Some implications of postnatal hippocampal development

Nadel, Lynn

doi:10.1002/hipo.23369

Cited by 5 publications

(7 citation statements)

References 32 publications

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“… 12 , 66 In the first few days of postnatal life, the cortical development continues as neurons are gradually attaining their postmitotic state 50 and hippocampal neurogenesis continues into adulthood. 51 These models can be used to study the dysregulation of the cell cycle, which is critically dependent on depolarization states mediated by GABA and glutamate, 67 ionic balance, 68 and calcium regulation, 69 which are all affected by seizures. The suppression of RNA and synaptic protein synthesis in these models 70 , 71 may be linked to circuit modifications and later cognitive deficits.…”

Section: Even In the Absence Of Neuronal Death Seizures May Cause Las...mentioning

confidence: 99%

“…11,12,14 This is a period where active cell-cycle genes are still being expressed in the superficial layers of the cortex 50 and when neurogenesis is robust in the developing dentate gyrus. 51 These seizure-related effects on growth wane as the CNS exits the "brain growth spurt" when critical periods of development begin to close. 14 Wasterlain and Plum (1973) showed long ago that repeated electroconvulsive seizures and status epilepticus 14 significantly reduce RNA and DNA synthesis and that the outcome is critically dependent on the timing of the insult.…”

Section: Even In the Absence Of Neuronal Death Seizures May Cause Las...mentioning

confidence: 99%

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Status epilepticus and early development: Neuronal injury, neurodegeneration, and their consequences

Thompson

2022

Epilepsia Open

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Evidence showing that the immature brain is vulnerable to seizure‐induced damage has been accumulating for decades. Clinical data have always suggested that some early‐life seizures are associated with negative sequelae, but clinical observations are frequently obscured by multiple uncontrolled contributing factors and can rarely establish causality. Determining with certainty that seizures, per se, can cause neuronal death and can irreversibly disrupt critical developmental processes, required the development of suitable model systems. Several experimental seizure models clearly show that the immature brain can sustain neuronal injury as a result of uncontrolled seizure activity and that even in the absence of observable neuronal death, the developing brain is selectively vulnerable to interruptions of required growth programs. Severe early‐life seizures inhibit DNA, RNA, and protein synthesis, and they can reduce the accumulation of myelin and synaptic markers in the developing nervous system, leading to functional delays in development. Depending on the seizure pathway involved, and the developmental period under study, classic neurodegeneration, excitotoxicity, and apoptosis can result in permanent damage to critical neural networks in the temporal lobe and in many other brain regions. This conclusion is further supported by recent clinical studies showing that prolonged febrile status epilepticus can lead to hippocampal injury, which evolves into hippocampal atrophy and hippocampal sclerosis. A growing body of experimental data demonstrates that the metabolic compromise and cellular loss produced by seizures during critical phases of brain development negatively affect later hippocampal physiology including learning and memory functions in maturity.

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Section: Even In the Absence Of Neuronal Death Seizures May Cause Las...mentioning

confidence: 99%

Section: Even In the Absence Of Neuronal Death Seizures May Cause Las...mentioning

confidence: 99%

Status epilepticus and early development: Neuronal injury, neurodegeneration, and their consequences

Thompson

2022

Epilepsia Open

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“…Investigations into hippocampal ontogeny and the influence of intrinsic and extrinsic factors on its developmental trajectory and neurobehavioral outcomes have gained more attention ( Birnie and Baram, 2022 ; Ohana et al, 2022 ). A rich literature has found that interfering with hippocampal function during postnatal days 19–21 (P19–21) impede optimal hippocampal development and disrupt the emergence of hippocampal-based behavioral functions such as spatial learning and memory ( Holahan et al, 2019 ; Nadel, 2022 ). The influence of environmental signals on the maturation of hippocampal circuits that underlie social memory, however, remains poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Preadolescent exposure to a sexually mature, unrelated male rat reduces postadolescent social recognition memory and CA2 c-Fos labeling

Maletta

Palummieri

Correa

et al. 2023

Front. Behav. Neurosci.

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IntroductionSocial memory involves social recognition: the ability to discriminate between two or more conspecifics when one has been previously encountered. The CA2 region of the hippocampus has been implicated in social memory, as lesions and dysfunction to this area lead to social memory impairments. A variety of psychogenic manipulations during postnatal sensitive developmental periods are associated with social memory impairments later in life.MethodsIn this study, we exposed preadolescent rats to a sexually, mature unrelated male and examined whether this was associated with changes in postadolescent social memory and c-Fos labeling in the CA2 region. Male and female Long-Evans rats were exposed to a male, adult rat on postnatal days 19–21 (P19–21). Social memory was measured during the postadolescent period and defined as increased interactions towards a novel age-matched rat in contrast to a previously-encountered age-matched rat. After the test, rats were euthanized and brain tissue was then collected to quantify c-Fos labeling within the CA2 region.ResultsCompared to home cage controls and controls not exposed to the adult male, male and female rats exposed to the unrelated adult during preadolescence were unable to discriminate between a novel and previously encountered conspecific during the postadolescent test showing social memory deficits. The groups that showed social recognition deficits also had significantly fewer c-Fos-positive cells within the CA2 region compared to the control groups.DiscussionThese findings indicate that threatening psychogenic encounters during preadolescence can have detrimental long-term effects on social memory potentially via disrupted activity in the CA2 hippocampal region.

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“…Hippocampal-dependent memories are not innate ( Westbrook et al, 2014 ; Ramsaran et al, 2016 , 2019 ; Contreras et al, 2019 ), and their postnatal expression has remained controversial. The appearance of episodic memory has been closely related to the maturation of the hippocampus ( Jabès et al, 2011 ; Farooq and Dragoi, 2019 ; Muessig et al, 2019 ; Nadel, 2021 ) and its role in spatial navigation, including place cells, grid cells, head direction cells, among others, providing all the spatial information that the animal would need ( O’Keefe and Dostrovsky, 1971 ; Taube et al, 1990 ; Sargolini et al, 2006 ; Ainge and Langston, 2012 ). The first signs of hippocampal-dependent memory have been reported to emerge as early as postnatal day 17 (P17) ( Westbrook et al, 2014 ); however, it is not fully expressed until late adolescence of the rat (i.e., postnatal weeks 4–6) ( Westbrook et al, 2014 ; Contreras et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Cortico-Hippocampal Oscillations Are Associated With the Developmental Onset of Hippocampal-Dependent Memory

García-Pérez

Irani²,

Tiznado³

et al. 2022

Front. Neurosci.

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Hippocampal-dependent memories emerge late during postnatal development, aligning with hippocampal maturation. During sleep, the two-stage memory formation model states that through hippocampal-neocortical interactions, cortical slow-oscillations (SO), thalamocortical Spindles, and hippocampal sharp-wave ripples (SWR) are synchronized, allowing for the consolidation of hippocampal-dependent memories. However, evidence supporting this hypothesis during development is still lacking. Therefore, we performed successive object-in-place tests during a window of memory emergence and recorded in vivo the occurrence of SO, Spindles, and SWR during sleep, immediately after the memory encoding stage of the task. We found that hippocampal-dependent memory emerges at the end of the 4th postnatal week independently of task overtraining. Furthermore, we observed that those animals with better performance in the memory task had increased Spindle density and duration and lower density of SWR. Moreover, we observed changes in the SO-Spindle and Spindle-SWR temporal-coupling during this developmental period. Our results provide new evidence for the onset of hippocampal-dependent memory and its relationship to the oscillatory phenomenon occurring during sleep that helps us understand how memory consolidation models fit into the early stages of postnatal development.

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Some implications of postnatal hippocampal development

Cited by 5 publications

References 32 publications

Status epilepticus and early development: Neuronal injury, neurodegeneration, and their consequences

Status epilepticus and early development: Neuronal injury, neurodegeneration, and their consequences

Preadolescent exposure to a sexually mature, unrelated male rat reduces postadolescent social recognition memory and CA2 c-Fos labeling

Cortico-Hippocampal Oscillations Are Associated With the Developmental Onset of Hippocampal-Dependent Memory

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