The possible physiological and pathophysiological role of monoamines-adrene
rgic transmitter (norepinephrine), serotonin; cholinergic transmitter (acet
ylcholine); inhibitory (gamma-aminobutyric acid) and excitatory (glutamate)
amino acids; opioid and nonopioid peptides, enkephalins, beta-endorphin an
d substance P, neurokinin-A, neurokinin-B, neurotensin, cytokines, calciton
ine gene-related peptide, galanin, neuropeptide Y, nerve growth factor, cho
lecystokinin; purines; nitric oxide; vanilloid receptor agonists (capasaici
n); and nociceptin-in spinal transmission of pain is reviewed, The role of
substance P, neurokinin-A and neurokinin-B in the dorsal horn has been iden
tified. These were suggested to be primary afferent transmitters mediating
or facilitating the expression of nociceptive inputs. Pronociceptive modula
tors will be discussed later. Recent findings showing that N-methyl-D-aspar
tate (NMDA) receptor activation generates nitric oxide and prostanoids that
enhance pain transmission whereas adenosine release acts to control these
NMDA-mediated events are also mentioned. The clinical importance of central
ly acting alpha(2)-adrenoceptor agonists (clonidine and dexmedetomidine) is
also discussed. Antinociceptive and morphine-potentiating drugs are ideal
adjuvants for anesthesia; their application in spinal anesthesia is highlig
hted. The recent development in understanding the importance of noradrenerg
ic transmission and subtypes of alpha(2)-adrenoceptors (alpha(2A) and alpha
(2B)) for the first time is reviewed. (C) 1999 Elsevier Science Inc.