Corticotrophin-releasing factor inhibits neuromedin U mRNA expressing neuron in the rat hypothalamic paraventricular nucleus in vitro

In the present study, we examined the effects of corticotrophin-releasing factor (CRF) on neuromedin U (NMU) mRNA-expressing neurons in the rat paraventricular nucleus (PVN) by whole-cell patch-clamp recordings and single-cell reverse transcription-multiplex polymerase chain reaction (single-cell RT-mPCR) techniques. In total, of 116 PVN putative parvocellular neurons screened for NMU mRNA, 14.7% (17/116) of them expressed NMU mRNA. The electrophysiological properties observed in the NMU mRNA-expressing neurons were generation of a low-threshold Ca2+ spike (LTS) and robust low voltage-activated (T-type) Ca2+ currents. Under current-clamp conditions, CRF (100 nM) induced a reversible decrease in spike firing and significantly diminished the LTS in 88.2% (15/17) of NMU mRNA-expressing neurons. Extracellular application of 1 μM α-helical CRF-(9–14) (α-hCRF), a selective CRF receptor antagonist, completely blocked the CRF-induced decrease in spike firing in the NMU mRNA-expressing neurons. Under voltage-clamp conditions, CRF (100 nM) significantly decreased the peak value of the T-type Ca2+ currents by 35.6 ± 7.8%. These findings suggest that CRF decreases neuronal excitability and diminishes T-type Ca2+ currents in a population of rat PVN NMU phenotype neurons in vitro.

► In rat PVN, 14.7% of putative parvocellular neurons expressed NMU mRNA.
► The NMU mRNA-expressing neurons generated an LTS and robust T-type Ca2+ currents.
► CRF decreased spike firing and T-type Ca2+ currents in the NMU mRNA-expressing neurons.