Senktide is an agonist of tachykinin NK3 receptor.

A subpopulation of dopamine-sensitive neurones were encountered which were potently excited by bath application of the NK3 receptor agonist, senktide.?On these senktide-sensitive neurones, NK1 and NK2 receptor agonists were inactive.?The excitatory action of senktide supports a role for tachykinins as putative neurotransmitters in the basal ganglia[1].

locomotor activity induced by the tachykinin NK(3) receptor agonist senktide was characterized.?Injection of senktide i.c.v. was found to dose-dependently induce hyperlocomotion from a dose of 0.06 nmol to the maximal dose tested, 0.6 nmol.?Locomotion induced by 0.1 nmol of senktide could be blocked by injection of the tachykinin NK(3) receptor antagonists SB222200 (10 and 30 mg/kg i.p.) and talnetant (SB223412;?10 and 30 mg/kg i.p.), as well as by osanetant (SR142801;?10 and 30 mg/kg i.p.) when administered in a vehicle containing vitamin E and glycofurol.?Senktide-induced activity was also reversed by the antipsychotics haloperidol (0.3 and 1 mg/kg p.o.) and risperidone (1 mg/kg p.o.), but not by the serotonin 5HT(2a/c) receptor antagonist MDL100907 (tested at 0.1, 0.3 and 1 mg/kg p.o.).?Hyperlocomotion induced by 0.03 nmol of senktide was potentiated by antagonism of the tachykinin NK(1) receptor with aprepitant (1, 3 and 10 mg/kg, p.o.).?Thus, hyperlocomotion induced by senktide in gerbils is a tachykinin NK(3) receptor-mediated behavior that is appropriate for use in testing tachykinin NK(3) receptor activity of novel compounds[2].