title: Large neurotoxic amygdala lesion impairs reinforcement omission effects.
abstract: The amygdala has been implicated in a variety of motivational and attentional functions related to appetitive learning. Some studies showed that electrolytic lesions of the amygdaloid complex disrupted reinforcement omission effects (ROEs). However, recent studies that investigated ROEs employing neurotoxic lesions in specific amygdala areas - the central nucleus (CeA) or basolateral complex (BLA) of the amygdala - showed that CeA lesions or BLA lesions can interfere with, but do not eliminate ROEs. Although the effects of neurotoxic lesions in particular areas of the amygdala differed from those of a large gross lesion, these studies have indicated that it is possible that the amygdala is involved in ROE modulation. Furthermore, the effect that a neurotoxic lesion involving both areas (CeA and BLA) has on ROEs remains unexplored. Thus, the present study aimed to clarify whether the functional impairment related to large amygdala activation affects ROEs, in a neurotoxic lesion procedure. If this is the case, the underlying process may contribute to a better understanding of the involvement of the amygdala in ROEs modulation. After acquisition of stable performance during pre-lesion training in which rats were trained to respond on a fixed-interval 6 s with limited hold 6 s schedules (FI 6 s LH 6 s), lesions were made including both the CeA and BLA areas. In test sessions, the partial omission of reinforcement was introduced. The results showed that bilateral lesion of both CeA and BLA impaired ROEs, suggesting that amygdala is part of ROEs' modulation circuitry.
authors.affiliation: Departamento de Psicologia, Faculdade de Filosofia, Ciências e Letras de Ribeirão Preto, Universidade de São Paulo, Avenida Bandeirantes, 3900 14040-901, Ribeirão Preto, São Paulo, Brazil. Electronic address: paratatiane@yahoo.com.br.
authors.forename: Tatiane F
authors.initials: TF
authors.lastname: Tavares
authors.affiliation: Departamento de Psicologia, Faculdade de Filosofia, Ciências e Letras de Ribeirão Preto, Universidade de São Paulo, Avenida Bandeirantes, 3900 14040-901, Ribeirão Preto, São Paulo, Brazil. Electronic address: dadatrabalho@yahoo.com.br.
authors.forename: Danielle M
authors.initials: DM
authors.lastname: Judice-Daher
authors.affiliation: Departamento de Psicologia, Faculdade de Filosofia, Ciências e Letras de Ribeirão Preto, Universidade de São Paulo, Avenida Bandeirantes, 3900 14040-901, Ribeirão Preto, São Paulo, Brazil. Electronic address: jldobuen@usp.br.
authors.forename: José Lino O
authors.initials: JL
authors.lastname: Bueno
mesh_terms: D000818:Animals; D066272:Basolateral Nuclear Complex / Q000293:injuries / Q000502:physiology*; D066274:Central Amygdaloid Nucleus / Q000293:injuries / Q000502:physiology*; D003216:Conditioning, Operant / Q000502:physiology*; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity; D005108:Extinction, Psychological / Q000502:physiology*; D007051:Ibotenic Acid / Q000633:toxicity; D008297:Male; D051381:Rats; D012055:Reinforcement Schedule; D012054:Reinforcement, Psychology; D018709:Statistics, Nonparametric
chemical_list: D018690:Excitatory Amino Acid Agonists; D007051:Ibotenic Acid
keywords: Amygdala; Omission effect; Operant behavior; Rat