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Neuropeptide FF and prolactin-releasing peptide decrease cortical excitability through activation of NPFF receptors.

Ine Buffel1, Alfred Meurs, Jeanelle Portelli

  • 1Laboratory for Clinical and Experimental Neurophysiology, Neurobiology and Neuropsychology, Department of Neurology, Ghent University Hospital, Ghent University, Ghent, Belgium.

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|February 17, 2015
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Summary

Neuropeptide FF (NPFF) and prolactin-releasing peptide (PrRP) were found to decrease cortical excitability in rats by activating NPFF receptors. The NPFF1 receptor is essential for NPFF's anticonvulsant effects, offering potential new epilepsy treatments.

Keywords:
EpilepsyKisspeptinMotor cortex stimulation modelNeuropeptide FFProlactin releasing peptideRF-amides

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Epilepsy Research

Background:

  • Epilepsy treatment requires novel mechanisms of action due to drug resistance in many patients.
  • Neuropeptide systems, including galanin, ghrelin, and neuropeptide Y (NPY), are being investigated for anticonvulsant properties.
  • The anticonvulsant potential of several RF-amide neuropeptides remains unexplored.

Purpose of the Study:

  • To investigate the anticonvulsant activities of neuropeptide FF (NPFF), prolactin-releasing peptide (PrRP), and kisspeptin (Kp).
  • To assess the role of their respective receptors (NPFF1/2 R, GPR10, and GRP54) in modulating cortical excitability.
  • To evaluate these neuropeptides in a rat motor cortex stimulation model.

Main Methods:

  • Rats underwent motor cortex stimulation with increasing pulse intensity to determine the motor threshold, a measure of cortical excitability.
  • The motor threshold was assessed before, during, and after intracerebroventricular (i.c.v.) administration of NPFF, PrRP, and Kp receptor ligands.
  • The effects of NPFF and PrRP were further evaluated using NPFF1/2 R antagonists (RF9) and a selective NPFF1 R antagonist.

Main Results:

  • Intracerebroventricular NPFF and PrRP significantly increased the motor threshold, indicating reduced cortical excitability.
  • The anticonvulsant effects of NPFF and PrRP were blocked by the NPFF1/2 R antagonist RF9 and a selective NPFF1 R antagonist.
  • Kisspeptin (Kp) did not demonstrate any significant effect on the motor threshold.

Conclusions:

  • Intracerebroventricular administration of NPFF and PrRP decreases cortical excitability in rats via NPFF receptor activation.
  • The NPFF1 receptor is specifically required for the anticonvulsant effect of NPFF.
  • These findings highlight NPFF and PrRP as potential therapeutic agents for epilepsy, particularly targeting NPFFRs.