Role of the basolateral amygdala and NMDA receptors in higher-order conditioned fear

Shauna L. Parkes, R. Frederick Westbrook
Reviews in the Neurosciences. 2011-01-01; 22(3):
DOI: 10.1515/RNS.2011.025

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1. Rev Neurosci. 2011;22(3):317-33. doi: 10.1515/RNS.2011.025. Epub 2011 May 13.

Role of the basolateral amygdala and NMDA receptors in higher-order conditioned
fear.

Parkes SL(1), Westbrook RF.

Author information:
(1)Brain and Mind Research Institute, The University of Sydney, NSW 2050,
Australia.

Laboratory rats learn to fear relatively innocuous stimuli which signal the
imminent arrival of an innate source of danger, typically brief but aversive foot
shock. Much is now known about the neural substrates underlying the acquisition,
consolidation and subsequent expression of this fear. Rats also learn to fear
stimuli which signal learned sources of danger but relatively little is known
about the neural substrates underlying this form of fear. Two Pavlovian
conditioning paradigms used to study this form of fear are second-order
conditioning and sensory preconditioning. In second-order conditioning, rats are
first exposed to a signaling relationship between one stimulus, such as a tone,
and aversive foot shock, and then to a signaling relationship between a second
stimulus, such as a light, and the now dangerous tone. In sensory
preconditioning, these phases are reversed: rats are first exposed to a signaling
relationship between the light and the tone and then to a signaling relationship
between the tone and the foot shock. In both paradigms, rats exhibit fear when
tested with the light. In this review paper, we describe the evidence for
higher-order forms of conditioning, the conditions which promote this learning
and its contents. We compare and contrast the substrates of the learning
underlying second-order and sensory preconditioning fear with those known to
underlie the better studied first-order conditioned fear. We conclude with some
comments as to the role of higher-order processes in anxiety disorders.

DOI: 10.1515/RNS.2011.025
PMID: 21591909 [Indexed for MEDLINE]


Auteurs Bordeaux Neurocampus