ArticleJournal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology2014
Riluzole suppresses postinhibitory rebound in an excitatory motor neuron of the medicinal leech.
Article in Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Multiple intrinsic membrane properties are modulated in a switch from single- to dual-network activity.Journal of neurophysiology · 2022Article
- Altered neocortical oscillations and cellular excitability in an in vitro Wwox knockout mouse model of epileptic encephalopathy.Neurobiology of disease · 2021Article
- Effects of calcium-activated potassium channel modulators on afterhyperpolarizing potentials in identified motor and mechanosensory neurons of the medicinal leech.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2021Article
- Circuit feedback increases activity level of a circuit input through interactions with intrinsic properties.Journal of neurophysiology · 2017Article
- 9-Phenanthrol modulates postinhibitory rebound and afterhyperpolarizing potentials in an excitatory motor neuron of the medicinal leech.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2017Article
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Authors and funding
2 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Postinhibitory rebound (PIR) is an intrinsic property often exhibited by neurons involved in generating rhythmic motor behaviors. Cell DE-3, a dorsal excitatory motor neuron in the medicinal leech exhibits PIR responses that persist for several seconds following the offset of hyperpolarizing stimuli and are suppressed in reduced Na(+) solutions or by Ca(2+) channel blockers. The long duration and Na(+) dependence of PIR suggest a possible role for persistent Na(+) current (I NaP). In vertebrate neurons, the neuroprotective agent riluzole can produce a selective block of I NaP. This study demonstrates that riluzole inhibits cell DE-3 PIR in a concentration- and Ca(2+)-dependent manner. In 1.8 mM Ca(2+) solution, 50-100 µM riluzole selectively blocked the late phase of PIR, an effect similar to that of the neuromodulator serotonin. However, 200 µM riluzole blocked both the early and late phases of PIR. Increasing extracellular Ca(2+) to 10 mM strengthened PIR, but high riluzole concentrations continued to suppress both phases of PIR. These results indicate that riluzole may suppress PIR via a nonspecific inhibition of Ca(2+) conductances and suggest that a Ca(2+)-activated nonspecific current (I(CAN)), rather than I NaP, may underlie the Na(+)-dependent component of PIR.
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