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Acute Exposure to Pacific Ciguatoxin Reduces Electroencephalogram Activity and Disrupts Neurotransmitter Metabolic Pathways in Motor Cortex.
Mol Neurobiol. 2017 09; 54(7):5590-5603.MN

Abstract

Ciguatera fish poisoning (CFP) is a common human food poisoning caused by consumption of ciguatoxin (CTX)-contaminated fish affecting over 50,000 people worldwide each year. CTXs are classified depending on their origin from the Pacific (P-CTXs), Indian Ocean (I-CTXs), and Caribbean (C-CTXs). P-CTX-1 is the most toxic CTX known and the major source of CFP causing an array of neurological symptoms. Neurological symptoms in some CFP patients last for several months or years; however, the underlying electrophysiological properties of acute exposure to CTXs remain unknown. Here, we used CTX purified from ciguatera fish sourced in the Pacific Ocean (P-CTX-1). Delta and theta electroencephalography (EEG) activity was reduced remarkably in 2 h and returned to normal in 6 h after a single exposure. However, second exposure to P-CTX-1 induced not only a further reduction in EEG activities but also a 2-week delay in returning to baseline EEG values. Ciguatoxicity was detected in the brain hours after the first and second exposure by mouse neuroblastoma assay. The spontaneous firing rate of single motor cortex neuron was reduced significantly measured by single-unit recording with high spatial resolution. Expression profile study of neurotransmitters using targeted profiling approach based on liquid chromatography-tandem mass spectrometry revealed an imbalance between excitatory and inhibitory neurotransmitters in the motor cortex. Our study provides a possible link between the brain oscillations and neurotransmitter release after acute exposure to P-CTX-1. Identification of EEG signatures and major metabolic pathways affected by P-CTX-1 provides new insight into potential biomarker development and therapeutic interventions.

Authors+Show Affiliations

Department of Biomedical Sciences, City University of Hong Kong, Tat Chee Avenue, Kowloon Tong, Hong Kong.Department of Biomedical Sciences, City University of Hong Kong, Tat Chee Avenue, Kowloon Tong, Hong Kong.Department of Biology and Chemistry, City University of Hong Kong, Tat Chee Avenue, Kowloon Tong, Hong Kong.State Key Laboratory in Marine Pollution, City University of Hong Kong, Tat Chee Avenue, Kowloon Tong, Hong Kong. Shenzhen Key Laboratory for the Sustainable Use of Marine Biodiversity, Research Centre for the Oceans and Human Health, City University of Hong Kong Shenzhen Research Institute, Shenzhen, China.Department of Electronic Engineering, City University of Hong Kong, Tat Chee Avenue, Kowloon Tong, Hong Kong. Centre for Biosystems, Neuroscience, and Nanotechnology, City University of Hong Kong, Tat Chee Avenue, Kowloon Tong, Hong Kong.Department of Biology and Chemistry, City University of Hong Kong, Tat Chee Avenue, Kowloon Tong, Hong Kong.Department of Biomedical Sciences, City University of Hong Kong, Tat Chee Avenue, Kowloon Tong, Hong Kong. State Key Laboratory in Marine Pollution, City University of Hong Kong, Tat Chee Avenue, Kowloon Tong, Hong Kong. Shenzhen Key Laboratory for the Sustainable Use of Marine Biodiversity, Research Centre for the Oceans and Human Health, City University of Hong Kong Shenzhen Research Institute, Shenzhen, China.Department of Biology and Chemistry, City University of Hong Kong, Tat Chee Avenue, Kowloon Tong, Hong Kong. State Key Laboratory in Marine Pollution, City University of Hong Kong, Tat Chee Avenue, Kowloon Tong, Hong Kong. Shenzhen Key Laboratory for the Sustainable Use of Marine Biodiversity, Research Centre for the Oceans and Human Health, City University of Hong Kong Shenzhen Research Institute, Shenzhen, China.Department of Biomedical Sciences, City University of Hong Kong, Tat Chee Avenue, Kowloon Tong, Hong Kong. eddiema@cityu.edu.hk. State Key Laboratory in Marine Pollution, City University of Hong Kong, Tat Chee Avenue, Kowloon Tong, Hong Kong. eddiema@cityu.edu.hk. Centre for Biosystems, Neuroscience, and Nanotechnology, City University of Hong Kong, Tat Chee Avenue, Kowloon Tong, Hong Kong. eddiema@cityu.edu.hk.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

27613284

Citation

Kumar, Gajendra, et al. "Acute Exposure to Pacific Ciguatoxin Reduces Electroencephalogram Activity and Disrupts Neurotransmitter Metabolic Pathways in Motor Cortex." Molecular Neurobiology, vol. 54, no. 7, 2017, pp. 5590-5603.
Kumar G, Au NPB, Lei ENY, et al. Acute Exposure to Pacific Ciguatoxin Reduces Electroencephalogram Activity and Disrupts Neurotransmitter Metabolic Pathways in Motor Cortex. Mol Neurobiol. 2017;54(7):5590-5603.
Kumar, G., Au, N. P. B., Lei, E. N. Y., Mak, Y. L., Chan, L. L. H., Lam, M. H. W., Chan, L. L., Lam, P. K. S., & Ma, C. H. E. (2017). Acute Exposure to Pacific Ciguatoxin Reduces Electroencephalogram Activity and Disrupts Neurotransmitter Metabolic Pathways in Motor Cortex. Molecular Neurobiology, 54(7), 5590-5603. https://doi.org/10.1007/s12035-016-0093-y
Kumar G, et al. Acute Exposure to Pacific Ciguatoxin Reduces Electroencephalogram Activity and Disrupts Neurotransmitter Metabolic Pathways in Motor Cortex. Mol Neurobiol. 2017;54(7):5590-5603. PubMed PMID: 27613284.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Acute Exposure to Pacific Ciguatoxin Reduces Electroencephalogram Activity and Disrupts Neurotransmitter Metabolic Pathways in Motor Cortex. AU - Kumar,Gajendra, AU - Au,Ngan Pan Bennett, AU - Lei,Elva Ngai Yu, AU - Mak,Yim Ling, AU - Chan,Leanne Lai Hang, AU - Lam,Michael Hon Wah, AU - Chan,Leo Lai, AU - Lam,Paul Kwan Sing, AU - Ma,Chi Him Eddie, Y1 - 2016/09/10/ PY - 2016/02/02/received PY - 2016/09/01/accepted PY - 2016/9/11/pubmed PY - 2018/5/19/medline PY - 2016/9/11/entrez KW - Ciguatera fish poisoning KW - Delta and theta power KW - Electroencephalography KW - Metabolomics KW - Neurotransmitters KW - Pacific ciguatoxin-1 SP - 5590 EP - 5603 JF - Molecular neurobiology JO - Mol Neurobiol VL - 54 IS - 7 N2 - Ciguatera fish poisoning (CFP) is a common human food poisoning caused by consumption of ciguatoxin (CTX)-contaminated fish affecting over 50,000 people worldwide each year. CTXs are classified depending on their origin from the Pacific (P-CTXs), Indian Ocean (I-CTXs), and Caribbean (C-CTXs). P-CTX-1 is the most toxic CTX known and the major source of CFP causing an array of neurological symptoms. Neurological symptoms in some CFP patients last for several months or years; however, the underlying electrophysiological properties of acute exposure to CTXs remain unknown. Here, we used CTX purified from ciguatera fish sourced in the Pacific Ocean (P-CTX-1). Delta and theta electroencephalography (EEG) activity was reduced remarkably in 2 h and returned to normal in 6 h after a single exposure. However, second exposure to P-CTX-1 induced not only a further reduction in EEG activities but also a 2-week delay in returning to baseline EEG values. Ciguatoxicity was detected in the brain hours after the first and second exposure by mouse neuroblastoma assay. The spontaneous firing rate of single motor cortex neuron was reduced significantly measured by single-unit recording with high spatial resolution. Expression profile study of neurotransmitters using targeted profiling approach based on liquid chromatography-tandem mass spectrometry revealed an imbalance between excitatory and inhibitory neurotransmitters in the motor cortex. Our study provides a possible link between the brain oscillations and neurotransmitter release after acute exposure to P-CTX-1. Identification of EEG signatures and major metabolic pathways affected by P-CTX-1 provides new insight into potential biomarker development and therapeutic interventions. SN - 1559-1182 UR - https://www.unboundmedicine.com/medline/citation/27613284/Acute_Exposure_to_Pacific_Ciguatoxin_Reduces_Electroencephalogram_Activity_and_Disrupts_Neurotransmitter_Metabolic_Pathways_in_Motor_Cortex_ L2 - https://dx.doi.org/10.1007/s12035-016-0093-y DB - PRIME DP - Unbound Medicine ER -