No abstract

The lamina II, also called the substantia gelatinosa (SG), of the trigeminal subnucleus caudalis (Vc), is thought to play an essential role in the control of orofacial nociception. Glycine and serotonin (5-hydroxytryptamine, 5-HT) are the important neurotransmitters that have the individual parts on the modulation of nociceptive transmission. However, the electrophysiological effects of 5-HT on the glycine receptors on SG neurons of the Vc have not been well studied yet. For this reason, we applied the whole-cell patch clamp technique to explore the interaction of intracellular signal transduction between 5-HT and the glycine receptors on SG neurons of the Vc in mice. In nine of 13 neurons tested (69.2%), pretreatment with 5-HT potentiated glycine-induced current (I Gly ). Firstly, we examined with a 5-HT 1 receptor agonist (8-OH-DPAT, 5-HT 1/7 agonist, co-applied with SB-269970, 5-HT 7 antagonist) and antagonist (WAY-100635), but 5-HT 1 receptor agonist did not increase I Gly and in the presence of 5-HT 1 antagonist, the potentiation of 5-HT on I Gly still happened. However, an agonist (α-methyl-5-HT) and antagonist (ketanserin) of the 5-HT 2 receptor mimicked and inhibited the enhancing effect of 5-HT on I Gly in the SG neurons, respectively. We also verified the role of the 5-HT 7 receptor by using a 5-HT 7 antagonist (SB-269970) but it also did not block the enhancement of 5-HT on I Gly . Our study demonstrated that 5-HT facilitated I Gly in the SG neurons of the Vc through the 5-HT 2 receptor. The interaction between 5-HT and glycine appears to have a significant role in modulating the transmission of the nociceptive pathway.

No abstract

Lamina II, also called the substantia gelatinosa (SG) of the medullary dorsal horn (the trigeminal subnucleus caudalis, Vc), is thought to play an essential role in the control of orofacial nociception because it receives the nociceptive signals from primary afferents, including thin myelinated Aδ-and unmyelinated C-fibers. Glycine, the main inhibitory neurotransmitter in the central nervous system, plays an essential role in the transference of nociceptive messages from the periphery to higher brain regions. Bisphenol A (BPA) is reported to alter the morphological and functional characteristics of neuronal cells and to be an effector of a great number of ion channels in the central nervous system. However, the electrophysiological effects of BPA on the glycine receptors of SG neurons in the Vc have not been well studied. Therefore, in this study, we used the whole-cell patch-clamp technique to determine the effect of BPA on the glycine response in SG neurons of the Vc in male mice. We demonstrated that in early neonatal mice (0−3 postnatal day mice), BPA did not affect the glycine-induced inward current. However, in the juvenile and adult groups, BPA enhanced the glycine-mediated responses. Heteromeric glycine receptors were involved in the modulation by BPA. The interaction between BPA and glycine appears to have a significant role in regulating transmission in the nociceptive pathway.