Table 1:

At least six categories of abused drugs strongly influence RMTg activity. Among these, cocaine is the most widely studied, but other drugs, particularly opioids and cannabinoids, appear to have large acute effects. In several cases, activity appears protective against acquisition of drug-seeking, but this topic is overall relatively understudied.

Drug	RMTg neural response:	Relevant receptors	References
Cocaine	Biphasic: reduced firing for several minutes, followed by excitation in some neurons 15–30 min after exposure. Marked cFos seen at 1–2 hours.	CP-AMPARs, 5HT2CR	(Colussi-Mas et al., 2007; Geisler et al., 2008; Jhou et al., 2009; Lavezzi et al., 2010; Jhou et al., 2013; Li et al., 2019; Parrilla-Carrero et al., 2021)
Methamphetamine	Firing rate unknown, but cFos increased at 2 hours.	Unknown.	(Lecca et al., 2011)
Morphine	Large acute reduction in firing. Increased cFos during withdrawal in dependent rats. Morphine blocks RMTg’s ability to suppress DA firing.	Mu opioid receptor	(Jalabert et al., 2011; Lecca et al., 2011; Lecca et al., 2012; Kaufling and Aston-Jones, 2015)
Nicotine	Acute increase in firing.	Alpha-7 nicotinic receptors on presynaptic glutamate inputs to RMTg	(Lecca et al., 2011; Castillo-Rolon et al., 2020)
Alcohol	Modest acute firing increase in firing, large cFos increase during withdrawal in dependent rats.	Unknown	(Melis et al., 2014; Glover et al., 2016; Glover et al., 2019)
Cannabinoids	Large acute firing inhibition, also blocks RMTg-induced suppression of DA firing	CB1 receptors on RMTg and presynaptically on its projections to VTA	(Lecca et al., 2011; Lecca et al., 2012; Melis et al., 2014)