title: Lesions of the medial prefrontal cortex enhance the early phase of psychogenic fever to unexpected sucrose concentration reductions, promote recovery from negative contrast and enhance spontaneous recovery of sucrose-entrained anticipatory activity.
abstract: Two groups of rats, one bearing bilateral excitotoxic lesions of the medial prefrontal cortex (mPFC) and one sham-lesioned group, were run in a successive negative contrast paradigm. Both groups had telemeters implanted to monitor core temperature and activity. After ad libitum baseline and food restriction to 85% body weights, rats received a sucrose solution once daily for 5 min and 30 s at 10:30 h. They received their preshift 32% sucrose solution for 14 days followed by a sucrose concentration reduction (downshift) to 4% sucrose for 12 days. Rats were then upshifted to 32% for six additional days before being downshifted to 4% for the next 6 days. There were no differences in intake of the 32% sucrose during the preshift. All rats showed profound suppression of intake upon the shift to 4% sucrose. On the first day of the unexpected 4% sucrose, lesioned rats showed an enhanced psychogenic fever compared with Shams, whereas on the second day of 4% sucrose they showed an impaired ability to blunt that fever compared with Shams. In addition, lesioned rats showed greater rates of recovery and asymptotic drinking of the subsequent 4% sucrose solution than Shams, indicating impairments in the encoding or retrieval of the shift. In addition, lesioned rats showed enhanced entrainment to the 32% sucrose meals, normal damping of anticipation, and enhanced spontaneous recovery of anticipatory thermal responses to the calorically impoverished 4% solutions. These failures to inhibit responding point to a failure in interference learning in rats bearing lesions of the mPFC.
authors.affiliation: Department of Physiology, School of Medicine, University of California-San Francisco, 415 Parnassus Avenue, San Francisco, CA 94143-0444, USA. norman.pecoraro@ucsf.edu
authors.forename: N
authors.initials: N
authors.lastname: Pecoraro
authors.forename: H
authors.initials: H
authors.lastname: de Jong
authors.forename: A B
authors.initials: AB
authors.lastname: Ginsberg
authors.forename: M F
authors.initials: MF
authors.lastname: Dallman
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000704:Analysis of Variance; D000818:Animals; D001522:Behavior, Animal; D001831:Body Temperature / Q000502:physiology; D001835:Body Weight; D003216:Conditioning, Operant; D003345:Corticosterone / Q000097:blood; D004305:Dose-Response Relationship, Drug; D004435:Eating / Q000502:physiology; D005334:Fever / Q000209:etiology*; D005508:Food Deprivation; D008297:Male; D009043:Motor Activity / Q000502:physiology; D017397:Prefrontal Cortex / Q000293:injuries* / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D020127:Recovery of Function / Q000502:physiology*; D012149:Restraint, Physical / Q000379:methods; D013315:Stress, Psychological / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D013395:Sucrose / Q000008:administration & dosage*; D013997:Time Factors
chemical_list: D013395:Sucrose; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone