The impact of stress on the hippocampal spatial code

Tomar, Anupratap; McHugh, Thomas J.

doi:10.1016/j.tins.2021.11.005

Cited by 16 publications

(8 citation statements)

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“…Earlier we showed that following PS, DA metabolism was impaired while concentrations of DA metabolites were increased [ 16 ]. The hippocampus participates in the regulation of anxiety [ 17 , 18 , 19 , 20 , 21 , 22 ]. The hippocampus interacts with both cortical and subcortical brain regions that regulate emotions and responses to stress.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Susceptibility and Resilience to PTSD: Role of Dopamine Metabolism and BDNF Expression in the Hippocampus

Tseĭlikman

Tseilikman

Pashkov

et al. 2022

IJMS

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Susceptibility and resilience to post-traumatic stress disorder (PTSD) are recognized, but their mechanisms are not understood. Here, the hexobarbital sleep test (HST) was used to elucidate mechanisms of PTSD resilience or susceptibility. A HST was performed in rats 30 days prior to further experimentation. Based on the HST, the rats were divided into groups: (1) fast metabolizers (FM; sleep duration < 15 min); (2) slow metabolizers (SM; sleep duration ≥ 15 min). Then the SM and FM groups were subdivided into stressed (10 days predator scent, 15 days rest) and unstressed subgroups. Among stressed animals, only SMs developed experimental PTSD, and had higher plasma corticosterone (CORT) than stressed FMs. Thus, resilience or susceptibility to PTSD was consistent with changes in glucocorticoid metabolism. Stressed SMs had a pronounced decrease in hippocampal dopamine associated with increased expressions of catecholamine-O-methyl-transferase and DA transporter. In stressed SMs, a decrease in monoaminoxidase (MAO) A was associated with increased expressions of hippocampal MAO-A and MAO-B. BDNF gene expression was increased in stressed FMs and decreased in stressed SMs. These results demonstrate relationships between the microsomal oxidation phenotype, CORT concentration, and anxiety, and they help further the understanding of the role of the liver–brain axis during PTSD.

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Section: Introductionmentioning

confidence: 99%

Mechanisms of Susceptibility and Resilience to PTSD: Role of Dopamine Metabolism and BDNF Expression in the Hippocampus

Tseĭlikman

Tseilikman

Pashkov

et al. 2022

IJMS

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“…The hippocampus interacts with a variety of brain regions, including the prefrontal cortex, amygdala, and hypothalamus, to adjust anxiety levels in response to a variety of stressful conditions [ 15 ]. Chronic stress impairs hippocampus-dependent plasticity with a simultaneous increase in anxiety response [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Paradoxical Anxiety Level Reduction in Animal Chronic Stress: A Unique Role of Hippocampus Neurobiology

Tseĭlikman

Akulov

Shevelev

et al. 2022

IJMS

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A paradoxical reduction in anxiety levels in chronic predator stress paradigm (PS) in Sprague–Dawley rats has recently been shown in previous works. In this paper, we studied the possible neurobiological mechanism of this phenomenon. We segregated PS-exposed Sprague–Dawley rats into the high- and low-anxiety phenotypes. The long-lasting effects of PS on corticosterone levels, blood flow speed in the carotid arteries, diffusion coefficient, and 1H nuclear magnetic resonance spectra in the hippocampus were compared in the high-anxiety and low-anxiety rats. In addition, we evaluated the gene BDNF expression in the hippocampus which is considered to be a main factor of neuroplasticity. We demonstrated that in low-anxiety rats, the corticosterone level was decreased and carotid blood flow speed was increased. Moreover, in the hippocampus of low-anxiety rats compared to the control group and high-anxiety rats, the following changes were observed: (a) a decrease in N-acetyl aspartate levels with a simultaneous increase in phosphoryl ethanol amine levels; (b) an increase in lipid peroxidation levels; (c) a decrease in apparent diffusion coefficient value; (d) an increase in BDNF gene expression. Based on these findings, we proposed that stress-induced anxiety reduction is associated with the elevation of BDNF gene expression directly. Low corticosterone levels and a rise in carotid blood flow speed might facilitate BDNF gene expression. Meanwhile, the decrease in apparent diffusion coefficient value and decrease in N-acetyl aspartate levels, as well as an increase in the lipid peroxidation levels, in the hippocampus possibly reflected destructive changes in the hippocampus. We suggested that in Sprague–Dawley rats, these morphological alterations might be considered as an impetus for further increase in neuroplasticity in the hippocampus.

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“…One study found that acute stress enhanced spatial encoding, expressed by computational models revealing increased spatial information contained in CA1 pyramidal place cell firing as well as sharper place cell tuning (reflected by lower sparsity; Markus et al, 1994 ; Tomar et al, 2021 ). Stress may also affect oscillatory activity in hippocampal ensembles; acute immobilization stress in rodents enhanced phase locking of single-cell firing, a critical component of the hippocampal temporal code that improves place encoding accuracy ( O'Keefe and Recce, 1993 ; Tomar and McHugh, 2022 ; Tomar et al, 2021 ).…”

Section: Within-context Bindingmentioning

confidence: 99%