Spontaneous
pain,
allodynia and
hyperalgesia are well known phenomena following peripheral nerve or tissue injury, and it is speculated that secondary
hyperalgesia and
allodynia, are generally thought to depend on a hyperexcitability (sensitization) of neurons in the dorsal horn. It is supposed that the sensitization may be due to various actions of
neurotransmitters (SP, CGRP,
excitatory amino acids) released from the primary afferent fibers. In this study, we examined effects of the iontophoretically applied SP and CGRP on the response to EAA receptor agonists (
NMDA and non-
NMDA) in the WDR dorsal horn neurones and see if the effects of SP or CGRP mimic the characteristic response pattern known in various
pain models. The main results are summarized as follows: 1) SP specifically potentiated
NMDA response. 2) CGRP non-specifically potentiated both
NMDA and
AMPA responses. Potentiation of
NMDA response, however, was significantly greater than that of
AMPA response. 3) 50% of SP applied cells and 15.8% of CGRP applied cells showed reciprocal changes(potentiation of
NMDA response and suppression of
AMPA response). These results are generally consistent with the sensitization characteristics in diverse
pain models and suggests that the modulatory effects of SP and CGRP on
NMDA and non-
NMDA (
AMPA) response are, at least in part, contribute to the development of sensitization in various
pain models.