Corticotrophin-Releasing Factor Augments the IH in Rat Hypothalamic Paraventricular Nucleus Parvocellular Neurons In Vitro
| Autor: | Takahiko Katoh, Hiromasa Tsukino, Hiroshi Kannan, Hiroyuki Nakao, Tetsuro Shirasaka, Takato Kunitake, Chun-Ping Chu, Delai Qiu, Kazuo Kato |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Male
endocrine system Patch-Clamp Techniques Potassium Channels Corticotropin-Releasing Hormone Physiology Action Potentials Cyclic Nucleotide-Gated Cation Channels In Vitro Techniques Receptors Corticotropin-Releasing Hormone Ion Channels Hormone Antagonists Parvocellular cell Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels medicine Animals Drug Interactions RNA Messenger Rats Wistar Neurons Dose-Response Relationship Drug Reverse Transcriptase Polymerase Chain Reaction Chemistry General Neuroscience Corticotrophin releasing factor Blotting Northern Peptide Fragments In vitro Rats Pyrimidines medicine.anatomical_structure Animals Newborn Whole cell Neuroscience Nucleus hormones hormone substitutes and hormone antagonists Paraventricular Hypothalamic Nucleus |
| Zdroj: | Journal of Neurophysiology. 94:226-234 |
| ISSN: | 1522-1598 0022-3077 |
| DOI: | 10.1152/jn.01325.2004 |
| Popis: | The goal of this study was to characterize the effects of corticotrophin-releasing factor (CRF) on rat paraventricular nucleus (PVN) putative parvocellular neurons using whole cell patch-clamp recordings and single-cell reverse transcription-multiplex polymerase chain reaction (single-cell RT-mPCR) techniques. Under current clamp, CRF (10–600 nM) increased the neuronal basal firing rate and depolarized neurons in a dose-dependent manner. CRF-induced depolarization was unaffected by co-perfusion with TTX, 6-cyano-7-nitroquinoxaline-2 3-dione (CNQX), and bicuculline but was completely inhibited by ZD7288. Under voltage clamp, 300 nM CRF significantly increased the hyperpolarization-activated cation current ( IH) in a voltage-dependent manner, shifted the IH conductance-voltage relationship ( V1/2) toward depolarization by ∼7.8 mV, and enhanced the IH kinetics without changing the slope constant (k). Extracellular application of ZD7288 completely blocked IH and the CRF-induced increase in IH. Furthermore, CRF-induced effects were completely blocked by extracellular application of 1 μM α-helical CRF-(9–14) (α-hCRF), a nonselective CRF receptor antagonist, but were not affected by extracellular application of antisauvagine-30, a selective CRF-receptor 2 antagonist. Single-cell RT-mPCR analysis showed that these neurons co-expressed CRF receptor 1 mRNA and CRF receptor 2 mRNA. Furthermore, CRF-sensitive neurons co-expressed HCN1 channel mRNA, HCN2 channel mRNA, and HCN3 channel mRNA, but not HCN4 channel mRNA. These results suggest that CRF modulates the subpopulation of PVN parvocellular neuronal function by CRF-receptor 1–mediated potentiation of HCN ion channel activity. |
| Databáze: | OpenAIRE |
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