Role of central NMDA versus non-NMDA receptor in spinal withdrawal reflex in spinal anesthetized rats under normal and hyperexcitable conditions.
The present study aimed to investigate the role of central N-methyl-D-aspartate (NMDA) and non-NMDA receptors in the spinal withdrawal reflex assessed by recording single motor unit (SMU) electromyogram (EMG) response to peripheral mechanical (pressure, pinch) stimuli and repeated electrical stimuli at 3 and 20 Hz. During normal conditions, intrathecal administration of MK-801 and CNQX apparently depressed mechanically and electrically (3 Hz) evoked EMG responses in a dose-dependent manner (10, 20 and 40 nmol in 10 microl). In contrast, the after-discharges to 20 Hz electrical stimuli were suppressed only by CNQX treatment, not by MK-801 treatment. This indicates that the central mechanisms underlying the different frequencies of electrically evoked withdrawal reflex may be different. During peripheral bee venom (BV, 0.2 mg/50 microl) induced inflammation and central sensitization, the enhanced SMU EMG responses including after-discharges to pinch stimuli and 3 Hz electrical stimuli were depressed significantly by treatments with both MK-801 and CNQX. However, the enhanced SMU activities to innocuous pressure stimuli were depressed only by treatment with CNQX. Likewise, enhanced long lasting after-discharges elicited by 20 Hz electrical stimuli were also only depressed by CNQX, indicating that different central mechanisms are involved in the persistent hyperexcitability during BV-induced inflammation. The data suggest that both central NMDA and non-NMDA receptors play important roles in the transmission of nociceptive information under normal conditions. In BV-induced inflammation, however, central non-NMDA receptors, but not NMDA receptors, play a pivotal role in the generation of persistent hyperexcitability to mechanical and electrical stimuli at different frequencies (3 Hz, 20 Hz).
You
Hao-Jun
HJ
Center for Sensory-Motor Interaction (SMI), Laboratory for Experimental Pain Research, Aalborg University, Fredrik Bajers Vej 7, Building D-3, DK-9220 Aalborg, Denmark.
Mørch
Carsten Dahl
CD
Chen
Jun
J
Arendt-Nielsen
Lars
L
D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000008:administration & dosage; D000704:Analysis of Variance; D000758:Anesthesia; D000818:Animals; D001514:Bee Venoms / Q000009:adverse effects; D002490:Central Nervous System / Q000187:drug effects / Q000502:physiology*; D016291:Dizocilpine Maleate / Q000008:administration & dosage; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D004576:Electromyography / Q000379:methods; D019054:Evoked Potentials, Motor / Q000502:physiology; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D006614:Hindlimb / Q000294:innervation; D007249:Inflammation / Q000139:chemically induced / Q000503:physiopathology; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects / Q000502:physiology; D016202:N-Methylaspartate / Q000008:administration & dosage; D010147:Pain Measurement; D017288:Pain Threshold; D010812:Physical Stimulation; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000145:classification / Q000187:drug effects / Q000502:physiology*; D012018:Reflex / Q000187:drug effects / Q000502:physiology*; D013116:Spinal Cord / Q000187:drug effects / Q000502:physiology*; D013119:Spinal Cord Injuries / Q000503:physiopathology
D001514:Bee Venoms; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D016194:Receptors, N-Methyl-D-Aspartate; D016202:N-Methylaspartate; D016291:Dizocilpine Maleate; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione