Peripheral administration of d-cycloserine rescues memory consolidation following bacterial endotoxin exposure

Kranjac, Dinko; Koster, Kyle M.; Kahn, Marielle S.; Eimerbrink, M.J.; Womble, Brent M.; Cooper, Brenton G.; Chumley, Michael J.; Boehm, Gary W.

doi:10.1016/j.bbr.2012.12.053

Cited by 14 publications

(6 citation statements)

References 73 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the current study, ifenprodil, a noncompetitive GluN2B-containing NMDA receptor antagonist, not only impaired the consolidation of the memory of novel object recognition task, but also reversed (at a dose that did not alter memory per se in our study) the improving effect of spermine on the memory of LPS-treated animals, supporting a role for NMDA receptors in this effect of spermine [ 72 - 74 ]. Interestingly, these results are in agreement with the study by Kranjac and colleagues [ 26 ], who have shown that partial NMDA receptor agonist D-cycloserine rescues memory consolidation following systemic bacterial endotoxin exposure. Furthermore, Velloso and colleagues [ 41 ] have found that post-training intrastriatal administration of spermine reverses the recognition memory deficits in the novel object recognition task induced by quinolinic acid, a model of Huntington’s disease.…”

Section: Discussionsupporting

confidence: 93%

“…This finding is in agreement with previous reports that neuroinflammation decreases total NMDA receptors (NR1 immunoreactivity) in the hippocampus and entorhinal cortex [ 24 ] and that LPS-treated animals present decreased MK801 binding [ 25 ]. Accordingly, the partial NMDA receptor agonist D-cycloserine prevents the deleterious effects of LPS [ 26 ] and closed head injury [ 27 ] on memory consolidation. Therefore, it sounds possible that other positive allosteric modulators of the NMDA receptor attenuate LPS-induced cognitive deficits.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Spermine reverses lipopolysaccharide-induced memory deficit in mice

Frühauf

Ineu

Tomazi

et al. 2015

J Neuroinflammation

View full text Add to dashboard Cite

BackgroundLipopolysaccharide (LPS) induces neuroinflammation and memory deficit. Since polyamines improve memory in various cognitive tasks, we hypothesized that spermine administration reverses LPS-induced memory deficits in an object recognition task in mice. The involvement of the polyamine binding site at the N-methyl-D-aspartate (NMDA) receptor and cytokine production in the promnesic effect of spermine were investigated.MethodsAdult male mice were injected with LPS (250 μg/kg, intraperitoneally) and spermine (0.3 to 1 mg/kg, intraperitoneally) or ifenprodil (0.3 to 10 mg/kg, intraperitoneally), or both, and their memory function was evaluated using a novel object recognition task. In addition, cortical and hippocampal cytokines levels were measured by ELISA four hours after LPS injection.ResultsSpermine increased but ifenprodil decreased the recognition index in the novel object recognition task. Spermine, at doses that did not alter memory (0.3 mg/kg, intraperitoneally), reversed the cognitive impairment induced by LPS. Ifenprodil (0.3 mg/kg, intraperitoneally) reversed the protective effect of spermine against LPS-induced memory deficits. However, spermine failed to reverse the LPS-induced increase of cortical and hippocampal cytokine levels.ConclusionsSpermine protects against LPS-induced memory deficits in mice by a mechanism that involves GluN2B receptors.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Spermine reverses lipopolysaccharide-induced memory deficit in mice

Frühauf

Ineu

Tomazi

et al. 2015

J Neuroinflammation

View full text Add to dashboard Cite

show abstract

“…There are numerous reports suggesting the beneficial influence of DCS on cognitive performance and other neurodegenerative diseases (Thompson et al, 1992 ; Baxter et al, 1994 ; Ohno and Watanabe, 1996 ; Gabriele and Packard, 2007 ; Yaka et al, 2007 ; Curlik and Shors, 2011 ; Kuriyama et al, 2011 ; Feld et al, 2013 ; Kranjac et al, 2013 ; Ren et al, 2013 ). Peripheral injection of DCS, which crosses the blood-brain barrier, has been shown to enhance learning rate and rescue impaired memory consolidation (Thompson et al, 1992 ; Kranjac et al, 2013 ). DCS can modulate NMDA receptor-mediated neurotransmission and has the potential to restore impaired NMDA receptor function associated with aging or pathological condition.…”

Section: Restoring Nmda Receptor Function With Advanced Agementioning

confidence: 99%

NMDA Receptor Function During Senescence: Implication on Cognitive Performance

Kumar

2015

Front. Neurosci.

View full text Add to dashboard Cite

N-methyl-D-aspartate (NMDA) receptors, a family of L-glutamate receptors, play an important role in learning and memory, and are critical for spatial memory. These receptors are tetrameric ion channels composed of a family of related subunits. One of the hallmarks of the aging human population is a decline in cognitive function; studies in the past couple of years have demonstrated deterioration in NMDA receptor subunit expression and function with advancing age. However, a direct relationship between impaired memory function and a decline in NMDA receptors is still ambiguous. Recent studies indicate a link between an age-associated NMDA receptor hypofunction and memory impairment and provide evidence that age-associated enhanced oxidative stress might be contributing to the alterations associated with senescence. However, clear evidence is still deficient in demonstrating the underlying mechanisms and a relationship between age-associated impaired cognitive faculties and NMDA receptor hypofunction. The current review intends to present an overview of the research findings regarding changes in expression of various NMDA receptor subunits and deficits in NMDA receptor function during senescence and its implication in age-associated impaired hippocampal-dependent memory function.

show abstract

“…While these pro-inflammatory molecules propagate throughout the brain, their proliferation has been shown to be greater in the dHC compared to other areas (Kranjac et al, 2012). The effects of LPS-induced inflammation Frustrative nonreward and the hippocampus -27 therefore has shown to acutely disrupt hippocampal CA3 and CA1 neural circuit activity (Czerniawski & Guzowski, 2014) and blunt production of hippocampal BDNF, a protein associated with hippocampal neurogenesis (Kranjac et al, 2012(Kranjac et al, , 2013. Cognitive impairments from LPS have also been shown to be HC dependent.…”

Section: Experiments 3: Hc Levels Of Tumor Necrosis Factor-α (Tnf-α) ...mentioning

confidence: 99%

Flexible behavioral adjustment to frustrative nonreward in anticipatory behavior, but not in consummatory behavior, requires the dorsal hippocampus

Hagen,

Hoxha,

Chitale

et al. 2024

Preprint

View full text Add to dashboard Cite

The hippocampus (HC) is recognized for its pivotal role in memory-related plasticity and facilitating adaptive behavioral responses to reward shifts. However, the nature of its involvement in the response to reward downshifts remains to be determined. To bridge this knowledge gap, we explored the HC's function through a series of experiments in various tasks involving reward downshifts and using several neural manipulations in rats. In Experiment 1, complete excitotoxic lesions of the HC impaired choice performance in an 8-maze task after reducing the quantity of sugar pellet rewards. In Experiment 2, whereas chemogenetic inhibition of the dorsal HC left consummatory responses unaffected after a sucrose downshift, it significantly disrupted anticipatory behavior following a food-pellet reward reduction. Experiments 3-5 used peripheral lipopolysaccharide (LPS) treatment and found an increase in cytokine levels in the dorsal HC (dHC, Experiment 3), impaired anticipatory choice (Experiment 4), but no effect on consummatory behavior in two reward-downshift tasks. In Experiment 6, after a sucrose downshift, we found no evidence of increased activation in either the dorsal or ventral HC, as measured by c-Fos expression. These findings highlight the HC's pivotal role in adaptively modulating anticipatory behavior in response to frustrative nonreward, while having no effect on adjustments of consummatory behavior. Spatial orientation, memory update, choice of reward signals of different value, and anticipatory vs. consummatory adjustments to reward downshift are discussed as potential mechanisms that could elucidate the specific effects observed from HC manipulations.

show abstract

Peripheral administration of d-cycloserine rescues memory consolidation following bacterial endotoxin exposure

Cited by 14 publications

References 73 publications

Spermine reverses lipopolysaccharide-induced memory deficit in mice

Spermine reverses lipopolysaccharide-induced memory deficit in mice

NMDA Receptor Function During Senescence: Implication on Cognitive Performance

Flexible behavioral adjustment to frustrative nonreward in anticipatory behavior, but not in consummatory behavior, requires the dorsal hippocampus

Contact Info

Product

Resources

About