Plasticity of NMDA Receptors at Ventral Hippocampal Synapses in the Infralimbic Cortex Regulates Cued Fear

Soler-Cedeño, Omar; Torres-Rodríguez, Orlando; Bernard, Faviola; Maldonado, Lizette; Hernández, Anixa; Porter, James T.

doi:10.1523/eneuro.0354-18.2019

Cited by 18 publications

(14 citation statements)

References 45 publications

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“…However, they do not necessarily influence memory intensity upon retrieval and expression. Instead, they could allow adjustments in mechanisms supporting the original aversive memory to retain the extinction one 21,[42][43][44] . For instance, whereas fear conditioning was sufficient to depress the IL intrinsic excitability 18,19 , fear extinction produced the opposite outcome 45 .…”

Section: Discussionmentioning

confidence: 99%

Infralimbic cortex controls fear memory generalization and susceptibility to extinction during consolidation

Bayer

Bertoglio

2020

Sci Rep

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Lesioning or inactivating the infralimbic (IL) subregion of the medial prefrontal cortex before acquisition produces more generalized and extinction-resistant fear memories. However, whether and how it modulates memory specificity and extinction susceptibility while consolidation takes place is still unknown. The present study aims to investigate these questions using muscimol-induced temporary inactivation and anisomycin-induced protein synthesis inhibition in the rat IL following contextual fear conditioning. Results indicate that the IL activity immediately after acquisition, but not six hours later, controls memory generalization over a week, regardless of its strength. Such IL function depends on the context-shock pairing since muscimol induced no changes in animals exposed to immediate shocks or the conditioning context only. Animals in which the IL was inactivated during consolidation extinguished similarly to controls within the session but were unable to recall the extinction memory the following day. Noteworthy, these post-acquisition IL inactivation-induced effects were not associated with changes in anxiety, as assessed in the elevated plus-maze test. Anisomycin results indicate that the IL protein synthesis during consolidation contributes more to producing extinction-sensitive fear memories than memory specificity. Collectively, present results provide evidence for the IL's role in controlling generalization and susceptibility to extinction during fear memory consolidation.

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Section: Discussionmentioning

confidence: 99%

Infralimbic cortex controls fear memory generalization and susceptibility to extinction during consolidation

Bayer

Bertoglio

2020

Sci Rep

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“…The glutamatergic projections from vCA1 to basolateral amygdala (BLA) encode conditioned fear memory whereas glutamatergic projections to the central amygdala (CeA) are necessary for the reinstatement of a cued fear response (e.g., freezing) following extinction (Xu et al, 2016 ; Jimenez et al, 2018 ). On the other hand, the regulation of conditioned fear extinction and renewal by vHPC seems to be via its glutamatergic projections to the infralimbic (IfL) and prelimbic (PrL) prefrontal cortices, respectively (Sierra-Mercado et al, 2011 ; Soler-Cedeño et al, 2019 ; Vasquez et al, 2019 ). Furthermore, there is a population of neurons within vCA1 that project monosynaptically to both the medial PFC and BLA that have been found to be preferentially activated during fear renewal (Jin and Maren, 2015 ) and are suspected to be important in conditioned fear extinction (Ishikawa and Nakamura, 2006 ; Kim and Cho, 2017 ).…”

Section: Vhpc As An Arbitrator Of Conflicting Stimulimentioning

confidence: 99%

Arbitration of Approach-Avoidance Conflict by Ventral Hippocampus

Bryant

Barker

2020

Front. Neurosci.

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When environmental cues or stimuli that represent both rewarding and aversive outcomes are presented, complex computations must be made in order to determine whether approach or avoidance is the better behavioral strategy. In many neuropsychiatric illnesses these computations can be skewed. In some instances, circumstances that may normally warrant avoidance instead promote approach, thus producing compulsive-like behavioral strategies that are inflexible in response to new or conflicting information. Alternatively, high sensitivity to aversion or low sensitivity to reward can result in the failure to achieve goals and loss of resilience that characterizes depressive disorders. Increases in compulsive-like behavior have been found to be associated with disrupted signaling in regions that regulate response to conflicting stimuli, including the hippocampus. Classic behavioral inhibition theories of hippocampus function in anxiety suggest that the hippocampus blocks aberrant behavior in response to anxiety related cues or stimuli. The hippocampus may act to block approach in the face of conflicting stimuli. Dysregulations of hippocampal function, as may be present in neuropsychiatric disorders, may therefore promote aberrant approach behavior. The ventral hippocampus (vHPC) subregion is key for coordinating this approach/avoidance conflict resolution, likely through its participation with cortico-striatal and mesolimbic circuits. We revisit Gray's behavioral inhibition theory of HPC function, first posited in the 1980s, and interpret in the context of new knowledge on vHPC function gained through modern technology. Taken together with the extant, classical literature on hippocampal function, we propose that these new findings suggest that vHPC circuits balance behavioral response to conflicting stimuli in a manner that is both state- and context-dependent and, further, that disruption of specific vHPC circuits tips the balance in favor of biased approach or avoidance behavioral strategies.

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“…shown that the subregions of the mPFC (such as the PrL, IL, and Cg1) play separate roles in fear conditioning and PTSD symptoms [33]. Previous studies have reported some controversial evidence in this regard [20,[34][35][36][37]. For example, a study of fear conditioning discrimination showed that Behavioural Neurology the subdivisions of the mPFC activated different responses to fear discrimination learning, and the PrL and IL seemingly contributed counterbalanced roles in fear discrimination learning [34].…”

Section: The Mpfc and Ptsd A Growing Body Of Evidence Hasmentioning

confidence: 99%

“…Using the single prolonged-stress footshock procedure of the PTSD model indicated that the prefrontal cortex has lower BDNF levels [19]. BDNF secretions in the ventral hippocampus-infralimbic cortex (IL) pathway could alter the fear contextual conditioning [20]. Under long-term restraint stress, the basolateral amygdala (BLA) exhibited higher levels in BDNF protein and BDNF mRNA expression; moreover, the CA3 of the hippocampus has lower BDNF protein and BDNF mRNA expression [21].…”

Section: Introductionmentioning

confidence: 99%

BDNF Protein and BDNF mRNA Expression of the Medial Prefrontal Cortex, Amygdala, and Hippocampus during Situational Reminder in the PTSD Animal Model

Chang

et al. 2021

Behavioural Neurology

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Whether BDNF protein and BDNF mRNA expression of the medial prefrontal cortex (mPFC; cingulated cortex area 1 (Cg1), prelimbic cortex (PrL), and infralimbic cortex (IL)), amygdala, and hippocampus (CA1, CA2, CA3, and dentate gyrus (DG)) was involved in fear of posttraumatic stress disorder (PTSD) during the situational reminder of traumatic memory remains uncertain. Footshock rats experienced an inescapable footshock (3 mA, 10 s), and later we have measured fear behavior for 2 min in the footshock environment on the situational reminder phase. In the final retrieval of situational reminder, BDNF protein and mRNA levels were measured. The results showed that higher BDNF expression occurred in the Cg1, PrL, and amygdala. Lower BDNF expression occurred in the IL, CA1, CA2, CA3, and DG. BDNF mRNA levels were higher in the mPFC and amygdala but lower in the hippocampus. The neural connection analysis showed that BDNF protein and BDNF mRNA exhibited weak connections among the mPFC, amygdala, and hippocampus during situational reminders. The present data did not support the previous viewpoint in neuroimaging research that the mPFC and hippocampus revealed hypoactivity and the amygdala exhibited hyperactivity for PTSD symptoms. These findings should be discussed with the previous evidence and provide clinical implications for PTSD.

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Plasticity of NMDA Receptors at Ventral Hippocampal Synapses in the Infralimbic Cortex Regulates Cued Fear

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Cited by 18 publications

References 45 publications

Infralimbic cortex controls fear memory generalization and susceptibility to extinction during consolidation

Infralimbic cortex controls fear memory generalization and susceptibility to extinction during consolidation

Arbitration of Approach-Avoidance Conflict by Ventral Hippocampus

BDNF Protein and BDNF mRNA Expression of the Medial Prefrontal Cortex, Amygdala, and Hippocampus during Situational Reminder in the PTSD Animal Model

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