Brain metabolism after extended training in a fear conditioning task

learning that involves the association of stimuli and their aversive consequences. In this paradigm, the animal receives pairings of an innocuous conditioned stimulus (CS), such as a tone or the context of the conditioning chamber, and a noxious unconditioned stimulus (US), such as a footshock. After a few such pairings, the CS comes to elicit a constellation of conditioned responses (CRs) that are characteristic of fear, including «freezing» or immobility (the species-typical behavioural response to a threatening stimulus), autonomic and endocrine responses (such as changes in heart rate and blood pressure, defecation, and increased levels of circulating stress hormones), and other changes including the potentiation of reflexes such as the acoustic startle response. Associated with the autonomic symptoms of the fear response there are, in humans, cognitive effects such as feelings of dread and despair (de Vicente Pérez and Díaz-Berciano, 2005; Gutiérrez Maldonado and Arbej Sánchez, 2005). Disorders of the storage or expression of fear responses are thought to underlie such mental disorders as panic attacks, anxiety and post traumatic stress disorder. Because fear conditioning is rapidly acquired and persistent, involves welldefined stimuli and responses, occurs in every species that has been examined from flies to humans, and implicates similar neural circuits in different vertebrate species, it has emerged as an especially useful paradigm for understanding the neurobiological mechanisms of this form of behavioural plasticity (e.g. LeDoux, 2000; Maren, 2001; Schafe and LeDoux, 2002; Fanselow and Poulos, 2005). In recent years, the neural circuitry that underlies fear conditioning, particularly auditory fear conditioning, has been characterized in great detail (Fendt and Fanselow, 1999; LeDoux, 2000; Maren, 2001; Fanselow and Poulos, 2005). One of the most studied brain regions is the amygdala, which seems to be critically involved in fear conditioning. However, there is no general agreement about the role of this structure on PFC. Several authors suggest that the amygdala is not required for the formation of the Brain metabolism after extended training in a fear conditioning task