Mechanisms of postinhibitory rebound and its modulation by serotonin in excitatory swim motor neurons of the medicinal leech

• Published in: Journal of Comparative Physiology 2005-08, Vol.191 (8), p.715-732
• Main Authors: Angstadt, James D, Grassmann, Jeffrey L, Theriault, Kraig M, Levasseur, Sarah M
• Format: Article
• Language: English
• Subjects: Animals; Barium - pharmacology; Cadmium - pharmacology; Calcium - pharmacology; Cesium - pharmacology; Chelating Agents - pharmacology; Egtazic Acid - analogs & derivatives; Egtazic Acid - pharmacology; Electrophysiology; Ganglia, Invertebrate - cytology; Ganglia, Invertebrate - physiology; Hirudinea; Hirudo medicinalis - physiology; In Vitro Techniques; Lithium - pharmacology; Membrane Potentials - drug effects; Membrane Potentials - physiology; Microelectrodes; Motor Neurons - drug effects; Motor Neurons - physiology; Neural Inhibition - physiology; Neurons; Nickel - pharmacology; Serotonin; Serotonin - pharmacology; Sodium - pharmacology; Swimming; Swimming - physiology
• ISSN: 0340-7594; 1432-1351
• DOI: 10.1007/s00359-005-0628-6

Postinhibitory rebound (PIR) is defined as membrane depolarization occurring at the offset of a hyperpolarizing stimulus and is one of several intrinsic properties that may promote rhythmic electrical activity. PIR can be produced by several mechanisms including hyperpolarization-activated cation current (I(h)) or de-inactivation of depolarization-activated inward currents. Excitatory swim motor neurons in the leech exhibit PIR in response to injected current pulses or inhibitory synaptic input. Serotonin, a potent modulator of leech swimming behavior, increases the peak amplitude of PIR and decreases its duration, effects consistent with supporting rhythmic activity. In this study, we performed current clamp experiments on dorsal excitatory cell 3 (DE-3) and ventral excitatory cell 4 (VE-4). We found a significant difference in the shape of PIR responses expressed by these two cell types in normal saline, with DE-3 exhibiting a larger prolonged component. Exposing motor neurons to serotonin eliminated this difference. Cs+ had no effect on PIR, suggesting that I(h) plays no role. PIR was suppressed completely when low Na+ solution was combined with Ca2+-channel blockers. Our data support the hypothesis that PIR in swim motor neurons is produced by a combination of low-threshold Na+ and Ca2+ currents that begin to activate near -60 mV.