is an antagonist (59)	5–40	Sigma-Aldrich
Epibatidine*	Agonist at all nAChRs except α9α10 heteromeric channels where it is an antagonist (59)	0.1	Sigma-Aldrich
NAChR antagonists
d-Tubocurarine (d-TC)	Broad nAChR competitive antagonist α1–4,7,9,10	10–30	Sigma-Aldrich
Mecamylamine	Noncompetitive open-channel block of α3, α6, and α9 nAChRs	50	Sigma-Aldrich
Methyllycaconitine (MLA)	Antagonist at α7 and α9 nAChRs	0.2–1.0	Tocris
Other
Neostigmine	Cholinesterase inhibitor (60)	20–30	Sigma-Aldrich
Atropine	Muscarinic receptor antagonist	10	Sigma-Aldrich
Picrotoxin	Antagonist at GABAARs by complex mechanisms	25	Tocris
Muscimol	Non-selective agonist at GABAARs	10	Tocris
GABA	Endogenous transmitter	100	Sigma-Aldrich
Nipecotic acid	GABA uptake inhibitor	100	Sigma-Aldrich
Tetrodotoxin (TTX)	Voltage-gated Na+ channel blocker	0.1	Sigma-Aldrich

Shown are the drugs used in the present study as well as their commonly reported sites of action (see Ref. 61). *Nicotine and epibatidine cause nAChRs to desensitize much more quickly than ACh (116).