Pretreatment with minocycline restores neurogenesis in the subventricular zone and subgranular zone of the hippocampus after ketamine exposure in neonatal rats

Lu, Yang; Giri, Praveen Kumar; Shan, Lei; Zheng, Juan; Li, Weisong; Wang, Ning; Chen, Xinlin; Lü, Haixia; Zuo, Zhiyi; Liu, Yong; Zhang, Pengbo

doi:10.1016/j.neuroscience.2017.03.057

Cited by 23 publications

(23 citation statements)

References 68 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The report from Zhu and his colleague showed greater impairments in performance on an objective recognition task at 10 weeks than at 4 weeks, suggesting that progressive decline in function mirrored progressive impairments in neurogenesis [15]. One of our recent works showed that pretreatment with minocycline restored neurogenesis in SVZ and SGZ of the hippocampus, and improved adult spatial learning and memory deficits induced by ketamine exposure in neonatal rats [12]. In this study isoflurane decreased neurogenesis and impaired cognitive functions, but pretreatment with simvastatin increased neurogenesis and improved isoflurane-induced learning and memory deficits, strengthening connection between neurogenesis and cognitive dysfunction in developmental anesthetic neurotoxicity.…”

Section: Discussionmentioning

confidence: 94%

“…It was speculated that progressive decline in cognitive function is a consequence of an early loss or suppression of pool of rapidly dividing, multipotent precursors, which might create an ongoing deficit in neurogenesis that worsened over time as the gap in NSC numbers between normal controls and exposed animals widened with rapid cell division [11]. Recently, we reported that pretreatment with minocycline restored neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ) of the hippocampus and improved adult spatial learning and memory deficits induced by ketamine exposure in neonatal rats [12]. Thus, the prevention of neurogenesis inhibition might be a new effective therapeutic approach for anesthetic-induced neurocognitive impairment in the developing brain.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Simvastatin Attenuates Neurogenetic Damage and Improves Neurocongnitive Deficits Induced by Isoflurane in Neonatal Rats

Wang¹,

Lu²,

Wang³

et al. 2018

Cell Physiol Biochem

Self Cite

View full text Add to dashboard Cite

Background/Aims: Isoflurane inhibited neurogenesis and induced subsequent neurocognitive deficits in developing brain. Simvastatin exerts neuroprotection in a wide range of brain injury models. In the present study, we investigated whether simvastatin could attenuate neurogenetic inhibition and cognitive deficits induced by isoflurane exposure in neonatal rats. Methods: Sprague-Dawley rats at postnatal day (PND) 7 and neural stem cells (NSCs) were treated with either gas mixture, isoflurane, or simvastatin 60 min prior to isoflurane exposure, respectively. The rats were decapitated at PND 8 and PND 10 for detection of neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ) of the hippocampus by immunostaining. NSC proliferation, viability and apoptosis were assessed by immunohistochemistry, CCK-8 and TUNEL, respectively. The protein expressions of caspase-3, p-Akt and p-GSK-3β both in vivo and vitro were assessed by western blotting. Cognitive functions were assessed by Morris Water Maze test and context fear conditioning test at the adult. Results: Isoflurane exposure inhibited neurogenesis in the SVZ and SGZ, decreased NSC proliferation and viability, promoted NSC apoptosis and led to late cognitive deficits. Furthermore, isoflurane increased caspase-3 expression and decreased protein expressions of p-Akt and p-GSK-3β both in vivo and in vitro. Pretreatment with simvastatin attenuated isoflurane-elicited changes in NSCs and cognitive function. Co-treatment with LY294002 reversed the effect of simvastatin on NSCs in vitro. Conclusion: We for the first time showed that simvastatin, by upregulating Akt/GSK-3β signaling pathway, alleviated isoflurane-induced neurogenetic damage and neurocognitive deficits in developing rat brain.

show abstract

Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Simvastatin Attenuates Neurogenetic Damage and Improves Neurocongnitive Deficits Induced by Isoflurane in Neonatal Rats

Wang¹,

Lu²,

Wang³

et al. 2018

Cell Physiol Biochem

Self Cite

View full text Add to dashboard Cite

show abstract

“…The pups ( n =5 in each group) received bromodeoxyuridine (BrdU) (50 mg/kg, intraperitoneal injection) every 24 h for 7 consecutive days, which started from the end of the anesthesia, and then they were killed for the detection of neurogenesis in the SVZ and SGZ at PND14. As we described in previous studies 18 , after anesthetization with 40 mg/kg sodium pentobarbital, the rats were perfused with 0.9% normal saline, followed by 4% paraformaldehyde transcardially. The brains were removed to 4% paraformaldehyde overnight for postfixation and then a 30% glucose solution overnight for dehydration.…”

Section: Methodsmentioning

confidence: 99%

“…The positive outcome of minocycline is associated with inhibition of microglia activation 14 , inhibition of caspase-1 and caspase-3 15 , and cytochrome c release 16 . Recently, we reported that minocycline attenuated ketamine-induced injury in neural stem cells (NSCs) 17 and restores neurogenesis in the subventricular zone (SVZ) and the subgranular zone (SGZ) of the hippocampus after ketamine exposure in neonatal rats 18 . However, whether minocycline can attenuate the developmental neurotoxicity of midazolam remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Pretreatment with minocycline improves neurogenesis and behavior performance after midazolam exposure in neonatal rats

Giri

Shan

et al. 2018

NeuroReport

Self Cite

View full text Add to dashboard Cite

Laboratory studies suggested that general anesthetics induce neuroapoptosis and inhibit neurogenesis in developing brains of animals. Minocycline exerts neuroprotection against a wide range of toxic insults in neurodegenerative diseases models. Here, we investigate whether minocycline can alleviate neurogenetic damage and improve cognition following midazolam exposure in neonatal rats. Postnatal 7 days rats were divided randomly into three groups: control group (C), midazolam group (M), and minocycline pretreatment group (MP). After exposure to midazolam, the cell proliferation in the subventricular zone (SVZ) and the subgranular zone (SGZ) of the hippocampus in pups was analyzed by bromodeoxyuridine immunochemistry at 7 days after the administration of anesthesia. Cognitive function was assessed using the Morris water-maze test at 35 days after midazolam exposure. Compared with the control, midazolam reduced cell proliferation both in the SVZ and in the SGZ of the hippocampus of neonatal rats, and decreased spatial learning and memory ability of rats in adulthood significantly. Pretreatment with minocycline increased cell proliferation both in the SVZ and in the SGZ of the hippocampus and improved spatial learning and memory ability compared with midazolam, but it did not mitigate the changes to the normal levels compared with the controls. Our results indicated that pretreatment with minocycline can alleviate midazolam-induced damage in neural stem cell proliferation of neonatal rats and improve spatial learning and memory ability of rats in adulthood.

show abstract

“…Beneficial effects of the drug have been shown in animal models of neuropathic pain, drug addiction, major depression, schizophrenia, cerebral ischaemia and also prevention of neurodegenerative disorders . In addition, a great deal of literature has shown that minocycline improves memory and cognition in animal models of sleep deprivation, transient ishchaemic reperfusion injury, alzheimer, brain injury, drug‐induced memory impairment, aging and also in human beings . Minocycline has been shown to be beneficial in decline of morphine tolerance and also morphine‐induced microglial activation by a suppression of microglial morphine‐induced p38 MAP kinase activation .…”

Section: Introductionmentioning

confidence: 99%

Effect of pretreatment with intracerebroventricular injection of minocycline on morphine‐induced memory impairment in passive avoidance test: Role of P‐CREB and c‐Fos expression in the dorsal hippocampus and basolateral amygdala regions

Hamidkhaniha

Bashiri

Omidi

et al. 2019

Clin Exp Pharma Physio

View full text Add to dashboard Cite

Summary Minocycline as a member of the tetracycline family is a lipophilic broad‐spectrum antibiotic, which can display some non‐antibiotic properties such as antioxidant, antiapoptosis, neuroprotection and modulation of pharmacological traits of drugs of abuse (ie, reward, sensitization and/or analgesia). Thus, the aim of the present study was to investigate the effect of intracerebroventricular (ICV) injection of minocycline on morphine‐induced memory impairment and motor function in male Wistar rats. The behavioural responses were measured by a passive avoidance test for evaluating memory, and in the open field for studying motor function. Furthermore, the expression of Phospho‐cAMP response element‐binding protein (P‐CREB) and c‐Fos were assessed using immunohistochemistry in the dorsal hippocampus and basolateral amygdala (BLA). Our results showed that morphine dose‐dependently impairs memory consolidation, but not motor function. Maximum effect was achieved with morphine at dose of 5 mg/kg. Pretreatment with ICV injection of minocycline (50 μg/rat) prevented morphine‐induced memory impairment, but there was no effect on motor function. The results of immunohistochemistry analysis demonstrated that morphine decreased expression of P‐CREB positive cells compared to saline control group in the BLA, but not in the dorsal hippocampus. On the other hand, pretreatment of animals with ICV injection of minocycline increased the expression of P‐CREB in both brain areas. Moreover, there was no significant change in the expression of c‐Fos positive cells in above‐mentioned regions. In summary, our results indicated that pretreatment with ICV injection of minocycline prevented morphine‐induced memory impairment and increased P‐CREB expression in the dorsal hippocampus and BLA, which may explain its memory improvement property.

show abstract

Pretreatment with minocycline restores neurogenesis in the subventricular zone and subgranular zone of the hippocampus after ketamine exposure in neonatal rats

Cited by 23 publications

References 68 publications

Simvastatin Attenuates Neurogenetic Damage and Improves Neurocongnitive Deficits Induced by Isoflurane in Neonatal Rats

Simvastatin Attenuates Neurogenetic Damage and Improves Neurocongnitive Deficits Induced by Isoflurane in Neonatal Rats

Pretreatment with minocycline improves neurogenesis and behavior performance after midazolam exposure in neonatal rats

Effect of pretreatment with intracerebroventricular injection of minocycline on morphine‐induced memory impairment in passive avoidance test: Role of P‐CREB and c‐Fos expression in the dorsal hippocampus and basolateral amygdala regions

Contact Info

Product

Resources

About