Activation of α1-adrenoceptors enhances excitatory synaptic transmission via a pre- and postsynaptic protein kinase C-dependent mechanism in the medial prefrontal cortex of rats

Signaling mechanism underlying α2A-adrenergic suppression of excitatory synaptic transmission in the medial prefrontal cortex of rats

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Norepinephrine Drives Persistent Activity in Prefrontal Cortex via Synergistic α1 and α2 Adrenoceptors

(2013) Zizhen Zhang et al.   PLoS One

Cyclothiazide-induced persistent increase in respiratory-related activityin vitro

(2012) Walter E. Babiec et al.   JOURNAL OF PHYSIOLOGY-LONDON

Neuromodulation of Thought: Flexibilities and Vulnerabilities in Prefrontal Cortical Network Synapses

(2012) Amy F.T. Arnsten et al.   NEURON

Too Much of a Good Thing: Blocking Noradrenergic Facilitation in Medial Prefrontal Cortex Prevents the Detrimental Effects of Chronic Stress on Cognition

(2012) Julianne D Jett et al.   NEUROPSYCHOPHARMACOLOGY

Pharmacotherapy for Attention-Deficit/Hyperactivity Disorder: From Cells to Circuits

(2012) Michael J. Minzenberg   Neurotherapeutics

Protein Kinase C PromotesN-Methyl-d-aspartate (NMDA) Receptor Trafficking by Indirectly Triggering Calcium/Calmodulin-dependent Protein Kinase II (CaMKII) Autophosphorylation

(2011) Jing-Zhi Yan et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

Activation of α1-adrenoceptors increases firing frequency through protein kinase C in pyramidal neurons of rat visual cortex

(2007) Masayuki Kobayashi et al.   NEUROSCIENCE LETTERS