Microstimulation reveals opposing influences of prelimbic and infralimbic cortex on the expression of conditioned fear.

By Ivan Vidal-Gonzalez, Benjamín Vidal-Gonzalez, Scott L. Rauch, Gregory J. Quirk. Learning & memory (Cold Spring Harbor, N.Y.), 2006

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Recent studies using lesion, infusion, and unit-recording techniques suggest that the infralimbic (IL) subregion of medial prefrontal cortex (mPFC) is necessary for the inhibition of conditioned fear following extinction. Brief microstimulation of IL paired with conditioned tones, designed to mimic neuronal tone responses, reduces the expression of conditioned fear to the tone. In the present study we used microstimulation to investigate the role of additional mPFC subregions: the prelimbic (PL), dorsal anterior cingulate (ACd), and medial precentral (PrCm) cortices in the expression and extinction of conditioned fear. These are tone-responsive areas that have been implicated in both acquisition and extinction of conditioned fear. In contrast to IL, microstimulation of PL increased the expression of conditioned fear and prevented extinction. Microstimulation of ACd and PrCm had no effect. Under low-footshock conditions (to avoid ceiling levels of freezing), microstimulation of PL and IL had opposite effects, respectively increasing and decreasing freezing to the conditioned tone. We suggest that PL excites amygdala output and IL inhibits amygdala output, providing a mechanism for bidirectional modulation of fear expression.

Subfields: Behavioral Neuroscience, Cellular and Molecular Neuroscience, Cognitive Neuroscience

View Paper: https://www.semanticscholar.org/paper/a0f35dc9c01e2aa8559caa7f3e14a8dd638d5564

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Citations in the corpus

Neurobiological Basis of Failure to Recall Extinction Memory in Posttraumatic Stress Disorder (2009, background): “, the prelimbic cortex, has been found to promote conditioned fear expression (45,46,47).”
Working Memory: Theories, Models, and Controversies (2015, neutral): “Finally, microstimulation of PL increased freezing responses to conditioned tones and impaired extinction (Vidal-Gonzalez et al. 2006).”
Dissociable roles of prelimbic and infralimbic cortices, ventral hippocampus, and basolateral amygdala in the expression and extinction of conditioned fear (2010, neutral): “Recent electrophysiological findings suggest that IL and PL have opposite influences on fear expression (Gilmartin and McEchron, 2005; Vidal-Gonzalez et al., 2006), and have different targets within the amygdala (Vertes, 2004; Gabbott et al., 2005).”
Extinction circuits for fear and addiction overlap in prefrontal cortex. (2009, background): “The prefrontal cortex has been strongly implicated in fear expression (Powell et al. 2001; Vidal-Gonzalez et al. 2006; Corcoran and Quirk 2007) and fear extinction (Herry and Garcia 2002; Milad and Quirk 2002; Gonzalez-Lima and Bruchey 2004; Hugues et al. 2004; Burgos-Robles et al. 2007; Hikind and…”
Synchronized activity between the ventral hippocampus and the medial prefrontal cortex during anxiety (2010, positive): “Stimulation of the prelimbic cortex decreases recall of fear extinction, consistent with the idea that this subregion of the mPFC acts to increase anxiety-like behaviors (Vidal-Gonzalez et al., 2006).”
Neural Mechanisms of Extinction Learning and Retrieval (2008, background): “Pharmacological inactivation of PL reduces conditioned fear expression (Corcoran and Quirk, 2007a; Blum et al, 2006), and microstimulation of PL increases conditioned fear expression (Vidal-Gonzalez et al, 2006).”
Fear Extinction as a Model for Translational Neuroscience: Ten Years of Progress (2012, background): “Finally, microstimulation of PL increased freezing responses to conditioned tones and impaired extinction (Vidal-Gonzalez et al 2006).”
Prefrontal control of fear: more than just extinction (2010, background): “PL-mediated excitation of fear expression Although earlier studies suggested a role of PL in excitation of fear [28,29], new studies using a variety of techniques have confirmed and extended that role [51].”
Brain structural and functional abnormalities in mood disorders: implications for neurocircuitry models of depression (2008, result): “…the remitted phases, the relationship between physiological activity and symptom severity differs in valence across some structures, compatible with preclinical evidence that distinct MPFC structures are involved in opponent processes with respect to emotional behavior (Vidal-Gonzalez et al. 2006).”
Theta oscillations between the ventromedial prefrontal cortex and amygdala support dynamic representations of threat and safety (2025, unknown): “We also observed increased theta input from the vmPFC to the amygdala under safety stimuli during fear acquisition, further supporting the role of the IL/vmPFC in modulating fear reduction (Do-Monte et al., 2015; Vidal-Gonzalez et al., 2006).”