%0 Journal Article
%T Milnacipran inhibits glutamatergic N-Methyl-D-Aspartate receptor activity in Spinal Dorsal Horn Neurons
%A Tatsuro Kohno
%A Masafumi Kimura
%A Mika Sasaki
%A Hideaki Obata
%A Fumimasa Amaya
%A Shigeru Saito
%J Molecular Pain
%D 2012
%I BioMed Central
%R 10.1186/1744-8069-8-45
%X Intrathecal injection of milnacipran (0.1£¿¦Ìmol), but not citalopram (0.1£¿¦Ìmol) and desipramine (0.1£¿¦Ìmol), followed by intrathecal injection of NMDA (1£¿¦Ìg) suppressed thermal hyperalgesia. Milnacipran (100 ¦ÌM) reduced the amplitude of NMDA (56£¿¡À£¿3£¿%, 64£¿¡À£¿5£¿% of control)-, but not AMPA (98£¿¡À£¿5£¿%, 97£¿¡À£¿5£¿% of control)-mediated currents induced by exogenous application and dorsal root stimulation, respectively. Citalopram (100 ¦ÌM) and desipramine (30 ¦ÌM) had no effect on the amplitude of exogenous NMDA-induced currents. The number of pERK-positive neurons in the group treated with milnacipran (100 ¦ÌM), but not citalopram (100 ¦ÌM) or desipramine (30 ¦ÌM), followed by NMDA (100 ¦ÌM) was significantly lower compared with the NMDA-alone group.The antinociceptive effect of milnacipran may be dependent on the drug¡¯s direct modulation of NMDA receptors in the superficial dorsal horn. Furthermore, in addition to inhibiting the reuptake of monoamines, glutamate NMDA receptors are also important for analgesia induced by milnacipran.
%K Antidepressants
%K N-methyl-D-aspartate (NMDA) Receptor
%K Spinal Analgesia
%U http://www.molecularpain.com/content/8/1/45/abstract