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Neuroprotective effects of ceftriaxone treatment on cognitive and neuronal deficits in a rat model of accelerated senescence. / Tikhonova, Maria A.; Ho, Shih Chun; Akopyan, Anna A. et al.

In: Behavioural Brain Research, Vol. 330, 14.07.2017, p. 8-16.

Research output: Contribution to journalArticlepeer-review

Harvard

Tikhonova, MA, Ho, SC, Akopyan, AA, Kolosova, NG, Weng, JC, Meng, WY, Lin, CL, Amstislavskaya, TG & Ho, YJ 2017, 'Neuroprotective effects of ceftriaxone treatment on cognitive and neuronal deficits in a rat model of accelerated senescence', Behavioural Brain Research, vol. 330, pp. 8-16. https://doi.org/10.1016/j.bbr.2017.05.002

APA

Tikhonova, M. A., Ho, S. C., Akopyan, A. A., Kolosova, N. G., Weng, J. C., Meng, W. Y., Lin, C. L., Amstislavskaya, T. G., & Ho, Y. J. (2017). Neuroprotective effects of ceftriaxone treatment on cognitive and neuronal deficits in a rat model of accelerated senescence. Behavioural Brain Research, 330, 8-16. https://doi.org/10.1016/j.bbr.2017.05.002

Vancouver

Tikhonova MA, Ho SC, Akopyan AA, Kolosova NG, Weng JC, Meng WY et al. Neuroprotective effects of ceftriaxone treatment on cognitive and neuronal deficits in a rat model of accelerated senescence. Behavioural Brain Research. 2017 Jul 14;330:8-16. doi: 10.1016/j.bbr.2017.05.002

Author

Tikhonova, Maria A. ; Ho, Shih Chun ; Akopyan, Anna A. et al. / Neuroprotective effects of ceftriaxone treatment on cognitive and neuronal deficits in a rat model of accelerated senescence. In: Behavioural Brain Research. 2017 ; Vol. 330. pp. 8-16.

BibTeX

@article{a0beb30145e242f4898e047646159b89,
title = "Neuroprotective effects of ceftriaxone treatment on cognitive and neuronal deficits in a rat model of accelerated senescence",
abstract = "Rats of OXYS strain are characterized by genetically defined accelerated senescence. Ceftriaxone (CEF) exerts neuroprotective effects by decreasing the excitotoxicity and activation of antioxidant system. Here, we studied the effects of CEF (50 or 100 mg/kg/day, i.p., 36 days) on cognitive and neuronal deficits in 5-month-old OXYS rats. Chronic CEF administration in a dose of 100 mg/kg partially inhibited impairments of movement and restored the deficit in the novel object recognition in OXYS rats. Neuromorphologically, control OXYS rats exhibited a lowered neuronal density in the hippocampal CA1 area and there was a tendency to decrease in the substantia nigra pars compacta compared to Wistar controls. Both doses of CEF increased the density of pyramidal neurons in the CA1 area in OXYS rats. Control OXYS rats demonstrated a tendency to lower tyrosine hydroxylase (TH) immunoreactivity in the striatum compared with Wistar rats, while CEF treatment at a dose of 50 mg/kg significantly augmented this parameter. In control OXYS rats, the levels of neurogenesis in the subgranular zone of the dentate gyrus of the hippocampus were significantly higher than in Wistar rats indicating compensatory processes that probably prevented the further induction of neurogenesis by CEF. Restoration of the recognition function and neuronal density in the CA1 area in OXYS rats after CEF treatment might be related to activation of the mechanisms that provide survival of newborn and mature neurons. The data suggested CEF as a promising pharmacological tool for the prevention of cognitive decline at accelerated aging.",
keywords = "Accelerated aging, Ceftriaxone, Cognitive deficit, Hippocampus, Neuroprotection, Rats, Tyrosine 3-Monooxygenase/analysis, Rats, Wistar, Male, Neurons/drug effects, Pars Compacta/drug effects, Dentate Gyrus/drug effects, Neurogenesis/drug effects, Dopaminergic Neurons/drug effects, Brain/drug effects, Hippocampus/drug effects, Disease Models, Animal, Aging/drug effects, Pyramidal Cells/drug effects, Antioxidants/pharmacology, Neuroprotective Agents/pharmacology, CA1 Region, Hippocampal/drug effects, Ceftriaxone/pharmacology, Animals, Cognition/drug effects",
author = "Tikhonova, {Maria A.} and Ho, {Shih Chun} and Akopyan, {Anna A.} and Kolosova, {Nataliya G.} and Weng, {Jun Cheng} and Meng, {Wan Yun} and Lin, {Chih Li} and Amstislavskaya, {Tamara G.} and Ho, {Ying Jui}",
note = "Copyright {\textcopyright} 2017 Elsevier B.V. All rights reserved.",
year = "2017",
month = jul,
day = "14",
doi = "10.1016/j.bbr.2017.05.002",
language = "English",
volume = "330",
pages = "8--16",
journal = "Behavioural Brain Research",
issn = "0166-4328",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Neuroprotective effects of ceftriaxone treatment on cognitive and neuronal deficits in a rat model of accelerated senescence

AU - Tikhonova, Maria A.

AU - Ho, Shih Chun

AU - Akopyan, Anna A.

AU - Kolosova, Nataliya G.

AU - Weng, Jun Cheng

AU - Meng, Wan Yun

AU - Lin, Chih Li

AU - Amstislavskaya, Tamara G.

AU - Ho, Ying Jui

N1 - Copyright © 2017 Elsevier B.V. All rights reserved.

PY - 2017/7/14

Y1 - 2017/7/14

N2 - Rats of OXYS strain are characterized by genetically defined accelerated senescence. Ceftriaxone (CEF) exerts neuroprotective effects by decreasing the excitotoxicity and activation of antioxidant system. Here, we studied the effects of CEF (50 or 100 mg/kg/day, i.p., 36 days) on cognitive and neuronal deficits in 5-month-old OXYS rats. Chronic CEF administration in a dose of 100 mg/kg partially inhibited impairments of movement and restored the deficit in the novel object recognition in OXYS rats. Neuromorphologically, control OXYS rats exhibited a lowered neuronal density in the hippocampal CA1 area and there was a tendency to decrease in the substantia nigra pars compacta compared to Wistar controls. Both doses of CEF increased the density of pyramidal neurons in the CA1 area in OXYS rats. Control OXYS rats demonstrated a tendency to lower tyrosine hydroxylase (TH) immunoreactivity in the striatum compared with Wistar rats, while CEF treatment at a dose of 50 mg/kg significantly augmented this parameter. In control OXYS rats, the levels of neurogenesis in the subgranular zone of the dentate gyrus of the hippocampus were significantly higher than in Wistar rats indicating compensatory processes that probably prevented the further induction of neurogenesis by CEF. Restoration of the recognition function and neuronal density in the CA1 area in OXYS rats after CEF treatment might be related to activation of the mechanisms that provide survival of newborn and mature neurons. The data suggested CEF as a promising pharmacological tool for the prevention of cognitive decline at accelerated aging.

AB - Rats of OXYS strain are characterized by genetically defined accelerated senescence. Ceftriaxone (CEF) exerts neuroprotective effects by decreasing the excitotoxicity and activation of antioxidant system. Here, we studied the effects of CEF (50 or 100 mg/kg/day, i.p., 36 days) on cognitive and neuronal deficits in 5-month-old OXYS rats. Chronic CEF administration in a dose of 100 mg/kg partially inhibited impairments of movement and restored the deficit in the novel object recognition in OXYS rats. Neuromorphologically, control OXYS rats exhibited a lowered neuronal density in the hippocampal CA1 area and there was a tendency to decrease in the substantia nigra pars compacta compared to Wistar controls. Both doses of CEF increased the density of pyramidal neurons in the CA1 area in OXYS rats. Control OXYS rats demonstrated a tendency to lower tyrosine hydroxylase (TH) immunoreactivity in the striatum compared with Wistar rats, while CEF treatment at a dose of 50 mg/kg significantly augmented this parameter. In control OXYS rats, the levels of neurogenesis in the subgranular zone of the dentate gyrus of the hippocampus were significantly higher than in Wistar rats indicating compensatory processes that probably prevented the further induction of neurogenesis by CEF. Restoration of the recognition function and neuronal density in the CA1 area in OXYS rats after CEF treatment might be related to activation of the mechanisms that provide survival of newborn and mature neurons. The data suggested CEF as a promising pharmacological tool for the prevention of cognitive decline at accelerated aging.

KW - Accelerated aging

KW - Ceftriaxone

KW - Cognitive deficit

KW - Hippocampus

KW - Neuroprotection

KW - Rats

KW - Tyrosine 3-Monooxygenase/analysis

KW - Rats, Wistar

KW - Male

KW - Neurons/drug effects

KW - Pars Compacta/drug effects

KW - Dentate Gyrus/drug effects

KW - Neurogenesis/drug effects

KW - Dopaminergic Neurons/drug effects

KW - Brain/drug effects

KW - Hippocampus/drug effects

KW - Disease Models, Animal

KW - Aging/drug effects

KW - Pyramidal Cells/drug effects

KW - Antioxidants/pharmacology

KW - Neuroprotective Agents/pharmacology

KW - CA1 Region, Hippocampal/drug effects

KW - Ceftriaxone/pharmacology

KW - Animals

KW - Cognition/drug effects

UR - http://www.scopus.com/inward/record.url?scp=85019550732&partnerID=8YFLogxK

U2 - 10.1016/j.bbr.2017.05.002

DO - 10.1016/j.bbr.2017.05.002

M3 - Article

C2 - 28487222

AN - SCOPUS:85019550732

VL - 330

SP - 8

EP - 16

JO - Behavioural Brain Research

JF - Behavioural Brain Research

SN - 0166-4328

ER -

ID: 9977270