[Abstract Title]. - Society for Neuroscience

intraorally administered sucrose solution. Since mu (µ) opioid stimulation of a similar dorsal
accumbens shell hotspot also enhances „liking,‟ and cannabinoids and opioids interact from the
behavioral to the molecular level, we asked if the opioid antagonist naloxone would block
„liking‟ enhancements by anandamide in the nucleus accumbens. We used a taste reactivity
paradigm, which measures the effects of brain manipulations on characteristic hedonic or
aversive orofacial reactions displayed by many species, from rats to humans, to intraorally
administered tastes. Two groups of rats were tested: males (n=15), and ovariectomized females
(n=6). All rats were given 0.2µl microinjections, to the medial accumbens shell, of vehicle,
anandamide alone, naloxone alone, and anandamide mixed with naloxone in randomized order
over four testing days. We examined taste reactivity to a 1mL of 1% sucrose solution orally
infused at 30, 45, and 60 minutes after drug injection. We found that anandamide enhanced
hedonic reactions to sucrose compared to vehicle, while this increase was totally abolished by
simultaneous co-infusion of naloxone. Naloxone itself had no effect on hedonic reactivity to
sucrose. These data support the idea that, within the nucleus accumbens, cannabinoid and opioid
circuits interact to modulate hedonic „liking‟ responses to a sweet reward. These findings have
implications for understanding the neural substrates of sensory pleasure involved in disorders
such as addiction and obesity.
Disclosures: M.R. Mitchell, None; S.V. Mahler, None; K.C. Berridge, None.
Poster
298. Neural Mechanisms of Reward: Self-Administration and Opioid Modulation
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 298.15/TT48
Topic: F.03.d. Reward
Title: Where in the ventral pallidum does neural inactivation cause aversive “disliking” and loss
of reward?
Authors: *C.-Y. HO, K. C. BERRIDGE;
Univ. Michigan, Ann Arbor, MI
Abstract: Ventral pallidum (VP) has been shown to be important for mediating „liking‟ and
„wanting‟ of natural rewards, such as food, and of drugs. Lesions of VP or inactivation of VP by
GABA agonist microinjections lead to a decrease in appetitive reward consumption or „wanting‟
along with a decrease of hedonic reward “liking” and an increase of aversive reward “disliking”.
However, it is unclear what substrate causes the loss of hedonic reward “liking” and the
replacement of aversive reward “disliking”. The goal of the present study is to identify the
specific “disliking” site in basal forebrain for lesions or local inactivation, with special attention