Hippocampal function in rodents

Zemla, Roland; Basu, Jayeeta

doi:10.1016/j.conb.2017.04.005

Cited by 53 publications

(36 citation statements)

References 95 publications

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“…The shortening of CA1 pyramidal cell dendrites in female mice alone could account for poor T-test behavioural results (the test relies on the detection of spatial novelty). The distant apical dendrites of CA1 neurons receive direct input from the entorhinal cortex that may help to discriminate between different instances of memories for the same location ( Remondes and Schuman, 2004 ; Zemla and Basu, 2017 ). In addition, a large number of long spines in aged female mice could indicate a general weakening of synaptic connections and hence weaker memory traces.…”

Section: Discussionmentioning

confidence: 99%

OPA1 deficiency accelerates hippocampal synaptic remodelling and age-related deficits in learning and memory

Bevan

Williams

Waters

et al. 2020

Brain Communications

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A healthy mitochondrial network is essential for the maintenance of neuronal synaptic integrity. Mitochondrial and metabolic dysfunction contributes to the pathogenesis of many neurodegenerative diseases including dementia. OPA1 is the master regulator of mitochondrial fusion and fission and is likely to play an important role during neurodegenerative events. To explore this, we quantified hippocampal dendritic and synaptic integrity and the learning and memory performance of aged Opa1 haploinsufficient mice carrying the Opa1Q285X mutation (B6;C3-Opa1Q285STOP; Opa1+/-). We demonstrate that heterozygous loss of Opa1 results in premature age-related loss of spines in hippocampal pyramidal CA1 neurons and a reduction in synaptic density in the hippocampus. This loss is associated with subtle memory deficits in both spatial novelty and object recognition. We hypothesise that metabolic failure to maintain normal neuronal activity at the level of a single spine leads to premature age-related memory deficits. These results highlight the importance of mitochondrial homeostasis for maintenance of neuronal function during ageing.

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Section: Discussionmentioning

confidence: 99%

OPA1 deficiency accelerates hippocampal synaptic remodelling and age-related deficits in learning and memory

Bevan

Williams

Waters

et al. 2020

Brain Communications

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“…It is important to note that the cognitive benefits of TLR4 deficiency appear to be task dependent, as TLR4 deficient mice show no differences in passive avoidance conditioning whereas they show impairments in contextual and cued fear conditioning (Li et al, 2016;Okun et al, 2012). While both contextual fear conditioning and spatial learning are hippocampus-dependent tasks, studies that employ lesion or optogenetic approaches indicate that dissociable cell ensembles, substructures, and circuits uniquely contribute to memory formation across the tasks (Burwell et al, 2004;Good and Honey, 1997;Zemla and Basu, 2017). Whether TLR4 differentially influences these circuits within the hippocampus, and potentially contributes to the different observations across the behavioral tasks, is presently unknown.…”

Section: Discussionmentioning

confidence: 99%

Young and aged TLR4 deficient mice show sex-dependent enhancements in spatial memory and alterations in interleukin-1 related genes

Potter

Giedraitis

Johnson

et al. 2019

Brain, Behavior, and Immunity

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Toll-like receptor-4 (TLR4) is a transmembrane receptor that initiates an immune response following a bacterial infection or host derived molecules associated with cellular distress. Beyond triggering inflammation, TLR4 has been implicated in modulating behavior and cognitive processes in a physiologically normal state, as young adult TLR4 deficient mice show learning enhancements in select tasks. Currently unknown is whether these benefits are present in both sexes and persist with aging. The present study evaluated spatial memory, anxiety-like behavior, and central levels of pro-and anti-inflammatory molecules in young (4-5 months) and aged (18-19 months) TLR4 deficient (TLR4−/−) and wild-type (WT) male and female mice. Results confirmed that TLR4−/− mice show enhanced spatial memory compared to WT mice. These effects were age-and sex-specific, as memory retention was superior in the TLR4−/− young males and aged females. While TLR4−/− mice showed age-related changes in behavior, these changes were attenuated relative to aged WT mice. Further, aged TLR4−/− mice showed differential expression of molecules involved in interleukin (IL)-1 signaling in the hippocampus. For instance, aged TLR4−/− females showed heightened expression of IL-1 receptor antagonist (IL-1ra) and the IL-1 accessory proteins AcP and AcPb. Collectively, these data provide the initial evidence that TLR4 deficiency enhances cognitive function and modulates the inflammatory profile of the hippocampus in a sex-and age-dependent manner.

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“…Electrode recordings are also unable to disentangle signals among the many different cell types. General dynamics of the CA1 response along the spatial dimension upon SC electrical stimulation have been described using multielectrode arrays (Gholmieh et al, 2006;Steidl et al, 2006) electrode and patch clamp recordings, report both excitatory and inhibitory inputs but they are confined in subcellular structures and are restricted to only a few cells (Zemla & Basu, 2017). Optical recordings using voltage sensitive dyes address the issue of spatial information and provide a more direct way to study depolarization and hyperpolarization of membrane potential by reporting membrane voltage rather than field potentials.…”

Section: Introductionmentioning

confidence: 99%

GEVI cell‐type specific labelling and a manifold learning approach provide evidence for lateral inhibition at the population level in the mouse hippocampal CA1 area

Nakajima

Laskaris

Rhee

et al. 2021

Eur J of Neuroscience

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The CA1 area in the mammalian hippocampus is essential for spatial learning. Pyramidal cells are the hippocampus output neurons and their activities are regulated by inhibition exerted by a diversified population of interneurons. Lateral inhibition has been suggested as the mechanism enabling the reconfiguration of pyramidal cell assembly activity observed during spatial learning tasks in rodents. However, lateral inhibition in the CA1 lacks the overwhelming evidence reported in other hippocampal areas such as the CA3 and the dentate gyrus. The use of genetically encoded voltage indicators and fast optical recordings permits the construction of cell-type specific response maps of neuronal activity. Here, we labelled mouse CA1 pyramidal neurons with the genetically encoded voltage indicator ArcLight and optically recorded their response to Schaffer Collaterals stimulation in vitro. By undertaking a manifold learning approach, we report a hyperpolarization-dominated area focused in the perisomatic region of pyramidal cells receiving late excitatory synaptic input.Functional network organization metrics revealed that information transfer was higher in this area. The localized hyperpolarization disappeared when GABA A receptors were pharmacologically blocked. This is the first report where the spatiotemporal pattern of lateral inhibition is visualized in the CA1 by expressing a genetically encoded voltage indicator selectively in principal neurons. Our analysis suggests a fundamental role of lateral inhibition in CA1 information processing.

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Hippocampal function in rodents

Cited by 53 publications

References 95 publications

OPA1 deficiency accelerates hippocampal synaptic remodelling and age-related deficits in learning and memory

OPA1 deficiency accelerates hippocampal synaptic remodelling and age-related deficits in learning and memory

Young and aged TLR4 deficient mice show sex-dependent enhancements in spatial memory and alterations in interleukin-1 related genes

GEVI cell‐type specific labelling and a manifold learning approach provide evidence for lateral inhibition at the population level in the mouse hippocampal CA1 area

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