PUBLICATION

Intradiencephalon injection of histamine inhibited the recovery of locomotor function of spinal cord injured zebrafish

Authors
Huang, S.B., Zhao, H.D., Wang, L.F., Sun, M.F., Zhu, Y.L., Wu, Y.B., Xu, Y.D., Peng, S.X., Cui, C., Shen, Y.Q.
ID
ZDB-PUB-170601-8
Date
2017
Source
Biochemical and Biophysical Research Communications   489(3): 275-280 (Journal)
Registered Authors
Keywords
Diencephalon, Histamine, Microenvironment, Spinal cord injury, Zebrafish
MeSH Terms
  • Animals
  • Histamine/administration & dosage*
  • Histamine/pharmacology*
  • Injections, Intraventricular
  • Locomotion/drug effects*
  • Neuroglia/drug effects
  • Neuroglia/metabolism
  • Spinal Cord Injuries/drug therapy*
  • Spinal Cord Injuries/pathology
  • Spinal Cord Injuries/physiopathology*
  • Structure-Activity Relationship
  • Zebrafish*/physiology
PubMed
28559136 Full text @ Biochem. Biophys. Res. Commun.
Abstract
Human spinal cord injury (SCI) usually causes irreversible disability beneath the injured site due to poor neural regeneration. On the contrary, zebrafish show significant regenerative ability after SCI, thus is usually worked as an animal model for studying neuroregeneration. Most of the previous SCI studies focused on the local site of SCI, the supraspinal-derived signals were rarely mentioned. Here we showed that intradiencephalon injection of histamine (HA) inhibited the locomotor recovery in adult zebrafish post-SCI. Immunofluorescence results showed that intradiencephalon HA administration increased the activated microglia 3 days post injury (dpi), promoted the proliferation of radial glial cells at 7 dpi and affected the morphology of radial glial cells at 11 dpi. Furthermore, quantitative real-time polymerase chain reaction (qRT-PCR) results showed that intradiencephalon HA administration also reduced the expression of neurotrophic factors including brain-derived neurotrophic factor (BDNF) and insulin-like growth factor1 (IGF-1) at the lesion site, however, had no effect on the expression of pro-inflammatory factors such as TNF-alpha and IL-1 beta. Hence, our data suggested that exogenous intradiencephalon HA retarded locomotor recovery in spinal cord injured zebrafish via modulating the repair microenvironment.
Errata / Notes
Correction.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping