Direct inhibition by cannabinoids of human 5‐HT3A receptors: probable involvement of an allosteric modulatory site

British Journal of Pharmacology - Tập 137 Số 5 - Trang 589-596 - 2002
Martin Barann1,2, Gerhard J. Molderings1, Michael Brüss1, Heinz Bönisch1, B. W. Urban2, M. Göthert1
1Institut für Pharmakologie und Toxikologie, Universität Bonn, Reuterstraße 2b, D-53113 Bonn, Germany
2Klinik für Anästhesiologie und spezielle Intensivmedizin, Universitätskliniken Bonn, Sigmund-Freud-Straße 25, D-53105 Bonn, Germany

Tóm tắt

Excised outside‐out patches from HEK293 cells stably transfected with the human (h) 5‐HT3A receptor cDNA were used to determine the effects of cannabinoid receptor ligands on the 5‐HT‐induced current using the patch clamp technique. In addition, binding studies with radioligands for 5‐HT3 as well as for cannabinoid CB1 and CB2 receptors were carried out.

The 5‐HT‐induced current was inhibited by the following cannabinoid receptor agonists (at decreasing order of potency): Δ9‐THC, WIN55,212‐2, anandamide, JWH‐015 and CP55940. The WIN55,212‐2‐induced inhibition was not altered by SR141716A, a CB1 receptor antagonist. WIN55,212‐3, an enantiomer of WIN55,212‐2, did not affect the 5‐HT‐induced current.

WIN55,212‐2 did not change the EC50 value of 5‐HT in stimulating current, but reduced the maximum effect.

The CB1 receptor ligand [3H]‐SR141716A and the CB1/CB2 receptor ligand [3H]‐CP55940 did not specifically bind to parental HEK293 cells. In competition experiments on membranes of HEK293 cells transfected with the h5‐HT3A receptor cDNA, WIN55,212‐2, CP55940, anandamide and SR141716A did not affect [3H]‐GR65630 binding, but 5‐HT caused a concentration dependent‐inhibition.

In conclusion, cannabinoids stereoselectively inhibit currents through recombinant h5‐HT3A receptors independently of cannabinoid receptors. Probably the cannabinoids act allosterically at a modulatory site of the h5‐HT3A receptor. Thus the functional state of the receptor can be controlled by the endogenous ligand anandamide. This site is a potential target for new analgesic and antiemetic drugs.

British Journal of Pharmacology (2002) 137, 589–596. doi:10.1038/sj.bjp.0704829

Từ khóa


Tài liệu tham khảo

10.2165/00003495-199142040-00002

10.1016/0165-6147(92)90064-D

10.1016/S0301-0082(98)00087-2

BARANN M., 2001, Inhibition by cannabinoid1 receptor agonists of currents through human 5‐HT3A receptors, Soc. Neurosci., 27, 2126

10.1007/s002100000288

10.1016/0028-3908(94)90059-0

10.1016/0003-2697(76)90527-3

10.1016/S0028-3908(01)00074-0

10.1007/s002100000342

10.1093/emboj/20.24.7033

10.1128/MCB.7.8.2745

COSTALL B., 1997, Handbook of Experimental Pharmacology, 409

10.1016/S0091-3057(01)00531-7

10.1038/16941

10.1126/science.1470919

10.1074/jbc.274.43.30799

FAN P., 1995, Cannabinoid agonists inhibit the activation of 5‐HT3 receptors in rat nodose ganglion neurones, J. Neurophysiol., 73, 907, 10.1152/jn.1995.73.2.907

FELDER C.C., 1998, LY320135, a novel cannabinoid CB1 receptor antagonist, unmasks coupling of the CB1 receptor to stimulation of cAMP accumulation, J. Pharmacol. Exp. Ther., 284, 291

10.1016/0014-2999(93)90468-W

GODLEWSKI G., 2002, Inhibitory effects of cannabinoid receptor agonists on the 5‐HT3 receptor‐mediated Bezold‐Jarisch Reflex in rats and human 5‐HT3A receptors in HEK 293 cells, Naunyn Schmiedeberg's Arch. Pharmacol., 365, R28

10.1073/pnas.87.5.1932

10.1016/0006-2952(96)00346-2

10.1016/S0006-3495(91)82068-9

10.1016/0304-3940(92)90265-9

10.1007/s00210-001-0498-6

10.1016/S0006-8993(98)01368-7

10.1038/346561a0

10.1093/emboj/20.1.47

MIYAKE A., 1995, Molecular cloning of human 5‐hydroxytryptamine3 receptor: heterogeneity in distribution and function among species, Mol. Pharmacol., 48, 407

10.2165/00003495-199243030-00002

10.1038/365061a0

10.1002/j.1552-4604.1975.tb02348.x

10.1038/sj.bjp.0704327

10.1517/13543784.9.7.1553

10.1016/0165-6147(92)90119-Q

10.1016/S0165-6147(00)01482-6

10.1016/0028-3908(96)00130-X

10.1016/S0163-7258(01)00130-9

10.1016/0024-3205(96)00085-9

10.1016/j.neuropharm.2005.11.008

10.2165/00003495-200059060-00008

TAO Q., 1998, Mutation of a highly conserved aspartate residue in the second transmembrane domain of the cannabinoid receptors, CB1 and CB2, disrupts G‐protein coupling, J. Pharmacol. Exp. Ther., 285, 651

THOMAS B.F., 1990, Characterization of the lipophilicity of natural and synthetic analogs of delta‐9‐tetrahydrocannabinol and its relationship to pharmacological potency, J. Pharmacol. Exp. Ther., 255, 624

10.1136/bmj.323.7303.16

10.1016/S0024-3205(00)00965-6

10.1038/22761