期刊
CHANNELS
卷 10, 期 4, 页码 282-296出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/19336950.2016.1164373
关键词
Ca2+ and TRP channels; cell firing; K-ATP and BK channels; Leptin; NMDA and AMPA receptors; PI3K
资金
- Telethon grant [GGP15110]
- Compagnia di San Paolo [2008.1155]
- Torino University
Leptin is produced by adipose tissue and identified as a satiety signal, informing the brain when the body has consumed enough food. Specific areas of the hypothalamus express leptin receptors (LEPRs) and are the primary site of leptin action for body weight regulation. In response to leptin, appetite is suppressed and energy expenditure allowed. Beside this hypothalamic action, leptin targets other brain areas in addition to neuroendocrine cells. LEPRs are expressed also in the hippocampus, neocortex, cerebellum, substantia nigra, pancreatic -cells, and chromaffin cells of the adrenal gland. It is intriguing how leptin is able to activate different ionic conductances, thus affecting excitability, synaptic plasticity and neurotransmitter release, depending on the target cell. Most of the intracellular pathways activated by leptin and directed to ion channels involve PI3K, which in turn phosphorylates different downstream substrates, although parallel pathways involve AMPK and MAPK. In this review we will describe the effects of leptin on BK, K-ATP, K-V, Ca-V, TRPC, NMDAR and AMPAR channels and clarify the landscape of pathways involved. Given the ability of leptin to influence neuronal excitability and synaptic plasticity by modulating ion channels activity, we also provide a short overview of the growing potentiality of leptin as therapeutic agent for treating neurological disorders.
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