Altered hippocampal function before emotional trauma in rats susceptible to PTSD-like behaviors

Nalloor, Rebecca; Bunting, Kristopher M.; Vazdarjanova, Almira

doi:10.1016/j.nlm.2014.02.006

Cited by 18 publications

(15 citation statements)

References 56 publications

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“…Compared with our published findings in dHC that were based on tissue from the same animals, the current results suggest that sucrose ingestion produces less Arc expression in vHC than dHC. This is consistent with other findings that have compared Arc expression in dHC and vHC (Gusev et al, 2005;Nalloor et al, 2012Nalloor et al, , 2014 and with results suggesting that dHC expresses higher levels of synaptic plasticity than vHC (Papatheodoropoulos and Kostopoulos, 2000a, 200b;Maruki et al, 2001;Maggio and Segal, 2007).…”

Section: Discussionsupporting

confidence: 93%

Ventral hippocampal neurons inhibit postprandial energy intake

et al. 2017

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Evidence suggests that the memory of a recently ingested meal limits subsequent intake. Given that ventral hippocampal (vHC) neurons are involved in memory and energy intake, the present experiment tested the hypothesis that vHC neurons contribute to the formation of a memory of a meal and inhibit energy intake during the postprandial period. We tested (1) whether pharmacological inactivation of vHC neurons during the period following a sucrose meal, when the memory of the meal would be undergoing consolidation, accelerates the onset of the next sucrose meal and increases intake and (2) whether sucrose intake increases vHC expression of the synaptic plasticity marker activity-regulated cytoskeletal-associated protein (Arc). Adult male Sprague-Dawley rats were trained to consume a 32% sucrose solution daily at the same time and location. On the experimental day, the rats were given intra-vHC infusions of the GABA receptor agonist muscimol or vehicle after they finished their first sucrose meal. Compared to vehicle infusions, postmeal intra-vHC muscimol infusions decreased the latency to the next sucrose meal, increased the amount of sucrose consumed during that meal, increased the total number of sucrose meals and the total amount of sucrose ingested. In addition, rats that consumed sucrose had higher levels of Arc expression in both vHC CA1 and CA3 subfields than cage control rats. Collectively, these findings are the first to show that vHC neurons inhibit energy intake during the postprandial period and support the hypothesis that vHC neurons form a memory of a meal and inhibit subsequent intake. © 2016 Wiley Periodicals, Inc.

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Section: Discussionsupporting

confidence: 93%

Ventral hippocampal neurons inhibit postprandial energy intake

et al. 2017

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“…Subsequently, Arc mRNA becomes perinuclear and accumulates in the cytoplasm and dendrites where it can be detected for approximately 45 min after induction (Vazdarjanova et al, ). The percent of Arc positive cells in this report is lower than that cited in previous reports (e.g., Nalloor et al, ). One possibility is that the repeated exposure to the sweet solutions in the same context may have attenuated dCA1 Arc activation over time, likely due to decreased mnemonic demand.…”

Section: Discussioncontrasting

confidence: 80%

Sweet orosensation induces Arc expression in dorsal hippocampal CA1 neurons in an Experience‐dependent manner

et al. 2015

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There is limited knowledge regarding how the brain controls the timing of meals. Similarly, there is a large gap in our understanding of how top-down cognitive processes, such as memory influence energy intake. We hypothesize that dorsal hippocampal (dHC) neurons, which are critical for episodic memory, form a memory of a meal and inhibit meal onset during the postprandial period. In support, we showed previously that reversible inactivation of these neurons during the period following a sucrose meal accelerates the onset of the next meal. If dHC neurons form a memory of a meal, then consumption should induce synaptic plasticity in dHC neurons. To test this, we determined (1) whether a sucrose meal increases the expression of the synaptic plasticity marker activity-regulated cytoskeleton-associated protein (Arc) in dHC CA1 neurons, (2) whether previous experience with sucrose influences sucrose-induced Arc expression, and (3) whether the orosensory stimulation produced by the noncaloric sweetener saccharin is sufficient to induce Arc expression. Male Sprague-Dawley rats were trained to consume a sweetened solution at a scheduled time daily. On the experimental day, they were given a solution for 7 min, euthanized, and then fluorescence in situ hybridization procedures were used to measure meal-induced Arc mRNA. Compared to caged control rats, Arc expression was significantly higher in rats that consumed sucrose or saccharin. Interestingly, rats given additional experience with sucrose had less Arc expression than rats with less sucrose experience, even though both groups consumed similar amounts on the experimental day. Thus, this study is the first to suggest that orosensory stimulation produced by consuming a sweetened solution and possibly the hedonic value of that sweet stimulation induces synaptic plasticity in dHC CA1 neurons in an experience-dependent manner. Collectively, these findings are consistent with our hypothesis that dHC neurons form a memory of a meal.

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“…Rats classified as SUS or RES, without having experienced trauma, show a different degree of overlap in the hippocampus after exploring a novel place twice, 25 min apart. SUS, compared to RES, rats show less overlap of ensembles in the dorsal/septal CA1 region, as well as a smaller neuronal ensemble in the ventral CA3 region (Figure 4; Nalloor et al, 2014). These findings demonstrate that SUS rats have impaired hippocampal function (interpreted as low fidelity in episodic memory encoding) before experiencing emotional trauma.…”

Section: Impaired Function Of the Hippocampus Is A Putative Susceptibmentioning

confidence: 74%

Investigating Individual Pre-trauma Susceptibility to a PTSD-Like Phenotype in Animals

Alexander

Nalloor

Bunting

et al. 2020

Front. Syst. Neurosci.

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• Susceptibility to developing a PTSD-like phenotype exists in animals. It can be identified behaviorally and therefore can be studied. • Susceptibility can be studied by identifying susceptibility factors (pre-trauma) and sequalae factors (peri-and posttrauma) to a PTSD-like phenotype. • Some susceptible individuals have impaired functioning in the hippocampus BEFORE emotional trauma. • Understanding susceptibility can inform ways to successfully build resilience. • Investigations into susceptibility also highlight the important idea that susceptibility is a dynamic feature of PTSD. Susceptibility is not strictly determined by genetics but requires an interaction with environmental factors, making it modifiable over time.

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Altered hippocampal function before emotional trauma in rats susceptible to PTSD-like behaviors

Cited by 18 publications

References 56 publications

Ventral hippocampal neurons inhibit postprandial energy intake

Ventral hippocampal neurons inhibit postprandial energy intake

Sweet orosensation induces Arc expression in dorsal hippocampal CA1 neurons in an Experience‐dependent manner

Investigating Individual Pre-trauma Susceptibility to a PTSD-Like Phenotype in Animals

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