Abstract
The cyclic peptide Melanin Concentrating Hormone (MCH) is known to control a large number of brain functions in mammals such as food intake and metabolism, stress response, anxiety, sleep/wake cycle, memory, and reward. Based on neuro-anatomical and electrophysiological studies these functions were attributed to neuronal circuits expressing MCHR1, the single MCH receptor in rodents. In complement to our recently published work (1) we provided here new data regarding the action of MCH on ependymocytes in the mouse brain. First, we establish that MCHR1 mRNA is expressed in the ependymal cells of the third ventricle epithelium. Second, we demonstrated a tonic control of MCH-expressing neurons on ependymal cilia beat frequency using in vitro optogenics. Finally, we performed in vivo measurements of CSF flow using fluorescent micro-beads in wild-type and MCHR1-knockout mice. Collectively, our results demonstrated that MCH-expressing neurons modulate ciliary beating of ependymal cells at the third ventricle and could contribute to maintain cerebro-spinal fluid homeostasis.
Highlights
First identified in the early 80s from chum salmon pituitaries, the melanin concentrating hormone (MCH) draw its name from its capability to induced the concentration of melanin in the skin melanophores [2]
Developing new techniques to measure and analyze the ependymal cilia beat frequency (CBF) in acute mouse brain slice preparations, we showed that the CBF is increased by MCH application or lateral hypothalamic area (LHA) stimulation, an effect blocked by a selective MCHR1 antagonist and absent in MCHR1-knockout (MCHR1-KO) mice
RT-PCR results indicate that mRNA coding for MCHR1 were present in the 3V epithelium (Figure 1C)
Summary
First identified in the early 80s from chum salmon pituitaries, the melanin concentrating hormone (MCH) draw its name from its capability to induced the concentration of melanin in the skin melanophores [2] This function seems to be restricted to teleosts [reviewed in Ref. All of these seem to converge to the adaptation of global physiologic state to metabolic needs by promoting memory processes and reward pathways activation on one hand and by decreasing arousal and thermogenesis on the other hand Activation of these cognitive and neuroendocrine networks leads to an increase in food intake and energy storage, respectively [reviewed in Ref. Activation of these cognitive and neuroendocrine networks leads to an increase in food intake and energy storage, respectively [reviewed in Ref. [9, 10]]
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