کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4344484 | 1296660 | 2012 | 6 صفحه PDF | دانلود رایگان |
The arousal peptides, orexins, play an important role in regulating the function of the prefrontal cortex (PFC). Although orexins have been shown to increase the excitability of deep-layer neurons in the medial prefrontal cortex (mPFC), little is known about their effect on layer 2/3, the main intracortical processing layer. In this study, we investigated the effect of orexin-A on pyramidal neurons in layer 2/3 of the mPFC using whole-cell recordings in rat brain slices. We observed that orexin-A reversibly depolarized layer 2/3 pyramidal neurons through a postsynaptic action. This depolarization was concentration-dependent and mediated via orexin receptor 1. In voltage-clamp recordings, the orexin-A-induced current was reduced by the replacement of internal K+ with Cs+, removal of external Na+, or an application of flufenamic acid (an inhibitor of nonselective cation channels). A blocker of Na+/Ca2+ exchangers (SN-6) did not influence the excitatory effect of orexin-A. Moreover, the current induced by orexin-A reversed near Ek when the external solution contained low levels of Na+. When recording with Cs+-containing pipettes in normal external solution, the reversal potential of the current was approximately −25 mV. These data suggest an involvement of both K+ channels and nonselective cation channels in the effect of orexin-A. The direct excitatory action of orexin-A on layer 2/3 mPFC neurons may contribute to the modulation of PFC activity, and play a role in cognitive arousal.
► Orexin-A directly excited the layer 2/3 pyramidal neurons in the rat mPFC.
► This excitatory effect was mediated via OX1R.
► The ionic mechanisms involved K+ channels and nonselective cation channels.
Journal: Neuroscience Letters - Volume 520, Issue 1, 27 June 2012, Pages 92–97