Selective lesion of the hippocampus increases the differentiation of immature neurons in the monkey amygdala

Chareyron, Loïc J.; Amaral, David G.; Lavenex, Pierre

doi:10.1073/pnas.1604288113

Cited by 27 publications

(58 citation statements)

References 44 publications

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“…In the PVN of the male and female mice, abundance of a genetically encoded reporter, mEGFP, which is specifically expressed in Sim1 neurons, is decreased. This effect is paralleled by apoptosis, detected by the Tunel assay, and decreased population of mature PVN neurons, detected by the NeuN staining (Mullen et al 1992;Chareyron et al 2016). These results suggest that exposure to HF diet induces injury, rather than complete loss, of Sim1 neurons, which may in turn disrupt control of energy homeostasis in mice of both sexes.…”

Section: Discussionmentioning

confidence: 95%

Injury to hypothalamic Sim1 neurons is a common feature of obesity by exposure to high‐fat diet in male and female mice

Nyamugenda

Trentzsch

Russell

et al. 2019

Journal of Neurochemistry

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The hypothalamus is essential for regulation of energy homeostasis and metabolism. Feeding hypercaloric, high‐fat (HF) diet induces hypothalamic arcuate nucleus injury and alters metabolism more severely in male than in female mice. The site(s) and extent of hypothalamic injury in male and female mice are not completely understood. In the paraventricular nucleus (PVN) of the hypothalamus, single‐minded family basic helix‐loop helix transcription factor 1 (Sim1) neurons are essential to control energy homeostasis. We tested the hypothesis that exposure to HF diet induces injury to Sim1 neurons in the PVN of male and female mice. Mice expressing membrane‐bound enhanced green fluorescent protein (mEGFP) in Sim1 neurons (Sim1‐Cre:Rosa‐mEGFP mice) were generated to visualize the effects of exposure to HF diet on these neurons. Male and female Sim1‐Cre:Rosa‐mEGFP mice exposed to HF diet had increased weight, hyperleptinemia, and developed hepatosteatosis. In male and female mice exposed to HF diet, expression of mEGFP was reduced by > 40% in Sim1 neurons of the PVN, an effect paralleled by cell apoptosis and neuronal loss, but not by microgliosis. In the arcuate nucleus of the Sim1‐Cre:Rosa‐mEGFP male mice, there was decreased alpha‐melanocyte‐stimulating hormone in proopiomelanocortin neurons projecting to the PVN, with increased cell apoptosis, neuronal loss, and microgliosis. These defects were undetectable in the arcuate nucleus of female mice exposed to the HF diet. Thus, injury to Sim1 neurons of the PVN is a shared feature of exposure to HF diet in mice of both sexes, while injury to proopiomelanocortin neurons in arcuate nucleus is specific to male mice. Open Science Badges This article has received a badge for *Open Materials* because it provided all relevant information to reproduce the study in the manuscript. The complete Open Science Disclosure form for this article can be found at the end of the article. More information about the Open Practices badges can be found at https://cos.io/our-services/open-science-badges/.

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Section: Discussionmentioning

confidence: 95%

Injury to hypothalamic Sim1 neurons is a common feature of obesity by exposure to high‐fat diet in male and female mice

Nyamugenda

Trentzsch

Russell

et al. 2019

Journal of Neurochemistry

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“…We propose that other neuronal factors may contribute, such as ( i ) the maturation of a large population of immature neurons within the paralaminar nucleus ( 6 , 14 – 17 ) and/or ( ii ) the migration of postnatally generated neurons ( 18 , 19 ). Immature neurons have been identified in both monkey and human amygdala using immunohistochemistry with protein markers such as doublecortin (DCX) and B cell lymphoma 2 (bcl-2) ( 14 , 16 – 18 , 20 , 21 ). The protracted maturational trajectory of the amygdala well beyond the perinatal period allows it to continually be shaped by external stimuli.…”

mentioning

confidence: 99%

“…The protracted maturational trajectory of the amygdala well beyond the perinatal period allows it to continually be shaped by external stimuli. In fact, the immature neurons within the paralaminar nucleus may develop in an activity-dependent manner ( 20 , 22 ). This lengthened maturational process, however, may also make the amygdala more susceptible to developmental or environmental insults.…”

mentioning

confidence: 99%

Neuron numbers increase in the human amygdala from birth to adulthood, but not in autism

Avino

Barger

Vargas

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

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140

164

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SignificanceWe demonstrate that the number of mature neurons in the human amygdala increases from childhood into adulthood. This trajectory may be due to the incorporation of immature neurons from the paralaminar nucleus in the ventral amygdala. In contrast, individuals with autism spectrum disorder (ASD) show an initial excess of mature neurons followed by a decline into adulthood. Our results suggest a degenerative component in ASD and highlight the need for a more comprehensive understanding of the protracted cellular development of the human amygdala for multiple psychiatric disorders.

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“…Neurons with immature features are present in the adolescent and adult human amygdala [57]. In patients with ASD, the process that governs postnatal cellular maturation, like the trajectory of neuronal development, is altered in the human amygdala with a persistence of neurons endowed with immature features [58,59]. This "immaturity" of impacted neurons stands at the core of the "neuroarchaeology" concept positing that the inaugurating insult in utero deviates developmental sequences leading to misplaced or misconnected neurons that present signs of immaturity and generate patterns that disturb behaviorally relevant oscillations [60].…”

Section: Discussionmentioning

confidence: 99%

Pregnancy data enable identification of relevant biomarkers and a partial prognosis of autism at birth

Caly

Rabiei

Coste-Mazeau

et al. 2020

Preprint

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AbstractAttempts to extract early biomarkers and expedite detection of Autism Spectrum Disorder (ASD) have been centered on postnatal measures of babies at familial risk. Here, we suggest that it might be possible to do these tasks already at birth relying on ultrasound and biological measurements routinely collected from pregnant mothers and fetuses during gestation and birth. We performed a gradient boosting decision tree classification analysis in parallel with statistical tests on a population of babies with typical development or later diagnosed with ASD. By focusing on minimization of the false positive rate, the cross-validated specificity of the classifier reached to 96% with a sensitivity of 41% and a positive predictive value of 77%. Extracted biomarkers included sex, maternal familial history of auto-immune diseases, maternal immunization to CMV, IgG CMV level, timing of fetal rotation on head, femoral length in the 3rd trimester, white cells in the 3rd trimester, fetal heart rate during labour, newborn feeding and newborn’s temperature difference between birth and one day after. Statistical models revealed that 38% of babies later diagnosed with ASD had significantly larger fetal cephalic perimeter than age matched neurotypical babies, suggesting an in-utero origin of the bigger brains of toddlers with ASD. Results pave the way to use pregnancy follow-up measurements to provide an early prognosis of ASD and implement pre-symptomatic behavioral interventions to attenuate efficiently ASD developmental sequels.

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Selective lesion of the hippocampus increases the differentiation of immature neurons in the monkey amygdala

Cited by 27 publications

References 44 publications

Injury to hypothalamic Sim1 neurons is a common feature of obesity by exposure to high‐fat diet in male and female mice

Injury to hypothalamic Sim1 neurons is a common feature of obesity by exposure to high‐fat diet in male and female mice

Neuron numbers increase in the human amygdala from birth to adulthood, but not in autism

Pregnancy data enable identification of relevant biomarkers and a partial prognosis of autism at birth

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