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. 2009 Nov 4;35(3):665–673. doi: 10.1038/npp.2009.171

Figure 4.

Figure 4

α-Conotoxin MII (α-CTX MII) infusion into the nucleus accumbens (NAc) shell did not depress locomotor activity in an open field. Animals received s.c. injection of 0.175 mg/kg nicotine (by weight of freebase) in 0.9% saline (NIC) or saline vehicle (VEH). Sessions were preceded by intra-accumbens shell infusion of saline vehicle (VEH), 5 pmol, or 10 pmol of the α6β2*nAChR antagonist, α-CTX MII. (a) Planned comparisons between VEH–VEH and VEH–NIC showed a significant increase in distance traveled following nicotine injection (n=8, p=0.002), indicating that the dose of nicotine used in these studies resulted in locomotor activation. Locomotor-activating effects of nicotine were not affected by antagonism of α6β2*nAChRs in the NAc shell. (b) Intra-accumbens shell infusion of α-CTX MII also had no effect on basal locomotor activity. Data are expressed as mean±SEM; *p<0.05 compared with activity following vehicle infusion and vehicle injection.