Feldman Jack L, Neverova Natalia V, Saywell Shane A
Systems Neurobiology Laboratory, Department of Neurobiology, David Geffen School of Medicine at UCLA, University of California, Los Angeles Box 951763, Los Angeles, CA 90095-1763, USA.
Respir Physiol Neurobiol. 2005 Jul 28;147(2-3):131-43. doi: 10.1016/j.resp.2005.03.014.
Motoneuronal excitability is highly modulated by various inputs; however, comparatively little is known about postsynaptic signal transduction cascades that affect motoneuron excitability. In this review, we discuss the role of intracellular signaling cascades in the modulation of respiratory motoneuronal excitability. In particular, protein kinases and phosphatases dynamically and constitutively modulate respiratory-modulated inputs to XII motoneurons: (i) activation of protein kinase A (PKA) potentiates both excitatory and inhibitory drive currents; (ii) protein kinase G (PKG) depresses excitatory currents, and (iii) inhibition of protein phosphatases potentiates excitatory drive currents. We also describe a novel form of persistent plasticity (in vitro long-term facilitation; ivLTF) of motoneuronal output. ivLTF is induced by episodic activation of 5-HT(2) or alpha(1)-adrenoreceptors and is manifested as an increase in the amplitude of XII nerve output due to an increase in alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-mediated motoneuronal drive currents. Blockade of Group 1 metabotropic glutamate receptors or protein kinase C (PKC) prevents the induction of ivLTF.
运动神经元的兴奋性受到多种输入的高度调节；然而，关于影响运动神经元兴奋性的突触后信号转导级联反应，我们了解得相对较少。在这篇综述中，我们讨论了细胞内信号级联反应在调节呼吸运动神经元兴奋性中的作用。特别是，蛋白激酶和磷酸酶动态且持续地调节对 XII 运动神经元的呼吸调节输入：（i）蛋白激酶 A（PKA）的激活增强了兴奋性和抑制性驱动电流；（ii）蛋白激酶 G（PKG）抑制兴奋性电流，以及（iii）蛋白磷酸酶的抑制增强了兴奋性驱动电流。我们还描述了运动神经元输出的一种新型持续性可塑性（体外长期易化；ivLTF）。ivLTF 由 5-HT(2) 或 α(1)-肾上腺素能受体的间歇性激活诱导，并表现为由于 α-氨基-3-羟基-5-甲基异恶唑-4-丙酸（AMPA）介导的运动神经元驱动电流增加，导致 XII 神经输出幅度增加。I 组代谢型谷氨酸受体或蛋白激酶 C（PKC）的阻断可防止 ivLTF 的诱导。
