Abstract

Apelin, an endogenous neuropeptide, has been identified as the cognate ligand for the G-protein-coupled receptor APJ. Apelin, APJ messenger RNA, and protein are widely expressed in the central nervous system and peripheral tissues of humans and animals. The apelin/APJ system has been implicated in diverse physiological and pathological processes. The present article reviews the progress of the latest research investigating the apelin/APJ system in pain, depression, anxiety, memory, epilepsy, neuroprotection, stroke, and brain injury and protection, and highlights its promising potential as a therapeutic target for treatment of psychosis and neuropathy.

Highlights

  • Apelin (APLN), an endogenous ligand of the APJ receptor (APLNR), was first isolated from bovine stomach tissue (Tatemoto et al, 1998)

  • This article provides an overview of the latest advances in the understanding of the signaling pathways and physiological and pathophysiological role of apelin/APJ in pain, depression, anxiety, memory, epilepsy, neuroprotection, stroke, brain injury, and protection

  • Central apelin has a regulatory effect on memory and epilepsy, and it could protective memory impairment in rodents. apln/ aplnr mRNA and APLN/APLNR protein have been found in the hippocampus, amygdala, and cerebral cortex (Hosoya et al, 2000; Lee et al, 2000; Medhurst et al, 2003), areas known to be closely related to learning and memory. This indicates that the apelin/APJ system may potentially play a role in regulating memory processes

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Summary

Introduction

Apelin (APLN), an endogenous ligand of the APJ receptor (APLNR), was first isolated from bovine stomach tissue (Tatemoto et al, 1998). This article provides an overview of the latest advances in the understanding of the signaling pathways and physiological and pathophysiological role of apelin/APJ in pain, depression, anxiety, memory, epilepsy, neuroprotection, stroke, brain injury, and protection. Chronic apelin-13 (3 μg/rat) injection resulted in tolerance to its antinociceptive effect and a decrease in APLNR protein expression in the lumbar spinal cord (Abbasloo et al, 2016).

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