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Vasoactive intestinal polypeptide excites medial pontine reticular formation neurons in the brainstem rapid eye

K A Kohlmeier1, P B Reiner

  • 1Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia, Vancouver, British Columbia, V6T 1Z3 Canada.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|May 11, 1999
PubMed

Insights

Vasoactive intestinal polypeptide (VIP) excites brainstem neurons in the medial pontine reticular formation (mPRF), potentially playing a role in rapid eye movement (REM) sleep induction. This peptide activates a sodium current, suggesting a physiological mechanism for REM sleep regulation.

Area of Science:

  • Neuroscience
  • Neurophysiology
  • Sleep Research

Background:

  • The medial pontine reticular formation (mPRF) is known to regulate behavioral states, including rapid eye movement (REM) sleep.
  • Cholinergic agonists like carbachol can induce REM sleep-like states when microinjected into the mPRF.
  • Vasoactive intestinal polypeptide (VIP) is a peptide neurotransmitter found in the mPRF and has been shown to induce REM sleep.

Purpose of the Study:

  • To investigate the cellular mechanisms by which VIP affects neurons in the mPRF.
  • To determine the specific ionic currents and signaling pathways involved in VIP-induced neuronal excitation.
  • To explore the potential physiological role of VIP in the induction of REM sleep.

Main Methods:

  • Whole-cell patch-clamp recordings were performed on mPRF cells in an in vitro rat brainstem slice preparation.
  • The effects of VIP on neuronal membrane potential and currents were measured.
  • Experiments were conducted in varying ionic conditions (low-sodium, low-calcium) and in the presence of specific antagonists and signaling pathway inhibitors.

Main Results:

  • VIP directly depolarized mPRF neurons by activating an inward sodium current.
  • The VIP-induced depolarization was slower and longer-lasting compared to carbachol-induced depolarization.
  • VIP receptor antagonism dose-dependently reduced the VIP-induced depolarization.
  • Inhibition of adenylyl cyclase, protein kinase A, or downstream effectors attenuated VIP's effects, suggesting a G-protein-coupled pathway involving cAMP and PKA.

Conclusions:

  • VIP excites mPRF neurons through the activation of a sodium current.
  • This excitatory effect is mediated, at least in part, by G-protein signaling leading to adenylyl cyclase, cAMP, and protein kinase A activation.
  • These findings suggest that VIP may physiologically contribute to the induction of REM sleep via its actions on mPRF neurons.

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