title: Inactivation of the central but not the basolateral nucleus of the amygdala disrupts learning in response to overexpectation of reward.
abstract: The amygdala is critical for associating predictive cues with primary rewarding and aversive outcomes. This is particularly evident in tasks in which information about expected outcomes is required for normal responding. Here we used a pavlovian overexpectation task to test whether outcome signaling by amygdala might also be necessary for changing those representations in the face of unexpected outcomes. Rats were trained to associate several different cues with a food reward. After learning, two of the cues were presented together, in compound, followed by the same reward. Before each compound training session, rats received infusions of 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide or saline into either the basolateral (ABL) or central nucleus (CeN) of amygdala. We found that infusions into CeN abolished the normal decline in responding to the compounded cue in a later probe test, whereas infusions into ABL had no effect. These results are inconsistent with the proposal that signaling of information about expected outcomes by ABL contributes to learning, at least in this setting, and instead implicate the CeN in this process, perhaps attributable to the hypothesized involvement of this area in attention and variations in stimulus processing.
authors.affiliation: Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
authors.forename: Richard Z
authors.initials: RZ
authors.lastname: Haney
authors.forename: Donna J
authors.initials: DJ
authors.lastname: Calu
authors.forename: Yuji K
authors.initials: YK
authors.lastname: Takahashi
authors.forename: Brian W
authors.initials: BW
authors.lastname: Hughes
authors.forename: Geoffrey
authors.initials: G
authors.lastname: Schoenbaum
mesh_terms: D000679:Amygdala / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001245:Association Learning / Q000187:drug effects / Q000502:physiology; D001288:Attention / Q000187:drug effects / Q000502:physiology; D003071:Cognition / Q000187:drug effects / Q000502:physiology*; D003463:Cues; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000502:physiology; D007858:Learning / Q000187:drug effects / Q000502:physiology*; D007859:Learning Disabilities / Q000139:chemically induced / Q000503:physiopathology*; D008032:Limbic System / Q000187:drug effects / Q000502:physiology*; D008297:Male; D008606:Mental Processes / Q000187:drug effects / Q000502:physiology; D009434:Neural Pathways / Q000187:drug effects / Q000502:physiology; D009483:Neuropsychological Tests; D011810:Quinoxalines / Q000494:pharmacology; D051381:Rats; D020318:Rats, Long-Evans; D017470:Receptors, Glutamate / Q000187:drug effects / Q000502:physiology; D012201:Reward; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D013663:Teaching
chemical_list: D018691:Excitatory Amino Acid Antagonists; D011810:Quinoxalines; D017470:Receptors, Glutamate; C062865:2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline; D018698:Glutamic Acid