INTRACISTERNALLY INJECTED GALANIN-(1-15) MODULATES THE CARDIOVASCULAR-RESPONSES OF GALANIN-(1-29) AND THE 5-HT1A RECEPTOR AGONIST 8-OH-DPAT

In view of the demonstration of specific binding sites for [I-125]gala nin-(1-15) in several brain areas including the nucleus of the solitar y tract, possibly indicating the existence of multiple galanin recepto r subtypes, the effects of intracisternal injections of galanin-(1-15) on cardiovascular parameters were studied. The effects of co-injectio ns of galanin-(1-15) and galanin-(1-29) and co-injections of galanin-( 1-15) and the 5-HT1A receptor agonist 8-OH-2-(di-n-propylamino)tetrali n (8-OH-DPAT) were also evaluated. Galanin-(1-15) produced a significa nt increase in mean arterial blood pressure (maximum effect 10% at 3 n mol of galanin-(1-15)) and in heart rate (maximum effect 12% at 1 nmol ). When threshold doses of galanin-(1-15) (0.1 nmol) and galanin-(1-29 ) (3 nmol) were injected simultaneously they elicited an increase in m ean arterial blood pressure. The vasodepressor response induced by an EDS, dose of 8-OH-DPAT (6 nmol) was not modulated by a threshold dose of galanin-(1-15), but the increase in heart rate area induced by gala nin-(1-15) alone was no longer observed. When threshold doses of both galanin-(1-15) and 8-OH-DPAT (0.3 nmol) were co-injected a vasodepress or response developed and on heart rate a tachycardic response was see n in the peak effects and the overall tachycardic response induced by galanin-(1-15) was sustained. The results show a different role for ga lanin-(1-15) as compared with galanin-(1-29) in central cardiovascular control. This effect could be mediated by the previously described su btype of galanin receptors recognizing N-terminal fragments. Thus, it may be suggested that galanin fragments could regulate the action of g alanin-(1-29).