Effects of m-CPP in altering neuronal function: Blocking depolarization in invertebrate motor and sensory neurons but exciting rat dorsal horn neurons

Garrett M. Sparks, Eugen Brailoiu, G. Cristina Brailoiu, Nae J. Dun, Jami Tabor, Robin L. Cooper

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

The compound m-chlorophenylpiperazine (m-CPP) is used clinically to manipulate serotonergic function, though its precise mechanisms of actions are not well understood. m-CPP alters synaptic transmission and neuronal function in vertebrates by non-selective agonistic actions on 5-HT1 and 5-HT2 receptors. In this study, we demonstrated that m-CPP did not appear to act through a 5-HT receptor in depressing neuronal function in the invertebrates (crayfish and Drosophila). Instead, m-CPP likely decreased sodium influx through voltage-gated sodium channels present in motor and primary sensory neurons. Intracellular axonal recordings showed that m-CPP reduced the amplitude of the action potentials in crayfish motor neurons. Quantal analysis of excitatory postsynaptic currents, recorded at neuromuscular junctions (NMJ) of crayfish and Drosophila, indicated a reduction in the number of presynaptic vesicular events, which produced a decrease in mean quantal content. m-CPP also decreased activity in primary sensory neurons in the crayfish. In contrast, serotonin produces an increase in synaptic strength at the crayfish NMJ and an increase in activity of sensory neurons; it produces no effect at the Drosophila NMJ. In the rat spinal cord, m-CPP enhances the occurrence of spontaneous excitatory postsynaptic potentials with no alteration in evoked currents.

Original languageEnglish
Pages (from-to)14-26
Number of pages13
JournalBrain Research
Volume969
Issue number1-2
DOIs
StatePublished - Apr 18 2003

Bibliographical note

Funding Information:
Funding was provided by NSF grants IBN-9808631 and IBN-0131459 (R.L. Cooper), NSF-ILI-DUE 9850907 (R.L. Cooper) and a G. Ribble Fellowship for undergraduate studies in the School of Biological Sciences at the University of Kentucky (J. Tabor and G.M. Sparks) and a Undergraduate Research Scholarship awarded by the Arnold and Mabel Beckman Foundation (G.M. Sparks), NIH NS18710 (N.J. Dun)

Funding

Funding was provided by NSF grants IBN-9808631 and IBN-0131459 (R.L. Cooper), NSF-ILI-DUE 9850907 (R.L. Cooper) and a G. Ribble Fellowship for undergraduate studies in the School of Biological Sciences at the University of Kentucky (J. Tabor and G.M. Sparks) and a Undergraduate Research Scholarship awarded by the Arnold and Mabel Beckman Foundation (G.M. Sparks), NIH NS18710 (N.J. Dun)

FundersFunder number
NSF-ILI-DUE9850907
National Science Foundation (NSF)IBN-0131459, IBN-9808631
National Institutes of Health (NIH)
National Institute of Neurological Disorders and StrokeR37NS018710
Arnold and Mabel Beckman Foundation
University of Kentucky

    Keywords

    • Crayfish
    • Neuromodulation
    • Presynaptic
    • Rat
    • Serotonin
    • Sodium
    • Synapse

    ASJC Scopus subject areas

    • General Neuroscience
    • Molecular Biology
    • Clinical Neurology
    • Developmental Biology

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