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Ghrelin alters neurite outgrowth and electrophysiological properties of mouse ventrolateral arcuate tyrosine hydroxylase neurons in culture.

Abstract：

:While the appetite-stimulating hormone ghrelin can act to acutely modulate electrical activity of neurons in the appetite regulating network, it also has a role in regulating neuronal outgrowth, synaptic connectivity and intrinsic electrophysiological properties. In this study, we investigated whether ghrelin may cause alteration in neurite outgrowth and electrophysiological properties of tyrosine hydroxylase (TH) neurons from the ventrolateral arcuate nucleus (VL-ARC), which are thought to contribute to regulation of energy balance. We prepared dissociated neuronal cultures from the VL-ARC of transgenic mice expressing EGFP under control of the tyrosine hydroxylase (TH) promoter, thus allowing visual identification of putative catecholaminergic (TH-EGFP) neurons. After five days of treatment with 100 nM ghrelin, TH-EGFP neurons exhibited significantly more and longer neurites than control treated neurons, and the effects of ghrelin were abolished by 100 μM ghrelin antagonist, D-Lys-GHRP-6. To investigate whether ghrelin altered electrophysiological properties of TH-EGFP neurons, we carried out patch clamp experiments measuring electrophysiological properties. No significant differences were identified for resting membrane potential or spontaneous action potential frequency, however we observed a hyperpolarization of threshold for action potentials and increased input resistance, indicating increased excitability. This increased excitability is consistent with an observed hyperpolarizing shift in the activation of voltage-gated Na(+) currents. These data indicate that the hunger signal ghrelin induces plastic changes in TH-neurons from VL-ARC.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Huang S,Lee SA,Oswald KE,Fry M

doi

10.1016/j.bbrc.2015.09.069

subject

Has Abstract

pub_date

2015-10-30 00:00:00

pages

682-8

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(15)30586-6

journal_volume

466

pub_type

杂志文章

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