| Abstrakt: |
Using an experimental model of postoperation hyperalgesia (incision of the tissues on the foot) on 45 mongrel Wistar rats, we demonstrated that postoperation hyperalgesia (24 h after surgical intervention) is accompanied by a rise in the concentration of astroglial proteins (glial fibrillary acidic protein, GFAP, and S-100β protein) in the medulla oblongata and thalamus/hypothalamus. An agonist of NMDA receptors, glutamate (1 mg/kg), injected 5 min prior to the surgical procedure caused a greater increase in the concentration of astroglial proteins, whereas a noncompetitive antagonist of the above receptors, MK-801 (0.5 mg/kg), injected according to the same protocol to a great extent prevented postoperation hyperalgesia-related changes in the level of astroglial proteins in the thalamus/hypothalamus and medulla oblongata. Our findings show that astroglia actively influences glutamate-mediated neurotransmission, which plays a leading role in the development of postoperation hyperalgesia. [ABSTRACT FROM AUTHOR] |
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