Event Abstract

Neuronal circuitry of fear conditioning and extinction

  • 1 Friedrich Miescher Institute for Biomedical Research, Switzerland

While many studies have demonstrated that neuronal plasticity in the basolateral amygdala (BLA) is necessary for the acquisition of Pavlovian fear conditioning, the role of the central nucleus of the amygdala (CEA) is poorly understood. In the classical circuit model, the CEA has been thought of as a passive relay station conveying BLA output to downstream targets in the hypothalamus and in the brain stem. However, recent in vivo pharmacological experiments suggest a more active role for the CEA during fear conditioning. To address the neuronal substrates of CEA plasticity during fear conditioning we have combined targeted pharmacological inactivation and single unit recordings from CEA neurons in behaving mice. We found that fear conditioning induced differential changes in stimulus-evoked and spontaneous firing of distinct types of CEA neurons. Moreover, targeted pharmacological inactivation revealed that discrete parts of CEA circuitry differentially contribute to the acquisition and expression of conditioned fear. Our results indicate that plasticity within CEA and/or of afferents to CEA contributes to fear memory acquisition and the formation of CS-US associations. Thus, fear conditioning-related neuronal plasticity is not limited to the BLA, and behavioral learning depends on plasticity at multiple levels within the amygdala circuitry. Extinction of conditioned fear is a form of learning that relies on the progressive inhibition of the memory trace previously acquired through the pairing of a conditioned tone (CS) with a footshock (US). During fear extinction, amygdala output is thought to become gradually inhibited through activation of local inhibitory circuits by inputs from the medial prefrontal cortex (mPFC). Converging evidence from animal and human studies, however, indicate that the basolateral complex of the amygdala (BLA), comprised of the lateral nucleus (LA) and the basal nucleus (BA) actively participates to fear extinction. This raises the question whether fear conditioning and extinction engage a common neural circuit within the amygdala, or whether the amygdala contains distinct sub-circuits dedicated to processing specific behavioral aspects. To distinguish between these possibilities and to disentangle the cellular substrates underlying fear conditioning and extinction, we used a combination of in vivo single unit recordings from amygdala neurons and targeted pharmacological inactivation in behaving mice. We found that the BA contains a specific sub-circuit reciprocally connected with the mPFC that mediates extinction of conditioned fear behavior. Our findings provide a new framework for understanding the neuronal substrates underlying fear conditioning and extinction.

Conference: 41st European Brain and Behaviour Society Meeting, Rhodes Island, Greece, 13 Sep - 18 Sep, 2009.

Presentation Type: Oral Presentation

Topic: Symposia lectures

Citation: Luthi A (2009). Neuronal circuitry of fear conditioning and extinction. Conference Abstract: 41st European Brain and Behaviour Society Meeting. doi: 10.3389/conf.neuro.08.2009.09.035

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Received: 04 Jun 2009; Published Online: 04 Jun 2009.

* Correspondence: Andreas Luthi, Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland, andreas.luthi@fmi.ch