Erratum: Functional Uncoupling NMDAR NR2A Subunit from PSD-95 in the Prefrontal Cortex: Effects on Behavioral Dysfunction and Parvalbumin Loss after Early-Life Stress

Ganguly, Prabarna; Holland, Freedom H.; Brenhouse, Heather C.

doi:10.1038/npp.2015.334

Cited by 3 publications

(2 citation statements)

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“…The reduction in PV + cellular density, observed in PrL is in line with the results of studies that employed a 3 h daily separation protocol during the first three postnatal weeks (Leussis et al, 2012;Ganguly et al, 2016;Grassi-Oliveira et al, 2016), as well as a previous result from our laboratory (Aksic et al, 2021). In another study, Helmeke et al (2008) reported an increase in the number of PV + neurons in the dorsal medial PFC of an adult Octogon degus which appeared strikingly opposite to our findings (Helmeke et al, 2008).…”

Section: Discussionsupporting

confidence: 90%

Effects of Maternal Deprivation on the Prefrontal Cortex of Male Rats: Cellular, Neurochemical, and Behavioral Outcomes

Poleksic

Aksić

Kapor

et al. 2021

Front. Behav. Neurosci.

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Stressful events experienced during early life are associated with increased vulnerability of developing psychopathology in adulthood. In the present study, we exposed 9-day-old Wistar rats to 24 h maternal deprivation (MD) with the aim to investigate the impact of early life stress (ELS) on morphological, biochemical, and functional aspects of the prefrontal cortex (PFC), a brain region particularly sensitive to stress. We found that in the superficial medial orbital cortex (MO), young adult male rats had reduced density of GAD67 and CCK immunopositive cells, while the rostral part of the ventral lateral orbital cortex (roVLO) showed a decrease in the density of GAD67 immunopositive cells in both superficial and deep layers. In addition, the superficial rostral part of area 1 of the cingulate cortex (roCg1) and deep prelimbic cortex (PrL) was also affected by MD indicated by the reduction in PV immunopositive cellular density. Furthermore, MD induced upregulation of brain-derived neurotrophic factor (BDNF), while it did not affect the overall expression of Iba1 in neonatal or young adult PFC as measured by Western blot, however, microglial activation in young adult MD rats was detected immunohistochemically in deep layers of MO and infralimbic cortex (IL). Interestingly, when young adult male rats were subjected to a behavioral flexibility test in a T-maze, MD rats showed a subtle impairment in T-maze reversal learning indicating a mildly affected PFC function. Taken together, our findings demonstrated that MD reduced the density of interneurons and induced microglial activation, in particular, PFC areas at young adulthood, and could alter synaptic plasticity accompanied by PFC dysfunction.

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Section: Discussionsupporting

confidence: 90%

Effects of Maternal Deprivation on the Prefrontal Cortex of Male Rats: Cellular, Neurochemical, and Behavioral Outcomes

Poleksic

Aksić

Kapor

et al. 2021

Front. Behav. Neurosci.

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“…While the effects of ES on cognition have been extensively studied in adult animals in our own and other research groups [4,52], it is worth highlighting that several recent studies have started to examine this issue in adolescent rodents. Studies with maternal separation or deprivation models reported that ES impaired spatial learning and memory in morris water maze test [38], novel object recognition memory [53], and temporary order memory [54] in adolescent rodents. To our knowledge, only one study has used the LBN paradigm and found that exposure to LBN during PND4-11 led to spatial object recognition memory loss in adolescent male mice [7].…”

Section: Discussionmentioning

confidence: 99%

The CRHR1→PN→PVI Pathway in Medial Prefrontal Cortex Mediates Early-life Stress-induced Cognitive Deficits in Adolescent Mice

Li,

Ma,

Yang

et al. 2024

Preprint

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Cognitive impairment, one core symptom of psychiatric disorders, is frequently observed in adolescents exposed to early-life stress (ES). However, the underlying neural mechanisms are unclear and the therapeutic efficacy is limited. Targeting at parvalbumin-expressing interneurons (PVIs) in the medial prefrontal cortex (mPFC), we report that mPFC PVI activity was reduced by ES and causally mediated ES-induced cognitive deficits in adolescent mice through chemogenetic or optogenetic experiments. We then demonstrate that ES reduced the excitatory inputs onto PVIs and pyramidal neuron (PN) activity and that ES negative effects were reversed by the knockout of corticotropin-releasing hormone receptor 1 (CRHR1, mainly expressed in PNs) in mouse mPFC, supporting the prefrontal CRHR1→PN→PVI pathway in mediating ES-induced cognitive deficits. Finally, antalarmin (a CRHR1 antagonist) treatment and environmental enrichment successfully restored PVI activity and cognitive deficits induced by ES. These findings highlight the critical role of PVIs in mediating and preventing ES-induced cognitive deficits in adolescent mice.

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Effects of autophagy on synaptic-plasticity-related protein expression in the hippocampus CA1 of a rat model of vascular dementia

Liu

Zhang

et al. 2019

Neuroscience Letters

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Erratum: Functional Uncoupling NMDAR NR2A Subunit from PSD-95 in the Prefrontal Cortex: Effects on Behavioral Dysfunction and Parvalbumin Loss after Early-Life Stress

Cited by 3 publications

References 0 publications

Effects of Maternal Deprivation on the Prefrontal Cortex of Male Rats: Cellular, Neurochemical, and Behavioral Outcomes

Effects of Maternal Deprivation on the Prefrontal Cortex of Male Rats: Cellular, Neurochemical, and Behavioral Outcomes

The CRHR1→PN→PVI Pathway in Medial Prefrontal Cortex Mediates Early-life Stress-induced Cognitive Deficits in Adolescent Mice

Effects of autophagy on synaptic-plasticity-related protein expression in the hippocampus CA1 of a rat model of vascular dementia

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