The N-terminal 1–16, but not C-terminal 17–29, galanin fragment affects the flexor reflex in rats

Abstract

The biological activity of two galanin (GAL) fragments, GAL-(1–16) and GAL-(17–29), was tested in vivo by using a spinal nociceptive flexor reflex model in the rat. Intrathecal (i.t.) GAL-(1–16) had a similar biphasic effect on the flexor reflex, with facilitation at lower doses and facilitation followed by depression at higher doses, as the full length peptide GAL-(1–29). GAL-(1–16) also effectively depressed the facilitation of the flexor reflex caused by i.t. substance P (SP) or C-fiber conditioning stimulation (CS) and potentiated the depressive effect of i.t. morphine on the reflex, both actions that have been reported earlier with GAL-(1–29). In contrast, i.t. GAL-(17–29), even at high doses, did not induce changes in the amplitude of the flexor reflex, nor did it interact with the effects of i.t. SP, morphine or C-fiber CS. It is concluded that the N-terminal portion of GAL-(1–29) is critical for the biological activity of the intact peptide in the dorsal horn of the rat spinal cord. The similarity between the effects GAL-(1–16) and GAL-(1–29) indicates that they probably act on the same GAL receptor.