Hopkins E, Spinella M, Pavlovic Z W, Bodnar R J
Neuropsychology Doctoral Subprogram, Queens College, City University of New York, Flushing 11367, USA.
Physiol Behav. 1998 Jun 1;64(3):219-25. doi: 10.1016/s0031-9384(98)00055-9.
Serotonergic, NMDA, or opioid antagonists in the rostral ventromedial medulla (RVM) reduce morphine analgesia elicited from the periaqueductal gray (PAG). Continuous (CCWS) and intermittent (ICWS) cold-water swims elicit respective naltrexone-insensitive and naltrexone-sensitive analgesic responses. CCWS analgesia is reduced by systemic NMDA receptor antagonism and by systemic, but not intrathecal serotonergic antagonism. ICWS analgesia is reduced by both systemic and intrathecal serotonergic antagonism, but unaffected by systemic NMDA antagonism. The present study evaluated whether serotonergic (methysergide: 5-10 microg) or competitive [AP7 (2-amino-7-phosphonoheptanoic acid): 0.01-0.1 microg] or non-competitive [MK-801 (dizocilipine maleate): 0.3-3 microg] NMDA antagonists in the RVM altered CCWS and ICWS analgesia and hypothermia as well as basal nociceptive latencies. Methysergide in the RVM significantly potentiated CCWS, but not ICWS analgesia. In contrast, AP7 in the RVM significantly potentiated ICWS analgesia. Antagonist-induced changes in either hypothermia or basal nociception failed to account for any alterations in stress-induced analgesia. These data suggest that serotonergic, but not NMDA, receptors in the RVM may mediate collateral inhibition between mesencephalic morphine analgesia and naltrexone-insensitive CCWS analgesia.
