PMID- 19336249 OWN - NLM STAT- MEDLINE DCOM- 20090824 LR - 20211020 IS - 1873-7544 (Electronic) IS - 0306-4522 (Print) IS - 0306-4522 (Linking) VI - 161 IP - 3 DP - 2009 Jul 7 TI - Convergent, not serial, striatal and pallidal circuits regulate opioid-induced food intake. PG - 718-33 LID - 10.1016/j.neuroscience.2009.03.057 [doi] AB - Mu opioid receptor (MOR) signaling in the nucleus accumbens (NAcc) elicits marked increases in the consumption of palatable tastants. However, the mechanism and circuitry underlying this effect are not fully understood. Multiple downstream target regions have been implicated in mediating this effect but the role of the ventral pallidum (VP), a primary target of NAcc efferents, has not been well defined. To probe the mechanisms underlying increased consumption, we identified behavioral changes in rats' licking patterns following NAcc MOR stimulation. Because the temporal structure of licking reflects the physiological substrates modulating consumption, these measures provide a useful tool in dissecting the cause of increased consumption following NAcc MOR stimulation. Next, we used a combination of pharmacological inactivation and lesions to define the role of the VP in hyperphagia following infusion of the MOR-specific agonist [D-Ala2, N-MePhe4, Gly-ol]-enkephalin (DAMGO) into the NAcc. In agreement with previous studies, results from lick microstructure analysis suggest that NAcc MOR stimulation augments intake through a palatability-driven mechanism. Our results also demonstrate an important role for the VP in normal feeding behavior: pharmacological inactivation of the VP suppresses baseline and NAcc DAMGO-induced consumption. However, this interaction does not occur through a serial circuit requiring direct projections from the NAcc to the VP. Rather, our results indicate that NAcc and VP circuits converge on a common downstream target that regulates food intake. FAU - Taha, S A AU - Taha SA AD - Department of Physiology, University of Utah School of Medicine, Salt Lake City, UT 84108, USA. s.taha@utah.edu FAU - Katsuura, Y AU - Katsuura Y FAU - Noorvash, D AU - Noorvash D FAU - Seroussi, A AU - Seroussi A FAU - Fields, H L AU - Fields HL LA - eng GR - R21 MH082325/MH/NIMH NIH HHS/United States GR - R21 MH082325-02/MH/NIMH NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, Non-P.H.S. DEP - 20090329 PL - United States TA - Neuroscience JT - Neuroscience JID - 7605074 RN - 0 (GABA Agonists) RN - 0 (Neurotoxins) RN - 0 (Neurotransmitter Agents) RN - 0 (Receptors, Opioid, mu) RN - 100929-53-1 (Enkephalin, Ala(2)-MePhe(4)-Gly(5)-) RN - 2763-96-4 (Muscimol) RN - F6F0HK1URN (Quinolinic Acid) SB - IM MH - Animals MH - Catheterization MH - Eating/drug effects/*physiology MH - Enkephalin, Ala(2)-MePhe(4)-Gly(5)-/administration & dosage MH - Feeding Behavior/drug effects/physiology MH - GABA Agonists/administration & dosage MH - Globus Pallidus/drug effects/*physiology MH - Hyperphagia/chemically induced/physiopathology MH - Male MH - Motor Activity/drug effects/physiology MH - Muscimol/administration & dosage MH - Neural Pathways/drug effects/physiology MH - Neurotoxins/toxicity MH - Neurotransmitter Agents/administration & dosage MH - Nucleus Accumbens/drug effects/*physiology MH - Quinolinic Acid/toxicity MH - Random Allocation MH - Rats MH - Rats, Long-Evans MH - Receptors, Opioid, mu/agonists/*metabolism MH - Time Factors PMC - PMC2699890 MID - NIHMS106551 EDAT- 2009/04/02 09:00 MHDA- 2009/08/25 09:00 PMCR- 2010/07/07 CRDT- 2009/04/02 09:00 PHST- 2008/10/07 00:00 [received] PHST- 2009/02/23 00:00 [revised] PHST- 2009/03/21 00:00 [accepted] PHST- 2009/04/02 09:00 [entrez] PHST- 2009/04/02 09:00 [pubmed] PHST- 2009/08/25 09:00 [medline] PHST- 2010/07/07 00:00 [pmc-release] AID - S0306-4522(09)00467-9 [pii] AID - 10.1016/j.neuroscience.2009.03.057 [doi] PST - ppublish SO - Neuroscience. 2009 Jul 7;161(3):718-33. doi: 10.1016/j.neuroscience.2009.03.057. Epub 2009 Mar 29.