Abstract
The glucagon-like peptide-1 (GLP-1) plays important roles in the regulation of food intake and energy metabolism. Peripheral or central GLP-1 suppresses food intake and reduces body weight. The electrophysiological properties of neurons in the mammalian central nervous system reflect the neuronal excitability and the functional organization of the brain. Recent studies focus on elucidating GLP-1-induced suppression of feeding behaviors and modulation of neuronal electrophysiological properties in several brain regions. Here, we summarize that activation of GLP-1 receptor (GLP-1R) suppresses food intake and induces postsynaptic depolarization of membrane potential and/or presynaptic modulation of glutamatergic or GABAergic neurotransmission in brain nuclei located within the medulla oblongata, pons, mesencephalon, diencephalon, and telencephalon. This review may provide a background to guide future research about the cellular mechanisms of GLP-1-induced feeding inhibition.
Highlights
The pre-proglucagon (Gcg) gene product peptides include glucagon-like peptide 1 (GLP-1), GLP2, oxyntomodulin (OXM), intervening peptide 1 (IP1), and glicentin
In contrast to the enhancement of spontaneous excitatory postsynaptic transmission (Mietlicki-Baase et al, 2013), using retrograde labeling of ventral tegmental area (VTA) to nucleus accumbens (NAc) medial shell projecting neurons, in vitro patch-clamp recordings showed that exendin-4 selectively inhibits the miniature excitatory postsynaptic currents within the dopaminergic VTA-to-NAc projection neurons (Wang et al, 2015; Figure 1B) suggesting the presynaptic inhibition of glutamatergic neurotransmission
Being a peptide involved in the regulation of food intake and energy metabolism, glucagon-like peptide-1 (GLP-1) has been demonstrated to suppress food intake and reduce body weight
Summary
The pre-proglucagon (Gcg) gene product peptides include glucagon-like peptide 1 (GLP-1), GLP2, oxyntomodulin (OXM), intervening peptide 1 (IP1), and glicentin. Many studies have demonstrated that GLP-1 suppresses feeding behaviors and modulates the spontaneous firing activities and/or glutamatergic or GABAergic neurotransmission in multiple brain regions. Electrophysiological studies revealed that GLP-1 or exendin-4 does not change the spontaneous firing activity as well as the synaptic transmission suggesting lack of functional GLP-1R in PPG neurons (Hisadome et al, 2010).
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