Exposure to far-infrared rays attenuates methamphetamine-induced recognition memory impairment via modulation of the muscarinic M1 receptor, Nrf2, and PKC.

摘要: We demonstrated that activation of protein kinase Cδ (PKCδ) and inactivation the glutathione peroxidase-1 (GPx-1)-dependent systems are critical for methamphetamine (MA)-induced recognition memory impairment. also exposure to far-infrared rays (FIR) causes induction (GSH)-dependent system, including GPx-1 gene. Here, we investigated whether FIR affects MA-induced impairment it modulates PKC, cholinergic receptors, GSH-dependent system. Because PKC activator bryostatin-1 mainly induces PKCα, PKCe, PKCδ, assessed expression these proteins after MA treatment. treatment selectively increased PKCδ its phosphorylation. Exposure significantly attenuated increases in Importantly, potentiated phosphorylation PKCδ. decreased M1, M3, M4 muscarinic acetylcholine receptors (mAChRs) β2 nicotinic receptor expression. Of these, decrease was most pronounced M1 mAChR. decreases mAChR phospho-ERK1/2, while facilitated Nrf2-dependent GSH induction. Dicyclomine, an antagonist, l-buthionine-(S, R)-sulfoximine (BSO), inhibitor synthesis, counteracted against protective potentials mediated by FIR. More importantly, memory-enhancing potential bryostatin-1, dicyclomine, BSO. Our results suggest attenuates via up-regulation mAChR, induction, ERK1/2 inhibiting bryostatin-1.