Submitted on August 21, 2007
Accepted on November 8, 2007
2-Adrenergic receptors modify dendritic spike generation via HCN channels in the prefrontal cortex
Albert MI Barth1, Sylvester E. Vizi1, Tibor Zelles1, and Balazs Lendvai1*
1 Department of Pharmacology, Institute of Experimental Medicine, Budapest, Hungary
* To whom correspondence should be addressed. E-mail: lendvai{at}koki.hu.
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-type dendritic Ca2+ transients associated with dendritic spikes in layer 5 pyramidal neurons of the prefrontal cortex. The block of hyperpolarization-activated currents (Ih) by ZD 7288 could shift the frequency threshold and decreased the number of action potentials required to produce the all-or-none-type Ca2+ transient. Activation of 
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 2-adrenergic receptors. This mechanism might be one cellular correlate of the 2-receptors-mediated actions on working memory.
