Updating memories: Changing the involvement of the prelimbic cortex in the expression of an infant fear memory

Li, S; Kim, Jee Hyun; Richardson, Rick

doi:10.1016/j.neuroscience.2012.06.038

Cited by 13 publications

(13 citation statements)

References 43 publications

(65 reference statements)

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“…In addition, these animals do not use the neural structures that have matured since the time of memory encoding. Juveniles use the prelimbic mPFC to retrieve/express fear that was learned during the juvenile developmental stage, but not if that memory was learned during infancy when this region was immature (Li et al 2012). However, rats trained as juveniles and extinguished as adolescents do not use NMDARs, or show pMAPK expression in the prefrontal cortex, during extinction-two features of the neural system that was in place when they acquired the fear as juvenile animals (Langton et al 2007;Baker and Richardson 2015).…”

Section: Discussionmentioning

confidence: 99%

Elucidating the mechanisms of fear extinction in developing animals: a special case of NMDA receptor-independent extinction in adolescent rats

2018

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NMDA receptors (NMDARs) are considered critical for the consolidation of extinction but recent work challenges this assumption. Namely, NMDARs are not required for extinction retention in infant rats as well as when extinction training occurs for a second time (i.e., reextinction) in adult rats. In this study, a possible third instance of NMDAR-independent extinction was tested. Although adolescents typically exhibit impaired extinction retention, rats that are conditioned as juveniles and then given extinction training as adolescents (JuvCond-AdolesExt) have good extinction retention. Unexpectedly, this good extinction retention is not associated with an up-regulation of a synaptic plasticity marker in the medial prefrontal cortex, a region implicated in extinction consolidation. In the current study, rats received either the noncompetitive NMDAR antagonist MK801 (0.1 mg/kg, s.c.) or saline before extinction training. In several experiments, rats conditioned and extinguished as juveniles, adolescents, or adults exhibited impaired extinction retention after MK801 compared to saline, but this effect was not observed in JuvCond-AdolesExt rats. Further experiments ruled out several alternative explanations for why NMDAR antagonism did not affect extinction retention in adolescents extinguishing fear learned as a juvenile. These results illustrate yet another circumstance in which NMDARs are not required for successful extinction retention and highlight the complexity of fear inhibition across development.

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Section: Discussionmentioning

confidence: 99%

Elucidating the mechanisms of fear extinction in developing animals: a special case of NMDA receptor-independent extinction in adolescent rats

2018

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“…Developmental changes in the mechanisms underlying retention of fear conditioning are seen in older rat pups. Prefrontal cortical engagement in the retention/retrieval of fear conditioning becomes evident between P17 and P24 (Kim, Li, Hamlin, McNally, & Richardson, 2012; Li, Kim, & Richardson, 2012a, 2012b). Prefrontal cortical development also plays a role in the development of spatial memory during this period (Freeman & Stanton, 1992; Jablonski, Watson, & Stanton, 2010; Watson & Stanton, 2009).…”

Section: Discussionmentioning

confidence: 99%

Ontogeny of septohippocampal modulation of delay eyeblink conditioning

Harmon

Freeman

2015

Developmental Psychobiology

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The current study investigated the effects of disrupting the septohippocampal theta system on the developmental emergence of delay eyeblink conditioning. Theta oscillations are defined as electroencephalographic (EEG) waveforms with a frequency between 3–8 Hz. Hippocampal theta oscillations are generated by inputs from the entorhinal cortex and the medial septum. Theta activity has been shown to facilitate learning in a variety of paradigms, including delay eyeblink conditioning. Lesions of the medial septum disrupt theta activity and slow the rate at which delay eyeblink conditioning is learned (Berry & Thompson, 1979). The role of the septohippocampal theta system in the ontogeny of eyeblink conditioning has not been examined. In the current study, infant rats received an electrolytic lesion of the medial septum on postnatal day (P)12. Rats were later given eyeblink conditioning for 6 sessions with an auditory conditioned stimulus on P17–P19, P21–23, or P24–P26. Lesions impaired eyeblink conditioning on P21–23 and P24–26 but not on P17–19. The results suggest that the septohippocampal system comes online to facilitate acquisition of eyeblink conditioning between P19 and P21. Developmental changes in septohippocampal modulation of the cerebellum may play a significant role in the ontogeny of eyeblink conditioning.

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“…Involvement of the PL vmPFC in fear learning begins later in life than that of the IL vmPFC (348), so the role of the former in fear learning acquisition must be carried out probably by the above-mentioned bidirectional nature of the IL-BLA connections (482) in younger animals (348); some fibers linking both structures go from BLA to IL and others go from IL to BLA.…”

Section: Hippocampus Amygdala Infralimbic Ventromedial Prefrontmentioning

confidence: 99%

Fear Memory

Izquierdo

Furini

Myskiw

2016

Physiological Reviews

377

259

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Fear memory is the best-studied form of memory. It was thoroughly investigated in the past 60 years mostly using two classical conditioning procedures (contextual fear conditioning and fear conditioning to a tone) and one instrumental procedure (one-trial inhibitory avoidance). Fear memory is formed in the hippocampus (contextual conditioning and inhibitory avoidance), in the basolateral amygdala (inhibitory avoidance), and in the lateral amygdala (conditioning to a tone). The circuitry involves, in addition, the pre-and infralimbic ventromedial prefrontal cortex, the central amygdala subnuclei, and the dentate gyrus. Fear learning models, notably inhibitory avoidance, have also been very useful for the analysis of the biochemical mechanisms of memory consolidation as a whole. These studies have capitalized on in vitro observations on long-term potentiation and other kinds of plasticity. The effect of a very large number of drugs on fear learning has been intensively studied, often as a prelude to the investigation of effects on anxiety. The extinction of fear learning involves to an extent a reversal of the flow of information in the mentioned structures and is used in the therapy of posttraumatic stress disorder and fear memories in general.

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Updating memories: Changing the involvement of the prelimbic cortex in the expression of an infant fear memory

Cited by 13 publications

References 43 publications

Elucidating the mechanisms of fear extinction in developing animals: a special case of NMDA receptor-independent extinction in adolescent rats

Elucidating the mechanisms of fear extinction in developing animals: a special case of NMDA receptor-independent extinction in adolescent rats

Ontogeny of septohippocampal modulation of delay eyeblink conditioning

Fear Memory

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