Acute inhibition of signalling phenotype of spinal GABAergic neurons by tumour necrosis factor‐α

摘要: Non-technical summary  Spinal application of tumour necrosis factor-α (TNFα) is shown to suppress inhibitory synaptic transmission and enhance excitatory in spinal dorsal horn, but the underlying mechanisms are not fully known. We show that acute TNFα inhibits excitability a subset GABAergic neurons through TNF receptor 1 probably by suppressing hyperpolarization-activated cation currents (Ih) activation p38 mitogen-activated protein kinase within these neurons. These results suggest novel cellular mechanism how modulates which may be involved development pain. Abstract  induces both allodynia hyperalgesia, at least part pronociceptive effects have been suggested as due impaired function (disinhibition). The present study explores on signalling phenotype identified transgenic mice expressing green fluorescent glutamic acid decarboxylase 67 (GAD67) promoter. Acute directly GAD67+ TNFα-induced inhibition was dependent (MAPK) (TNFR1) 2 (TNFR2) neurons, suggesting signals TNFR1. Voltage-clamp recordings indicated effect suppression current (Ih). This defines disinhibition mediated TNFα–TNFR1–p38 pathway interneurons.