Gastrin-releasing peptide (GRP) has been implicated in several aspects of physiology and behavior including digestion, cancer, lung development, and memory process. Increasing evidence in rodents shows that GRP may contribute to hippocampal circuit function. Though the central role of GRP in the brain has been established, the cellular and molecular mechanisms of its actions have not been well defined. Thus in this study, we verified the expression of GRPR in the rat hippocampal CA1 region. Then we examined the mechanisms closely related to neuronal excitability, the effects of GRP on voltage-gated ion channels in CA1 neurons using patch-clamp. The results showed that GRP could decrease voltage-gated sodium currents mainly by affecting the kinetics of recovery from the inactivated state. However, GRP enhanced both kinds of voltage-gated potassium channels, the A-type channels were more sensitive to GRP than K-type channels. In conclusion, we found that GRP could alter the voltage-gated Na+ and K+ ion channel characteristics which might be the ionic mechanisms of the physiological function of GRP in the brain.

中文翻译：

---

胃泌素释放肽对大鼠海马神经元电压门控通道的影响

胃泌素释放肽 (GRP) 与生理和行为的多个方面有关，包括消化、癌症、肺发育和记忆过程。越来越多的啮齿动物证据表明 GRP 可能有助于海马回路功能。尽管 GRP 在大脑中的核心作用已经确立，但其作用的细胞和分子机制尚未明确。因此，在本研究中，我们验证了 GRPR 在大鼠海马 CA1 区的表达。然后我们使用膜片钳检查了与神经元兴奋性密切相关的机制，GRP 对 CA1 神经元电压门控离子通道的影响。结果表明，GRP 主要通过影响从失活状态恢复的动力学来降低电压门控钠电流。然而，GRP对两种电压门控钾通道均有增强作用，A型通道对GRP的敏感性高于K型通道。总之，我们发现GRP可以改变电压门控Na+和K+离子通道特性，这可能是GRP在大脑中生理功能的离子机制。