Abstract
It has been reported that inflammation triggers the sprouting of Aβ afferents to substantia gelatinosa that originally terminate at deeper laminae. This sprouting could be mediated by a change occurring at the early state of inflammation. To elucidate mechanisms of the sprouting following inflammation in the spinal dorsal horn, blind patch-and in vivo patch-clamp recordings were made from substantia gelatinosa neurons of rats 2 days after inflammation. In vivo patch-clamp recordings showed an increase of spontaneous firing of afferents and elimination of accommodation that is a common property of non-nociceptive receptors. Consistently, the slice study demonstrated an increase of transmitter release that was mediated by newly synthesized BDNF. These changes occurring at the early state of inflammation would be an underlying mechanism that triggers the sprouting of Aβ afferents to substantia gelatinosa.
