Temporary inactivation reveals that the CA1 region of the mouse dorsal hippocampus plays an equivalent role in the retrieval of long-term object memory and spatial memory

Stackman, Robert W.; Cohen, Sarah J.; Lora, Joan C.; Rios, Lisa M.

doi:10.1016/j.nlm.2016.06.016

Cited by 52 publications

(34 citation statements)

References 44 publications

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“…In fact, increased number of Tunel‐positive cells in CA1 subfield of male rats was shown 24 h after neonatal anoxia in a previous work (Takada et al, 2015). These data, together with the result obtained in the Morris water maze task in adolescent male rats, corroborate the well‐described role of dorsal hippocampal CA1 subfield in spatial navigation (Blum et al, 1999; Danielson et al, 2016; Stackman et al, 2016), except for the same histological damage found in female adolescent rats that did not correlate to disruption of spatial memory. Interestingly, we found reduction in the number of cells in the ventral CA3‐2 subfields in anoxic male rats.…”

Section: Discussionsupporting

confidence: 88%

Behavioral, cognitive and histological changes following neonatal anoxia: Male and female rats' differences at adolescent age

Kumar

Motta-Teixeira

Takada

et al. 2018

Intl J of Devlp Neuroscience

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Neonatal anoxia induces long‐term brain injury that may underlie neurobehavioral deficits at adolescence. Neonatal anoxia, induced by exposure of 30‐hour old pups to 100% nitrogen, represents a non‐invasive and global stimulus, which simulates clinical conditions of human pre‐term babies (around 6 gestational months). Previous studies showed that neonatal anoxia induced impairments of spatial memory and altered anxiety‐like behaviors in male rats tested at adult age. This study evaluated if neonatal anoxia induces similar behavioral effects in female rats, as compared to males, by testing the animals at adolescence, and also searched for possible cell losses in hippocampal subfields. Results in the Elevated Plus Maze test showed that anoxic females spent proportionally more time within the open arms as compared to anoxic males, suggesting a less anxious‐like behavior. In the Morris Water Maze Test, latencies and path lengths of the anoxic subjects were longer as compared to control subjects, thus indicating that anoxia disrupted the cognitive functions required for spatial mapping. In addition, results showed that anoxia‐induced disruption was greater in male rats as compared to female rats. Stereological analysis revealed that anoxic male rats exhibited significant cell losses in the dorsal hippocampus dentate gyrus and CA1 subfields, but not in CA3‐2 subfield. Similar results were observed in the ventral hippocampus, but now with cell loss in the male CA3‐2 subfield. There were also significant cell loss differences of anoxic male rats as compared to anoxic female rats. In conclusion, neonatal anoxia induces deleterious and long lasting behavioral and cognitive disruptions, and these effects were stronger in male rats as compared to female rats. These changes are congruent with the pattern of cell losses observed in hippocampal subfields. Together, these results emphasize the relevance of scientific research, aiming at clinical strategies and treatments, consider the sex differential patterns of response to neonatal injury.

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Section: Discussionsupporting

confidence: 88%

Behavioral, cognitive and histological changes following neonatal anoxia: Male and female rats' differences at adolescent age

Kumar

Motta-Teixeira

Takada

et al. 2018

Intl J of Devlp Neuroscience

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“…Therefore, the reduction of the hippocampal subfield volumes would likely affect cognitive function. For example, the CA1 region is essential for retrieval of contextual memory (Ji & Maren, 2008), autobiographical memory (Bartsch, Dohring, Rohr, Jansen, & Deuschl, 2011), consolidation of long-term memory (Remondes & Schuman, 2004;Stackman, Cohen, Lora, & Rios, 2016). This is consistent with the finding of significantly poorer scores in the orientation subscales of MMSE in patients with deficient levels of vitamin D. The CA1 region connects the cortical regions via the subiculum.…”

Section: Hippocampal Volume Loss Is Associated With Disrupted Netwosupporting

confidence: 81%

“…For example, the CA1 region is essential for retrieval of contextual memory (Ji & Maren, 2008), autobiographical memory (Bartsch, Dohring, Rohr, Jansen, & Deuschl, 2011), consolidation of long-term memory (Remondes & Schuman, 2004;Stackman, Cohen, Lora, & Rios, 2016). For example, the CA1 region is essential for retrieval of contextual memory (Ji & Maren, 2008), autobiographical memory (Bartsch, Dohring, Rohr, Jansen, & Deuschl, 2011), consolidation of long-term memory (Remondes & Schuman, 2004;Stackman, Cohen, Lora, & Rios, 2016).…”

Section: Hippocampal Volume Loss Is Associated With Disrupted Netwomentioning

confidence: 99%

Vitamin D deficiency is associated with reduced hippocampal volume and disrupted structural connectivity in patients with mild cognitive impairment

Al-Amin

Bradford

Sullivan

et al. 2018

Human Brain Mapping

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Vitamin D deficiency may exacerbate adverse neurocognitive outcomes in the progression of diseases such as Parkinson's, Alzheimer's, and other dementias. Mild cognitive impairment (MCI) is prodromal for these neurocognitive disorders and neuroimaging studies suggest that, in the elderly, this cognitive impairment is associated with a reduction in hippocampal volume and white matter structural integrity. To test whether vitamin D is associated with neuroanatomical correlates of MCI, we analyzed an existing structural and diffusion MRI dataset of elderly patients with MCI. Based on serum 25‐OHD levels, patients were categorized into serum 25‐OHD deficient (<12 ng/mL, n = 27) or not‐deficient (>12 ng/mL, n = 29). Freesurfer 6.0 was used to parcellate the whole brain into 164 structures and segment the hippocampal subfields. Whole‐brain structural connectomes were generated using probabilistic tractography with MRtrix. The network‐based statistic (NBS) was used to identify subnetworks of connections that significantly differed between the groups. We found a significant reduction in total hippocampal volume in the serum 25‐OHD deficient group especially in the CA1, molecular layer, dentate gyrus, and fimbria. We observed a connection deficit in 13 regions with the right hippocampus at the center of the disrupted network. Our results demonstrate that low vitamin D is associated with reduced volumes of hippocampal subfields and connection deficits in elderly people with MCI, which may exacerbate neurocognitive outcomes. Longitudinal studies are now required to determine if vitamin D can serve as a biomarker for Alzheimer's disease and if intervention can prevent the progression from MCI to major cognitive disorders.

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“…Hippocampal damage is associated with a poor outcome in the NOR test [30, 39]; thus, we performed immunostaining to evaluate hippocampal neuronal and synaptic integrity. A higher overall thickness of NeuN-immunoreactive cells was detected in the neuronal CA1 layer of the GDM-HFS group compared to GDM-LF and lean offspring controls (Fig.…”

Section: Resultsmentioning

confidence: 99%

Exposure to gestational diabetes mellitus induces neuroinflammation, derangement of hippocampal neurons, and cognitive changes in rat offspring

Vuong

Odero

Rozbacher³

et al. 2017

J Neuroinflammation

116

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BackgroundBirth cohort studies link gestational diabetes mellitus (GDM) with impaired cognitive performance in the offspring. However, the mechanisms involved are unknown. We tested the hypothesis that obesity-associated GDM induces chronic neuroinflammation and disturbs the development of neuronal circuitry resulting in impaired cognitive abilities in the offspring.MethodsIn rats, GDM was induced by feeding dams a diet high in sucrose and fatty acids. Brains of neonatal (E20) and young adult (15-week-old) offspring of GDM and lean dams were analyzed by immunohistochemistry, cytokine assay, and western blotting. Young adult offspring of GDM and lean dams went also through cognitive assessment. Cultured microglial responses to elevated glucose and/or fatty acids levels were analyzed.ResultsIn rats, impaired recognition memory was observed in the offspring of GDM dams. GDM exposure combined with a postnatal high-fat and sucrose diet resulted in atypical inattentive behavior in the offspring. These cognitive changes correlated with reduced density and derangement of Cornu Ammonis 1 pyramidal neuronal layer, decreased hippocampal synaptic integrity, increased neuroinflammatory status, and reduced expression of CX3CR1, the microglial fractalkine receptor regulating microglial pro-inflammatory responses and synaptic pruning. Primary microglial cultures that were exposed to high concentrations of glucose and/or palmitate were transformed into an activated, amoeboid morphology with increased nitric oxide and superoxide production, and altered their cytokine release profile.ConclusionsThese findings demonstrate that GDM stimulates microglial activation and chronic inflammatory responses in the brain of the offspring that persist into young adulthood. Reactive gliosis correlates positively with hippocampal synaptic decline and cognitive impairments. The elevated pro-inflammatory cytokine expression at the critical period of hippocampal synaptic maturation suggests that neuroinflammation might drive the synaptic and cognitive decline in the offspring of GDM dams. The importance of microglia in this process is supported by the reduced Cx3CR1 expression as an indication of the loss of microglial control of inflammatory responses and phagocytosis and synaptic pruning in GDM offspring.

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Temporary inactivation reveals that the CA1 region of the mouse dorsal hippocampus plays an equivalent role in the retrieval of long-term object memory and spatial memory

Cited by 52 publications

References 44 publications

Behavioral, cognitive and histological changes following neonatal anoxia: Male and female rats' differences at adolescent age

Behavioral, cognitive and histological changes following neonatal anoxia: Male and female rats' differences at adolescent age

Vitamin D deficiency is associated with reduced hippocampal volume and disrupted structural connectivity in patients with mild cognitive impairment

Exposure to gestational diabetes mellitus induces neuroinflammation, derangement of hippocampal neurons, and cognitive changes in rat offspring

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