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J Neurophysiol 99: 394-401, 2008. First published November 14, 2007; doi:10.1152/jn.00943.2007
0022-3077/08 $8.00
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{alpha}2-Adrenergic Receptors Modify Dendritic Spike Generation Via HCN Channels in the Prefrontal Cortex

Albert M. I. Barth, E. Sylvester Vizi, Tibor Zelles and Balazs Lendvai

Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary

Submitted 21 August 2007; accepted in final form 8 November 2007

Although dendritic spikes are generally thought to be restricted to the distal apical dendrite, we know very little about the possible modulatory mechanisms that set the spatial limits of dendritic spikes. Our experiments demonstrated that high-frequency trains of backpropagating action potentials avoided filtering in the apical dendrite and initiated all-or-none dendritic Ca2+ transients associated with dendritic spikes in layer 5 pyramidal neurons of the prefrontal cortex. The block of hyperpolarization-activated currents (Ih) by ZD7288 could shift the frequency threshold and decreased the number of action potentials required to produce the all-or-none Ca2+ transient. Activation of {alpha}2-adrenergic receptors could also shift the frequency domain of spike induction to lower frequencies. Our data suggest that noradrenergic activity in the prefrontal cortex influences dendritic Ih and extends the zone of dendritic spikes in the apical dendrite via {alpha}2-adrenergic receptors. This mechanism might be one cellular correlate of the {alpha}2-receptor–mediated actions on working memory.

Address for reprint requests and other correspondence: B. Lendvai, Institute of Experimental Medicine, H-1083 Budapest, Szigony u. 43., Hungary (E-mail: lendvai{at}koki.hu)






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