1.Acute Myelitis after hepatitis B vaccination.
Hong Ki SONG ; Hyoung Cheol KIM ; Yeo Hoon YUN
Journal of Korean Medical Science 1997;12(3):249-251
We report a case of myelitis after plasma-derived hepatitis B vaccination. The patient was a 31-year-old man who presented with progressive sensory symptoms in extremities that developed 2 weeks after a third vaccination. MRI of the cervicothoracic region revealed swelling and T2 high signal at the level of C4 to C5 cord, and isolated enhancement in the posterior columns between C4 and C5 cord. The significance of MRI findings and HLA haplotype of the patient will be briefly discussed.
Acute Disease
;
Adult
;
Case Report
;
Hepatitis B Vaccines/adverse effects*
;
Human
;
Magnetic Resonance Imaging
;
Male
;
Myelitis/pathology
;
Myelitis/chemically induced*
2.Spinal CCL2 Promotes Central Sensitization, Long-Term Potentiation, and Inflammatory Pain via CCR2: Further Insights into Molecular, Synaptic, and Cellular Mechanisms.
Rou-Gang XIE ; Yong-Jing GAO ; Chul-Kyu PARK ; Ning LU ; Ceng LUO ; Wen-Ting WANG ; Sheng-Xi WU ; Ru-Rong JI
Neuroscience Bulletin 2018;34(1):13-21
Mounting evidence supports an important role of chemokines, produced by spinal cord astrocytes, in promoting central sensitization and chronic pain. In particular, CCL2 (C-C motif chemokine ligand 2) has been shown to enhance N-methyl-D-aspartate (NMDA)-induced currents in spinal outer lamina II (IIo) neurons. However, the exact molecular, synaptic, and cellular mechanisms by which CCL2 modulates central sensitization are still unclear. We found that spinal injection of the CCR2 antagonist RS504393 attenuated CCL2- and inflammation-induced hyperalgesia. Single-cell RT-PCR revealed CCR2 expression in excitatory vesicular glutamate transporter subtype 2-positive (VGLUT2) neurons. CCL2 increased NMDA-induced currents in CCR2/VGLUT2 neurons in lamina IIo; it also enhanced the synaptic NMDA currents evoked by dorsal root stimulation; and furthermore, it increased the total and synaptic NMDA currents in somatostatin-expressing excitatory neurons. Finally, intrathecal RS504393 reversed the long-term potentiation evoked in the spinal cord by C-fiber stimulation. Our findings suggest that CCL2 directly modulates synaptic plasticity in CCR2-expressing excitatory neurons in spinal lamina IIo, and this underlies the generation of central sensitization in pathological pain.
Animals
;
Benzoxazines
;
pharmacology
;
therapeutic use
;
Chemokine CCL2
;
antagonists & inhibitors
;
genetics
;
metabolism
;
pharmacology
;
Excitatory Amino Acid Agents
;
pharmacology
;
Excitatory Amino Acid Agonists
;
pharmacology
;
Female
;
Freund's Adjuvant
;
toxicity
;
Hyperalgesia
;
chemically induced
;
metabolism
;
prevention & control
;
Long-Term Potentiation
;
drug effects
;
physiology
;
Luminescent Proteins
;
genetics
;
metabolism
;
Male
;
Mice
;
Mice, Inbred C57BL
;
Mice, Transgenic
;
Myelitis
;
chemically induced
;
drug therapy
;
metabolism
;
Neurons
;
drug effects
;
Pain Management
;
Somatostatin
;
genetics
;
metabolism
;
Spinal Cord
;
cytology
;
Spiro Compounds
;
pharmacology
;
therapeutic use
;
Vesicular Glutamate Transport Protein 2
;
genetics
;
metabolism
;
Vesicular Inhibitory Amino Acid Transport Proteins
;
genetics
;
metabolism