Synapses, circuits, and the ontogeny of learning

Hunt, Pamela S.; Fanselow, Michael S.; Richardson, Rick; Mauk, Michael D.; Freeman, John H.; Stanton, Mark E.

doi:10.1002/dev.20250

Cited by 20 publications

(11 citation statements)

References 61 publications

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“…c). This is consistent with previous studies showing weaker retention of contextual fear conditioning for infant rats compared to juvenile and adult rats (Hunt et al, ; Rudy, ; Rudy & Morledge, ; Schiffino, Murawski, Rosen, & Stanton, ). It is important to note, however, that while PND17 rats do not show significant freezing to a context associated with presentation of a single footshock, more subtle indications of memory for the fear conditioning experience are present in these infant rats (Pisano et al, ).…”

Section: Discussionsupporting

confidence: 92%

Infant stress exposure produces persistent enhancement of fear learning across development

Quinn

Skipper

Claflin

2013

Developmental Psychobiology

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In recent years, it has become increasingly clear that early life stress experiences persistently impact subsequent physiological, cognitive, and emotional responses. In cases of trauma, these early experiences can result in anxiety disorders such as phobias and posttraumatic stress disorder. In the present paper, we examined the effects of infant footshock stress exposure at postnatal day (PND) 17 on subsequent contextual fear conditioning at postnatal days 18 (Experiment 1), 24 (Experiment 2), or 90 (Experiment 3). In each experiment, PND17 footshock stress exposure enhanced later fear conditioning, indicating that the stress enhancement of fear learning (SEFL) persists throughout development. Memory for the original stress exposure context was gradually forgotten, with significant fear expression evident at PND20, and a complete lack of fear expression in that same context at PND90. These data suggest that the stress-enhancing component of infant fear learning is dissociable from the infant contextual fear memory per se. In other words, early life stress produces persistent effects on subsequent cognition that are independent of the memory for that early life event.

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Section: Discussionsupporting

confidence: 92%

Infant stress exposure produces persistent enhancement of fear learning across development

Quinn

Skipper

Claflin

2013

Developmental Psychobiology

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“…Interestingly, those deficits were not present during the reversal learning task, which suggests the presence of cognitive flexibility in SCD mice. Animal and human studies indicate that intact hippocampal and cerebellar functions are required for normal cognitive learning and memory and that both spatial and reversal learning in the water T-maze are impaired after hippocampal lesions(Burgess et al, 2002; Gandhi et al, 2000; Hunt et al, 2007; Wang et al, 2011). However, during reversal learning, the striatum, frontal cortex, and nucleus accumbens neurons are engaged (Clarke et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Cognitive and behavior deficits in sickle cell mice are associated with profound neuropathologic changes in hippocampus and cerebellum

Wang

Almeida

Batista

et al. 2016

Neurobiology of Disease

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Strokes are perhaps the most serious complications of sickle cell disease (SCD) and by the fifth decade occur in approximately 25% of patients. While most patients do not develop strokes, mounting evidence indicates that even without brain abnormalities on imaging studies, SCD patients can present profound neurocognitive dysfunction. We sought to evaluate the neurocognitive behavior profile of humanized SCD mice (Townes, BERK) and to identify hematologic and neuropathologic abnormalities associated with the behavioral alterations observed in these mice. Heterozygous and homozygous Townes mice displayed severe cognitive deficits shown by significant delays in spatial learning compared to controls. Homozygous Townes also had increased depression- and anxiety-like behaviors as well as reduced performance on voluntary wheel running compared to controls. Behavior deficits observed in Townes were also seen in BERKs. Interestingly, most deficits in homozygotes were observed in older mice and were associated with worsening anemia. Further, neuropathologic abnormalities including the presence of large bands of dark/pyknotic (shrunken) neurons in CA1 and CA3 fields of hippocampus and evidence of neuronal dropout in cerebellum were present in homozygotes but not control Townes. These observations suggest that cognitive and behavioral deficits in SCD mice mirror those described in SCD patients and that aging, anemia, and profound neuropathologic changes in hippocampus and cerebellum are possible biologic correlates of those deficits. These findings support using SCD mice for studies of cognitive deficits in SCD and point to vulnerable brain areas with susceptibility to neuronal injury in SCD and to mechanisms that potentially underlie those deficits.

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“…Furthermore, HPA activity has been shown to be reduced to only the second exposure to a stressor despite a long interval of time between the first and second exposures, suggesting some sort of memory trace produced by prior stress which can influence subsequent HPA activity (Armario, Valles, Dal-Zotto, Marquez, & Belda, 2004; Vogel & Jensh, 1988). Finally, habituation of HPA activity involves activation of distributed limbic circuitry (Herman, Figueiredo, Muller, Ulrich-Lai, Ostrander, Choi, and Cullinan, 2003) that overlaps with circuitry important for associative learning (Hunt, Fanselow, Richardson, Mauk, Freeman, & Stanton, 2007). Though direct tests of whether habituation of HPA activity relies on associative learning will be challenging to design, this idea must be addressed for a full understanding of adaptation of physiological and behavioral responses to repeated stress.…”

Section: Discussionmentioning

confidence: 99%

Habituation to repeated stress: Get used to it

Grissom

Bhatnagar

2009

Neurobiology of Learning and Memory

428

301

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Habituation, as described in the landmark paper by Thompson and Spencer (1966), is a form of simple, nonassociative learning in which the magnitude of the response to a specific stimulus decreases with repeated exposure to that stimulus. A variety of neuronal and behavioral responses have been shown to be subject to habituation based on the criteria presented in that paper. It has been known for several decades that the magnitude of hypothalamic-pituitary-adrenal (HPA) activation occurring in response to a stressor declines with repeated exposure to that same stressor. For some time this decline has been referred to as “habituation” in the stress neurobiology literature. However, how this usage compares to the definition proposed by Thompson and Spencer has not been systematically addressed. For this special issue, we review the stress neurobiology literature and examine the support available for considering declines in HPA response to repeated stress to be response habituation in the sense defined by Thompson and Spencer. We conclude that habituation of HPA activity meets many, but not all, important criteria for response habituation, supporting the use of this term within the context of repeated stress. However, we also propose that response habituation can, at best, only partially explain the phenomenon of HPA habituation which also involves well-known negative feedback mechanisms, activation of broad stress-related neural circuitry and potentially more complex associative learning mechanisms.

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Synapses, circuits, and the ontogeny of learning

Cited by 20 publications

References 61 publications

Infant stress exposure produces persistent enhancement of fear learning across development

Infant stress exposure produces persistent enhancement of fear learning across development

Cognitive and behavior deficits in sickle cell mice are associated with profound neuropathologic changes in hippocampus and cerebellum

Habituation to repeated stress: Get used to it

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