Intracerebroventricular galanin and N-terminal galanin fragment enhance the morphine-induced analgesia in the rat.

Behavioral effect of galanin and its fragments, galanin1-15 and galanin16-29 (200 ng, 1 and 5 micrograms), after intracerebroventricular (i.c.v.) administration was studied in rats. The number of crossings and pippings and the time of locomotion (an open field test) showed a similar sedative action of galanin and galanin16-29, with no significant effect of galanin1-15. Galanin and its fragments, injected in doses of 200 ng, 1 and 5 micrograms, did not affect nociception, as measured by a tail-flick and paw pressure test. Galanin and galanin1-15, but not galanin16-29 (5 micrograms i.c.v.), injected together with morphine (2.5 micrograms i.c.v.), significantly potentiated the analgetic effect of morphine assessed by a paw pressure test; a similar tendency was also observed in a tail-flick test. Galanin and its two fragments injected in doses of 200 ng, 1 and 5 micrograms, did not change the effect of morphine given in a dose of 1 microgram. These data suggest that galanin, having no effect when given alone, potentiate the analgetic effect of morphine. The fact that the N-terminal fragment of galanin acts like a natural peptide suggests a receptor mediated action. In conclusion, the analgesic effect of morphine was potentiated by galanin and its N-terminal fragment galanin1-15. On the other hand, behavioral study showed a similar sedative action of galanin and C-terminal fragment galanin16-29. This suggests that the N- and C-terminal fragments of galanin are differentially involved in behavioral effects of the peptide.