Posterodorsal amygdala lesions reduce feeding stimulated by 8-OH-DPAT

Citation
Dv. Coscina et al., Posterodorsal amygdala lesions reduce feeding stimulated by 8-OH-DPAT, BRAIN RES, 883(2), 2000, pp. 243-249
Citations number
45
Categorie Soggetti
Neurosciences & Behavoir
Journal title
BRAIN RESEARCH
ISSN journal
00068993 → ACNP
Volume
883
Issue
2
Year of publication
2000
Pages
243 - 249
Database
ISI
SICI code
0006-8993(20001117)883:2<243:PALRFS>2.0.ZU;2-B
Abstract
Injections of the serotonin (5-HT)(1A) agonist, 8-hydroxy-2(di-n-propylamin o)tetralin, (8-OH-DPAT), either systemically or into the midbrain raphe nuc lei, elicit food intake in otherwise satiated rats. Lesions of the paravent ricular nucleus of the hypothalamus are well known for producing long-term overeating, but past research has excluded this site as a potential locus f or short-term 8-OH-DPAT feeding effects. More recent work shows that small lesions of the posterodorsal amygdala (PDA) elicit overeating in their own right. Since this and related regions of the amygdala receive 5-HT innervat ions from the dorsal raphe nucleus (DRN), we determined if PDA lesions migh t alter feeding after injecting 8-OH-DPAT into this midbrain region. Adult female rats received either bilateral electrolytic lesions of the PDA or sh am lesions. After recording weight gains for over 1 month, all rats were im planted with DRN cannulae, then randomly tested every 3-4 days for 1 h inta ke of standard lab chow after 0, 0.4, 0.8 or 1.6 nmol injections of 8-OH-DP AT. Additional 90 min measures of intake were also made after 0 vs. 250 mug (760 nmol) 8-OH-DPAT s.c. At the two highest DRN doses tested, lesioned ra ts showed 50% less intake compared to shams. A similar profile emerged afte r the single s.c. dose. These results suggest that the PDA may be an import ant locus at which reduced release of endogenous 5-HT stimulates feeding. A lternatively, the PDA may represent part of a larger brain circuit whose in tegrity is necessary for eliciting intake in response to a variety of feedi ng stimuli. (C) 2000 Elsevier Science B.V. All rights reserved.