The glial response in the rodent hippocampus to systemic administration of bacterial lipopolysaccharide

Tishkina, A. O.; Stepanichev, M. Yu.; Лазарева, Н. А.; Kulagina, A. O.; Gulyaeva, N. V.

doi:10.1134/s1819712414020111

Cited by 2 publications

(4 citation statements)

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“…We performed measurements in these regions 1 month after LPS administration at a much lower dose (2 mg kg −1 ), which showed an increased BI and proved that long‐term LPS‐induced changes were of a decidedly different character compared with those described by Tishkina et al. (). Moreover, our studies showed that long‐term changes could be observed when LPS was administered on P30 but were absent when LPS was given on P06.…”

Section: Discussionsupporting

confidence: 61%

“…In addition, in these brain structures, Tishkina et al. () discovered a reduction of density of GFAP + astrocytes already 1 day after LPS administration (5 mg kg −1 ). We performed measurements in these regions 1 month after LPS administration at a much lower dose (2 mg kg −1 ), which showed an increased BI and proved that long‐term LPS‐induced changes were of a decidedly different character compared with those described by Tishkina et al.…”

Section: Discussionmentioning

confidence: 95%

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Inflammation in the developing rat modulates astroglial reactivity to seizures in the mature brain

2017

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Astrocytes participate in neuronal development and excitability, and produce factors enhancing or suppressing inflammatory processes occurring due to neurodegenerative diseases, such as epilepsy. Seizures, in turn, trigger the release of inflammatory mediators, causing structural and functional changes in the brain. Therefore, it appears reasonable to determine whether generalized inflammation at developmental periods can affect astrocyte reactivity to epileptic seizures occurring in the adult brain. Lipopolysaccharide (LPS) was injected in 6- or 30-day-old rats (P6 or P30, respectively). At the age of 2 months, seizures were induced, and pilocarpine and morphological changes of astrocytes located within the hippocampal formation were assessed. Additionally, expression of glial fibrillary acidic protein (GFAP), glutamine synthetase (GS), aquaporin 4 (AQP4), and inwardly rectifying potassium channel Kir 4.1 (Kir4.1) was determined using Western blots. The animal group given LPS on P6 displayed maximal susceptibility to pilocarpine-induced seizures, significantly higher than the group that received LPS on P30. In the immunohistologically examined hippocampal formation, the GFAP-immunoreactive area was not affected by LPS alone. However, it was reduced following seizures in naïve controls but not in LPS-pretreated rats. Increases in the ramification of astrocytic processes were detected only in adult rats given LPS on P30, not on P6. Seizures abolished the effects. Following seizures, the process ramification showed no significant change in the two LPS-treated rat groups, whereas it was significantly reduced in the dentate gyrus of LPS-untreated controls. Glial fibrillary acidic protein (GFAP) expression showed no changes induced with LPS alone and rose slightly after seizures. AQP4 content was lower in rats given LPS on P6 and was seizure-resistant in the two LPS-treated groups, contrary to a decrease in untreated controls. GS expression was not affected by LPS treatments and was reduced after seizures without an intergroup difference. Kir4.1 underwent highly significant increases in all groups experiencing seizures, but LPS alone had no effect. It can be concluded that the generalized inflammatory status led to some important changes in astrocytes reflected, in part at least by permanent modifications of their morphology and molecular profile. Moreover, the previously experienced inflammation prevented the cells from much stronger changes in response to seizures observed in adult untreated controls. The obtained results point to a link between the activation of astrocytes by transient systemic inflammation occurring during the developmental period and their subsequent reactivity to seizures, which may play an important role in the functional features of the brain, including its susceptibility to seizures.

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Section: Discussionsupporting

confidence: 61%

Section: Discussionmentioning

confidence: 95%

Inflammation in the developing rat modulates astroglial reactivity to seizures in the mature brain

2017

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“…In the present study we did not observe an increase in GFAP after the treatments with Bromo, LPS or the combination. This effect may also be explained because we employed short-term treatments with the endotoxin, since LPS induces neuroinflammation at longer periods of time after administration (48 h) but not after short ones (4 h) (Tishkina et al, 2014), even when it can increase the BBB permeability at short times after its administration (Zhao et al, 2014). This same effect (increase in BBB permeability but no change in GFAP expression) was observed in the animals with PRL inhibition treatment.…”

Section: Discussionsupporting

confidence: 58%

“…An increase in BBB permeability is also related to glial activation (Tishkina et al, 2014), for this reason the analysis of the expression of the glial specific marker GFAP was performed. We found that none of the treatments modified the expression of this protein, compared to the control (Fig.…”

Section: Inhibition Of Prl Did Not Modify the Expression Of Gfapmentioning

confidence: 99%

Inhibition of prolactin with bromocriptine for 28days increases blood–brain barrier permeability in the rat

Rosas-Hernández¹,

Ramı́rez²,

Ramirez-Lee³

et al. 2015

Neuroscience

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The glial response in the rodent hippocampus to systemic administration of bacterial lipopolysaccharide

Cited by 2 publications

References 20 publications

Inflammation in the developing rat modulates astroglial reactivity to seizures in the mature brain

Inflammation in the developing rat modulates astroglial reactivity to seizures in the mature brain

Inhibition of prolactin with bromocriptine for 28days increases blood–brain barrier permeability in the rat

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