alpha2-Adrenergic Receptors Modify Dendritic Spike Generation Via HCN Channels in the Prefrontal Cortex

@article{citeulike:2365492, abstract = {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-receptormediated actions on working memory. 10.1152/jn.00943.2007}, author = {Barth, Albert M. and Vizi, Sylvester E. and Zelles, Tibor and Lendvai, Balazs }, citeulike-article-id = {2365492}, doi = {10.1152/jn.00943.2007}, journal = {J Neurophysiol}, keywords = {2pe, ca\_phys, critical\_frequency, dendrites, hcn, h-current, pfc}, month = {January}, number = {1}, pages = {394--401}, posted-at = {2008-05-12 14:02:16}, priority = {4}, title = {{alpha}2-Adrenergic Receptors Modify Dendritic Spike Generation Via HCN Channels in the Prefrontal Cortex}, url = {http://dx.doi.org/10.1152/jn.00943.2007}, volume = {99}, year = {2008} }

TY - JOUR ID - citeulike:2365492 L3 - citeulike-article-id:2365492 TI - {alpha}2-Adrenergic Receptors Modify Dendritic Spike Generation Via HCN Channels in the Prefrontal Cortex JF - J Neurophysiol VL - 99 IS - 1 SP - 394 EP - 401 N2 - 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-receptormediated actions on working memory. 10.1152/jn.00943.2007 KW - 2pe KW - ca_phys KW - critical_frequency KW - dendrites KW - hcn KW - h-current KW - pfc AU - Barth, Albert AU - Vizi, Sylvester AU - Zelles, Tibor AU - Lendvai, Balazs PY - 2008/01/01/ UR - http://dx.doi.org/10.1152/jn.00943.2007 ER -