Endogenous cannabinoid system alterations and their role in epileptogenesis after brain injury in rat

被引:10
作者
Wang, Xiu [1 ,2 ]
Wang, Yao [1 ,2 ]
Zhang, Chao [1 ,2 ]
Liu, Chang [2 ]
Yang, Hai-Feng [3 ]
Hu, Wen-Han [2 ,4 ,5 ]
Zhang, Jian-Guo [1 ,2 ,4 ,5 ]
Zhang, Kai [1 ,2 ,5 ]
机构
[1] Capital Med Univ, Beijing Tian Tan Hosp, Dept Neurosurg, 6 Tian Tan Xi Li, Beijing 100050, Peoples R China
[2] Beijing Key Lab Neurostimulat, Beijing 100050, Peoples R China
[3] Beijing Jingmei Grp Gen Hosp, Beijing 102300, Peoples R China
[4] Capital Med Univ, Beijing Neurosurg Inst, Stereotact & Funct Neurosurg Lab, Beijing 100050, Peoples R China
[5] Peking Univ, Hosp Fengtai Hosp 1, Med Alliance Beijing Tian Tan Hosp, Epilepsy Ctr, Beijing 100050, Peoples R China
基金
中国国家自然科学基金;
关键词
Cannabinoid; CB1; receptor; Post-traumatic epilepsy; Epileptogenesis; CLOSED-HEAD-INJURY; ENDOCANNABINOID SYSTEM; HIPPOCAMPAL-NEURONS; EPILEPSY; RECEPTOR; SEIZURE; ANTAGONIST; MODEL; HYPEREXCITABILITY; EXCITOTOXICITY;
D O I
10.1016/j.eplepsyres.2016.10.002
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Post-traumatic epilepsy (PTE) is one of the most common complications resulting from brain injury, however, antiepileptic drugs usually fail to prevent it. Several lines of evidence have demonstrated that the endogenous cannabinoid system (ECS) plays a pivotal role during epileptogenesis in several animal models. A recent study has shown that a cannabinoid type 1 (CB1) receptor antagonist could suppress long-term neuron hyperexcitability after brain injury, but the underlying mechanisms remain largely unknown. In this study, we first analyzed the dynamic expression of different components of the ECS at various time points after brain injury in rats. Then, we conducted a 12-month-long session of behavioral monitoring after the brain injury, and based on the results, the rats were divided into a PTE group and a non-PTE group. Finally, the changes in the ECS between the two groups were compared. We found that the ECS exhibited a biphasic alteration after brain injury; the expression of the CB1 receptor and 2-arachidonoylglycerol (2-AG) in the PTE group was significantly higher than that of the non-PTE group 12 months after traumatic brain injury. Our preliminary results indicated that the ECS might be involved in post-traumatic epileptogenesis. (C) 2016 Elsevier B.V. All rights reserved.
引用
收藏
页码:35 / 42
页数:8
相关论文
共 37 条
[1]   Enzymatic pathways that regulate endocannabinoid signaling in the nervous system [J].
Ahn, Kay ;
McKinney, Michele K. ;
Cravatt, Benjamin F. .
CHEMICAL REVIEWS, 2008, 108 (05) :1687-1707
[2]   A population-based study of seizures after traumatic brain injuries [J].
Annegers, JF ;
Hauser, WA ;
Coan, SP ;
Rocca, WA .
NEW ENGLAND JOURNAL OF MEDICINE, 1998, 338 (01) :20-24
[3]   Cloning of the first sn1-DAG lipases points to the spatial and temporal regulation of endocannabinoid signaling in the brain [J].
Bisogno, T ;
Howell, F ;
Williams, G ;
Minassi, A ;
Cascio, MG ;
Ligresti, A ;
Matias, I ;
Schiano-Moriello, A ;
Paul, P ;
Williams, EJ ;
Gangadharan, U ;
Hobbs, C ;
Di Marzo, V ;
Doherty, P .
JOURNAL OF CELL BIOLOGY, 2003, 163 (03) :463-468
[4]   Activation of the cannabinoid type-1 receptor mediates the anticonvulsant properties of cannabinoids in the hippocampal neuronal culture models of acquired epilepsy and status epilepticus [J].
Blair, Robert E. ;
Deshpande, Laxmikant S. ;
Sombati, Sompong ;
Falenski, Katherine W. ;
Martin, Billy R. ;
DeLorenzo, Robert J. .
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 2006, 317 (03) :1072-1078
[5]   EPILEPSY, A PRODUCT OF TRAUMA IN OUR TIME [J].
CAVENESS, WF .
EPILEPSIA, 1976, 17 (02) :207-215
[6]   Prevention of plasticity of endocannabinoid signaling inhibits persistent limbic hyperexcitability caused by developmental seizures [J].
Chen, Kang ;
Neu, Axel ;
Howard, Allyson L. ;
Foldy, Csaba ;
Echegoyen, Julio ;
Hilgenberg, Lutz ;
Smith, Martin ;
Mackie, Ken ;
Soltesz, Ivan .
JOURNAL OF NEUROSCIENCE, 2007, 27 (01) :46-58
[7]   Traumatic brain injury: Risks of epilepsy and implications for medicolegal assessment [J].
Christensen, Jakob .
EPILEPSIA, 2012, 53 :43-47
[8]   Long-term risk of epilepsy after traumatic brain injury in children and young adults: a population-based cohort study [J].
Christensen, Jakob ;
Pedersen, Marianne G. ;
Pedersen, Carsten B. ;
Sidenius, Per ;
Olsen, Jorn ;
Vestergaard, Mogens .
LANCET, 2009, 373 (9669) :1105-1110
[9]   Molecular characterization of an enzyme that degrades neuromodulatory fatty-acid amides [J].
Cravatt, BF ;
Giang, DK ;
Mayfield, SP ;
Boger, DL ;
Lerner, RA ;
Gilula, NB .
NATURE, 1996, 384 (6604) :83-87
[10]   Endocannabinoids: synthesis and degradation [J].
Di Marzo, V. .
REVIEWS OF PHYSIOLOGY, BIOCHEMISTRY AND PHARMACOLOGY, VOL 160, 2008, 160 :1-24