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J Physiol Volume 584, Number 2, 437-450, October 15, 2007 DOI: 10.1113/jphysiol.2007.141671
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NEUROSCIENCE

{alpha}2-Noradrenergic receptors activation enhances excitability and synaptic integration in rat prefrontal cortex pyramidal neurons via inhibition of HCN currents

 David B. Carr1, Glenn D. Andrews1, William B. Glen1 and A. Lavin1

1 Department of Neurosciences, Medical University of South Carolina, Charleston, SC 29425, USA

Stimulation of {alpha}2-noradrenergic (NA) receptors within the PFC improves working memory performance. This improvement is accompanied by a selective increase in the activity of PFC neurons during delay periods, although the cellular mechanisms responsible for this enhanced response are largely unknown. Here we used current and voltage clamp recordings to characterize the response of layer V–VI PFC pyramidal neurons to {alpha}2-NA receptor stimulation. {alpha}2-NA receptor activation produced a small hyperpolarization of the resting membrane potential, which was accompanied by an increase in input resistance and evoked firing. Voltage clamp analysis demonstrated that {alpha}2-NA receptor stimulation inhibited a caesium and ZD7288-sensitive hyperpolarization-activated (HCN) inward current. Suppression of HCN current by {alpha}2-NA stimulation was not dependent on adenylate cyclase but instead required activation of a PLC–PKC linked signalling pathway. Similar to direct blockade of HCN channels, {alpha}2-NA receptor stimulation produced a significant enhancement in temporal summation during trains of distally evoked EPSPs. These dual effects of {alpha}2-NA receptor stimulation – membrane hyperpolarization and enhanced temporal integration – together produce an increase in the overall gain of the response of PFC pyramidal neurons to excitatory synaptic input. The net effect is the suppression of isolated excitatory inputs while enhancing the response to a coherent burst of synaptic activity.

(Received 27 July 2007; accepted after revision 10 August 2007; first published online 16 August 2007)
Corresponding author A. Lavin: Department of Neurosciences, Medical University of South Carolina, 173 Ashley Avenue, Suite 403 BSB, Charleston, SC 29425, USA. Email: lavina{at}musc.edu






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