1 xhibit high binding affinities for the human 5-HT1D receptor.

2 VA Ca2+ currents were mediated by 5-HT1A and 5-HT1D receptors.

3           It has been observed that reported 5-HT1D receptor agonists have at least one heteroatom (N

4 y)alkylamines may represent a novel class of 5-HT1D receptor agonists.

5        Here, we also report the ability of a 5-HT1D receptor antagonist, GR127935, to antagonize 5-HT

6                            Our finding, that 5-HT1D receptors are distributed in nociceptors througho

7 ible explanation for this difference is that 5-HT1D receptors are preferentially expressed by cranial

8 d G protein subunits to membranes containing 5-HT1D receptors caused a small increase in affinity for

9 lves the activation of serotonin subtype 1D (5-HT1D) receptors expressed on "pain-responsive" trigemi

10 uggest that a "pain"-triggered regulation of 5-HT1D-receptor expression underlies the effectiveness o

11 g at least in part through the regulation of 5-HT1D-receptor gene expression.

12              We compared the distribution of 5-HT1D receptor-immunoreactive (5-HT1D-IR) peripheral af

13       Moreover, the widespread expression of 5-HT1D receptor in somatic nociceptive afferents suggest

14                At the ultrastructural level, 5-HT1D receptors in the spinal cord dorsal horn are loca

15                             In contrast, the 5-HT1D receptor produced both voltage-dependent and -ind

16                    Agonists at serotonin 1D (5-HT1D) receptors relieve migraine headache but are not

17 ptan (1 nM-1 microM), agonists at 5-HT1B and 5-HT1D receptors, respectively.

18  of EPSCs caused by 5-HT was mediated by the 5-HT1D receptor subtype, since the 5-HT1D agonist, sumat

19 e (8) binds with high affinity at calf brain 5-HT1D receptors, we explored the structure-affinity rel