Nicotine pretreatment alleviates MK-801-induced behavioral and cognitive deficits in mice by regulating Pdlim5/CRTC1 in the PFC

Wang, Qian; Wang, Mengwei; Sun, Yuanheng; Hu, Xiaoyan; Geng, Panpan; Shu, Hui; Wang, Xiaona; Wang, Hao; Zhang, Junfang; Cheng, Hongqiang; Wang, Wei; Jin, Xinchun

doi:10.1038/s41401-022-00974-8

Cited by 5 publications

(4 citation statements)

References 62 publications

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“…We demonstrated LPS‐produced CRTC1 decrease in PFC (Figure 3 ) which is known to be crucial for fear memory consolidation, 9 ischemic stroke‐produced memory deficit, 11 and schizophrenia‐induced WM deficiency. 45 We have shown that LPS impaired fear memory reconsolidation through downregulating CRTC1 expression. 13 Our current study indicates that CRTC1 is also involved in WM and could be a target for reducing LPS‐produced WM deficiency.…”

Section: Discussionmentioning

confidence: 86%

Chronic but not acute nicotine treatment ameliorates acute inflammation‐induced working memory impairment by increasing CRTC1 and HCN2 in adult male mice

Wang,

Song

et al. 2024

CNS Neurosci Ther

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BackgroundSystemic inflammation in which lipopolysaccharide (LPS) is released into circulation can cause cognitive dysfunction and we have previously shown that LPS impaired working memory (WM) which refers to the ability to guide incoming behavior by retrieving recently acquired information. However, the mechanism is not very clear, and currently, there is no approved strategy to improve inflammation‐induced WM deficit. Notably, epidemiological studies have demonstrated a lower occurrence rate of inflammatory‐related diseases in smoking patients, suggesting that inflammation‐induced WM impairment may be improved by nicotine treatment. Here, our object is to investigate the effect and potential mechanisms of acute and chronic nicotine treatment on LPS‐produced WM deficiency.MethodsDelayed alternation T‐maze task (DAT) was applied for evaluating WM which includes both the short‐term information storage and the ability to correct errors in adult male mice. Immunofluorescence staining and immunoblotting were used for assessing the levels and distribution of CREB‐regulated transcription coactivator 1 (CRTC1) and hyperpolarization‐activated cation channels 2 (HCN2) in the medial prefrontal cortex (mPFC) and hippocampus. Quantitative PCR and ELISA were employed for analyzing the mRNA and protein levels of TNF‐α and IL‐1β.ResultsOur results revealed that administration of LPS (i.p.) at a dose of 0.5 mg/kg significantly produced WM impairment in the DAT task accompanied by an increase in IL‐1β and TNF‐α expression in the mPFC. Moreover, intra‐mPFC infusion of IL‐1Ra, an IL‐1 antagonist, markedly alleviated LPS‐induced WM deficiency. More important, chronic (2 weeks) but not acute nicotine (0.2 mg/kg, subcutaneous) treatment significantly alleviated LPS‐induced WM deficiency by upregulating CRTC1 and HCN2. Of note, intra‐mPFC infusion of HCN blocker ZD7288 produced significant WM deficiency.ConclusionsIn summary, in this study, we show that chronic nicotine treatment ameliorates acute inflammation‐induced working memory deficiency by increasing CRTC1 and HCN2 in adult male mice.

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Section: Discussionmentioning

confidence: 86%

Chronic but not acute nicotine treatment ameliorates acute inflammation‐induced working memory impairment by increasing CRTC1 and HCN2 in adult male mice

Wang,

Song

et al. 2024

CNS Neurosci Ther

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“…Wang et al reported that chronic nicotine pretreatment (0.2 mg/kg for 2 weeks) diminished MK-801-induced memory impairments. 22 Shu et al showed acute nicotine injection alleviated memory deficits in lipopolysaccharide (LPS)-induced fear memory reconsolidation impairment. 23 Furthermore, Hambsch et al indicated that in a G72 mouse model of schizophrenia-like symptoms, chronic nicotine administration improved short-term memory impairments.…”

Section: Discussionmentioning

confidence: 99%

Effects of Nicotine Administration in an Enriched Environment on the Behavior of Male MK-801-Exposed Rats

Salmani,

Darvishzadeh Mahani,

Parvan

et al. 2023

Addict Health

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Background: Smoking is more common in patients with schizophrenia than in healthy populations. Some controversial hypotheses connect the disease with the high prevalence of smoking. Moreover, environmental factors affect the severity of the positive and negative symptoms of schizophrenia. The current study aimed to assess the effect of enriched environment (EE) and nicotine on the MK-801 animal model of schizophrenia. Methods: Male Wistar rat pups randomly received saline or MK-801 (dose:1 mg/kg) for five days from the sixth postnatal day (P) until the tenth. The pups were placed in EE or standard cages (SCs) after weaning (P21). Morris water maze (MWM) was used to assess spatial learning and memory. The rats received 0.6 mg/kg nicotine twice for three days at the end of the second month and were examined in an open-field box and three-chamber social interaction test. Findings: MK-801 rats’ behaviors were the same as those of the saline rats when they were exposed to nicotine. No positive effects of EE were observed when the animals were exposed to nicotine. Conclusion: The results suggested that nicotine decreased schizophrenia-like symptoms and covered the positive effects of EE.

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“…123 It is noteworthy that CRTC1 has been reported to critically contribute to regulating depression, 124 AD, 125 fear memory, 126 stroke-induced memory impairment, 127 LPSinduced fear memory impairment, 128 and schizophreniainduced memory impairment. 129 CRTC1 is necessary for the induction of ischemic tolerance 130 and can play pivotal roles in SIK2mediated neuron survival after ischemia. 131 The function of CRTC1 can be affected if CRTC1 is phosphorylated after ischemia.…”

Section: Possible Mechanisms and Treatment Strategymentioning

confidence: 99%

“… 123 It is noteworthy that CRTC1 has been reported to critically contribute to regulating depression, 124 AD, 125 fear memory, 126 stroke-induced memory impairment, 127 LPS-induced fear memory impairment, 128 and schizophrenia-induced memory impairment. 129 …”

Section: Role Of Crtc1 In Cognition and Aging-induced Crtc1 Changesmentioning

confidence: 99%

CRTC1 is a potential target to delay aging-induced cognitive deficit by protecting the integrity of the blood-brain barrier via inhibiting inflammation

Wang

Sun

et al. 2023

J Cereb Blood Flow Metab

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Aging can cause attenuation in the functioning of multiple organs, and blood-brain barrier (BBB) breakdown could promote the occurrence of disorders of the central nervous system during aging. Since inflammation is considered to be an important factor underlying BBB injury during aging, vascular endothelial cell senescence serves as a critical pathological basis for the destruction of BBB integrity. In the current review, we have first introduced the concepts related to aging-induced cognitive deficit and BBB integrity damage. Thereafter, we reviewed the potential relationship between disruption of BBB integrity and cognition deficit and the role of inflammation, vascular endothelial cell senescence, and BBB injury. We have also briefly introduced the function of CREB-regulated transcription co-activator 1 (CRTC1) in cognition and aging-induced CRTC1 changes as well as the critical roles of CRTC1/cyclooxygenase-2 (COX-2) in regulating inflammation, endothelial cell senescence, and BBB injury. Finally, the underlying mechanisms have been summarized and we propose that CRTC1 could be a promising target to delay aging-induced cognitive deficit by protecting the integrity of BBB through promoting inhibition of inflammation-mediated endothelial cell senescence.

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Nicotine pretreatment alleviates MK-801-induced behavioral and cognitive deficits in mice by regulating Pdlim5/CRTC1 in the PFC

Cited by 5 publications

References 62 publications

Chronic but not acute nicotine treatment ameliorates acute inflammation‐induced working memory impairment by increasing CRTC1 and HCN2 in adult male mice

Chronic but not acute nicotine treatment ameliorates acute inflammation‐induced working memory impairment by increasing CRTC1 and HCN2 in adult male mice

Effects of Nicotine Administration in an Enriched Environment on the Behavior of Male MK-801-Exposed Rats

CRTC1 is a potential target to delay aging-induced cognitive deficit by protecting the integrity of the blood-brain barrier via inhibiting inflammation

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