Effects of acute pro-inflammatory stimulation and 25-hydroxycholesterol on hippocampal plasticity & learning involve NLRP3 inflammasome and cellular stress responses DOI Creative Commons
Yukitoshi Izumi,

Kazuko A. O’Dell,

Steven Mennerick

и другие.

Research Square (Research Square), Год журнала: 2024, Номер unknown

Опубликована: Дек. 18, 2024

Abstract Neuroinflammation is an increasingly important target for therapeutics in neuropsychiatry and contributes to cognitive dysfunction, disability death across a range of illnesses. We previously found that acute effects pro-inflammatory stimulation with lipopolysaccharide (LPS) on hippocampal long-term potentiation (LTP), form synaptic plasticity involved learning memory, requires synthesis the oxysterol, 25-hydroxycholesterol (25HC) exogenous 25HC mimics LPS. However, downstream mechanisms engaged by LPS remain uncertain. Here we use rat slices vivo behavioral studies provide evidence modulation both activation NLRP3 inflammasome, caspase-1 interleukin-1 receptor. Furthermore, engage cellular stress responses including 5a-reduced neurosteroids are prevented modulators these responses. In using one-trial inhibitory avoidance task, inhibition pre-treatment inhibitor NLRP3. The present strong support role as mediator importance inflammasome deleterious inflammation.

Язык: Английский

Effects of acute pro-inflammatory stimulation and 25-hydroxycholesterol on hippocampal plasticity and learning involve NLRP3 inflammasome and cellular stress responses DOI Creative Commons
Yukitoshi Izumi,

Kazuko A. O’Dell,

Steven Mennerick

и другие.

Scientific Reports, Год журнала: 2025, Номер 15(1)

Опубликована: Фев. 20, 2025

Neuroinflammation is an increasingly important target for therapeutics in neuropsychiatry and contributes to cognitive dysfunction, disability death across a range of illnesses. We previously found that acute effects pro-inflammatory stimulation with lipopolysaccharide (LPS) on hippocampal long-term potentiation (LTP), form synaptic plasticity involved learning memory, requires synthesis the oxysterol, 25-hydroxycholesterol (25HC) exogenous 25HC mimics LPS. However, downstream mechanisms engaged by LPS remain uncertain. Here we use rat slices vivo behavioral studies provide evidence modulation both activation NLRP3 inflammasome, caspase-1 interleukin-1 receptor. Furthermore, engage cellular stress responses including 5α-reduced neurosteroids are prevented modulators these responses. In using one-trial inhibitory avoidance task, inhibition pre-treatment inhibitor NLRP3. The present strong support role as mediator importance inflammasome deleterious inflammation.

Язык: Английский

Процитировано

0
Effects of acute pro-inflammatory stimulation and 25-hydroxycholesterol on hippocampal plasticity & learning involve NLRP3 inflammasome and cellular stress responses DOI Creative Commons
Yukitoshi Izumi,

Kazuko A. O’Dell,

Steven Mennerick

и другие.

Research Square (Research Square), Год журнала: 2024, Номер unknown

Опубликована: Дек. 18, 2024

Abstract Neuroinflammation is an increasingly important target for therapeutics in neuropsychiatry and contributes to cognitive dysfunction, disability death across a range of illnesses. We previously found that acute effects pro-inflammatory stimulation with lipopolysaccharide (LPS) on hippocampal long-term potentiation (LTP), form synaptic plasticity involved learning memory, requires synthesis the oxysterol, 25-hydroxycholesterol (25HC) exogenous 25HC mimics LPS. However, downstream mechanisms engaged by LPS remain uncertain. Here we use rat slices vivo behavioral studies provide evidence modulation both activation NLRP3 inflammasome, caspase-1 interleukin-1 receptor. Furthermore, engage cellular stress responses including 5a-reduced neurosteroids are prevented modulators these responses. In using one-trial inhibitory avoidance task, inhibition pre-treatment inhibitor NLRP3. The present strong support role as mediator importance inflammasome deleterious inflammation.

Язык: Английский

Процитировано

0