Abstract
Extinction learning provides the ability to flexibly adapt to new contingencies by learning to inhibit previously acquired associations in a context-dependent manner. The neural networks underlying extinction learning were mostly studied in rodents using fear extinction paradigms. To uncover invariant properties of the neural basis of extinction learning, we employ pigeons as a model system. Since the prefrontal cortex (PFC) of mammals is a key structure for extinction learning, we assessed the role of N-methyl-D-aspartate receptors (NMDARs) in the nidopallium caudolaterale (NCL), the avian functional equivalent of mammalian PFC. Since NMDARs in PFC have been shown to be relevant for extinction learning, we locally antagonized NMDARs through 2-Amino-5-phosphonovalerianacid (APV) during extinction learning in a within-subject sign-tracking ABA-renewal paradigm. APV-injection slowed down extinction learning and in addition also caused a disinhibition of responding to a continuously reinforced control stimulus. In subsequent retrieval sessions, spontaneous recovery was increased while ABA renewal was unaffected. The effect of APV resembles that observed in studies of fear extinction with rodents, suggesting common neural substrates of extinction under both appetitive and aversive conditions and highlighting the similarity of mammalian PFC and the avian caudal nidopallium despite 300 million years of independent evolution.
Highlights
Learning enables organisms to survive in a permanently changing environment
Overall 36 cannulas were found to be within the nidopallium caudolaterale (NCL) and 28 cannulas were placed in the nidopallium caudocentrale (NCC) (Figure 2)
The present study investigated the role of Nmethyl-D-aspartate receptors (NMDARs) in the NCL for extinction memory by pharmacologically modulating these receptors with the antagonist APV during extinction
Summary
Learning enables organisms to survive in a permanently changing environment. During learning, stimuli that are initially neutral become associated with co-occurring unconditioned stimuli and acquire the ability to elicit conditioned responses. The transfer to a context other than that where extinction took place results in the reappearance of the conditioned behavior, a phenomenon termed renewal (Bouton and Bolles, 1979; Bouton and Ricker, 1994; Rauhut et al, 2001; Bouton, 2002; Crombag and Shaham, 2002). It illustrates that extinction does not erase the old memory trace but entails new learning (Pavlov, 1927; Bouton, 2004). Pharmacological manipulations of the hippocampus as well as the PFC demonstrate that these structures are involved in contextual coding during renewal and extinction retrieval (Corcoran and Maren, 2004; Burgos-Robles et al, 2007)
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