Direct action of noradrenaline on the medial prefrontal cortex (mPFC) pyramidal neurons in young rats

• Autorzy: Grzelka K. , Szulczyk P.J.
• Języki publikacji: EN

Abstrakty

EN

INTRODUCTION: Noradrenaline (NA) and adrenergic receptors (α1, α2 and β) are crucial in regulating medial prefrontal cortex (mPFC) functions. Impaired modulation of the mPFC by NA has been implicated in many neuropsychiatric diseases, e.g. posttraumatic stress disorder, attention deficit hyperactivity disorder, depression. However, the mechanisms by which NA modulates mPFC neurons are not well understood. AIM(S): The aim of this study was to investigate which adrenergic receptor subtype controls the resting membrane potential and holding currents in mPFC neurons and what are the cellular mechanisms underpinning the effects of NA. METHOD(S): The resting membrane potential and holding currents were recorded in layer V mPFC pyramidal neurons. Gramicidin perforated-patch and classical whole-cell recordings were obtained from neurons in brain slices of young rats. Tested compounds were applied to the bath and/or to the solution in the recording pipette. RESULTS: NA evoked depolarization of the membrane potential and the inward holding current. Stimulation of α1‑ and α2‑receptors failed to evoke similar effects. Meanwhile, the nonselective β‑receptor agonist as well as the selective β1‑receptor agonist mimicked the effect of NA on holding currents. The NA-dependent inward current was considerably reduced by the selective β1‑receptor antagonist. The β1‑related inward current was significantly decreased in the presence of Cs+ ions and the selective blocker of HCN channels – ZD7288. It was not affected by selective blockers of different signaling pathways known to be responsible for mediating the effects from β‑receptors (e.g. adenylyl cyclase-PKA, PLC-PKC, protein tyrosine kinases). CONCLUSIONS: We conclude that NA changes the membrane potential/holding currents of the mPFC pyramidal neurons acting via β1‑receptors. The effects occur due to HCN channel activation and are not mediated by the classical signaling pathways. FINANCIAL SUPPORT: Supported by National Science Centre, Poland, grant 2014/15/N/NZ4/04760 and FW5/ PM2/16.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2017
• Tom: 77
• Numer: Suppl.1
• Opis fizyczny: p.98

Twórcy

autor

Grzelka K.

• Medical University of Warsaw, Department of Physiology and Pathophysiology, Warsaw, Poland

autor

Szulczyk P.J.

• Medical University of Warsaw, Department of Physiology and Pathophysiology, Warsaw, Poland