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Citation Information : Acta Neurobiologiae Experimentalis. Volume 76, Issue 2, Pages 158-164, DOI: https://doi.org/10.21307/ane-2017-015
License : (CC BY 4.0)
Received Date : 08-March-2016 / Accepted: 08-May-2016 / Published Online: 25-July-2017
The aim of this perforated-patch study was to test the effect of isoproterenol on the membrane potential in mPFC (medial prefrontal cortex) pyramidal neurons. Isoproterenol depolarized the membrane potential recorded from the soma. This effect was absent in the presence of metoprolol, suggesting the involvement of β1-adrenergic receptors. The adenylate cyclase activator forskolin also depolarized the membrane potential. Moreover, the effect of isoproterenol was abolished by the adenylate cyclase inhibitor SQ 22536. This suggested that adenylate cyclase was involved in mediating the effect of the β-adrenergic receptor agonist. The isoproterenol-induced depolarization persisted after inhibition of protein kinase A with H-89. The effect of β-adrenergic receptor activation on the membrane potential was dependent on Ih channels because it was abolished in the presence of the Ih channel inhibitor ZD 7288. Dendritic recordings were also performed. In the dendritic segments between 100 μm and 150 μm from the soma and between 200 μm and 250 μm from the soma, isoproterenol also depolarized the membrane potential. The magnitude of the β-adrenergic receptor-stimulated depolarization was the same in the soma and in both dendritic localizations. The depolarization exerted by isoproterenol may influence PFC cognitive functions.