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Neuropeptide S Receptor Stimulation Excites Principal Neurons in Murine Basolateral Amygdala through a

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Neuropeptide S (NPS) activates its receptor (NPSR1) in mouse amygdala neurons, inhibiting potassium channels. This Gαq-dependent signaling increases neuronal excitability, offering insights into neuropeptide S system function.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cellular Signaling

Background:

  • The neuropeptide S system, comprising neuropeptide S (NPS) and its receptor NPSR1, is crucial in rodent behavior.
  • Intracellular signaling downstream of NPSR1 in endogenous neuronal expression remains poorly understood.

Purpose of the Study:

  • To investigate the intracellular signaling cascades activated by NPSR1 in mouse amygdalar neurons.
  • To elucidate the G-protein-dependent pathways and effector systems involved in NPSR1-mediated responses.

Main Methods:

  • Whole-cell patch-clamp recordings were performed on principal neurons in the anterior basolateral amygdala of mice.
  • Pharmacological agents were used to characterize the NPSR1-mediated current induced by NPS application.

Main Results:

  • NPS application induced inward currents in amygdalar neurons, associated with increased membrane input resistance.
  • The NPSR1-mediated current was dependent on intracellular Gαq signaling and calcium ions, and inhibited potassium channels.

Conclusions:

  • NPSR1 activation in amygdalar neurons inhibits voltage-gated potassium channels, likely of the delayed rectifier family.
  • Gαq signaling and intracellular calcium are essential for the NPS-evoked current and subsequent increase in neuronal excitability.