Physiol Rev 80(2): 767-852

Synaptic Control of Motoneuronal Excitability

Departments of Neurobiology and Physiological Science, University of California, Los Angeles, California; Department of Physiology, University of Auckland, Auckland, New Zealand; Department of Pharmacology, University of Virginia, Charlottesville, Virginia; and CNS/CV Biological Research, Schering-Plough Research Institute, Kenilworth, New Jersey

Address for reprint requests and other correspondence: J. L. Feldman, Dept. of Neurobiology, UCLA, Box 951763, Los Angeles, CA 90095-1763 (ude.alcu@namdlef)

^{Jens C. Rekling and Gregory D. Funk contributed equally to this work.}

Abstract

Movement, the fundamental component of behavior and the principal extrinsic action of the brain, is produced when skeletal muscles contract and relax in response to patterns of action potentials generated by motoneurons. The processes that determine the firing behavior of motoneurons are therefore important in understanding the transformation of neural activity to motor behavior. Here, we review recent studies on the control of motoneuronal excitability, focusing on synaptic and cellular properties. We first present a background description of motoneurons: their development, anatomical organization, and membrane properties, both passive and active. We then describe the general anatomical organization of synaptic input to motoneurons, followed by a description of the major transmitter systems that affect motoneuronal excitability, including ligands, receptor distribution, pre- and postsynaptic actions, signal transduction, and functional role. Glutamate is the main excitatory, and GABA and glycine are the main inhibitory transmitters acting through ionotropic receptors. These amino acids signal the principal motor commands from peripheral, spinal, and supraspinal structures. Amines, such as serotonin and norepinephrine, and neuropeptides, as well as the glutamate and GABA acting at metabotropic receptors, modulate motoneuronal excitability through pre- and postsynaptic actions. Acting principally via second messenger systems, their actions converge on common effectors, e.g., leak K^{current, cationic inward current, hyperpolarization-activated inward current, Ca}^{channels, or presynaptic release processes. Together, these numerous inputs mediate and modify incoming motor commands, ultimately generating the coordinated firing patterns that underlie muscle contractions during motor behavior.}

Abstract

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