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Publication : Cannabinoid modulation of backpropagating action potential-induced calcium transients in layer 2/3 pyramidal neurons.

First Author  Hsieh LS Year  2013
Journal  Cereb Cortex Volume  23
Issue  7 Pages  1731-41
PubMed ID  22693342 Mgi Jnum  J:211023
Mgi Id  MGI:5573035 Doi  10.1093/cercor/bhs168
Citation  Hsieh LS, et al. (2013) Cannabinoid modulation of backpropagating action potential-induced calcium transients in layer 2/3 pyramidal neurons. Cereb Cortex 23(7):1731-41
abstractText  Endocannabinoids (eCBs) play a prominent role in regulating synaptic signaling throughout the brain. In layer 2/3 of the neocortex, eCB-mediated suppression of GABA release results in an enhanced excitability of pyramidal neurons (PNs). The eCB system is also involved in spike timing-dependent plasticity that is dependent on backpropagating action potentials (bAPs). Dendritic backpropagation plays an important role in many aspects of neuronal function, and can be modulated by intrinsic dendritic conductances as well as by synaptic inputs. The present studies explored a role for the eCB system in modulating backpropagation in PN dendrites. Using dendritic calcium imaging and somatic patch clamp recordings from mouse somatosensory cortical slices, we found that activation of type 1 cannabinoid receptors potentiated bAP-induced calcium transients in apical dendrites of layer 2/3 but not layer 5 PNs. This effect was mediated by suppression of GABAergic transmission, because it was prevented by a GABAA receptor antagonist and was correlated with cannabinoid suppression of inhibitory synaptic activity. Finally, we found that activity-dependent eCB release during depolarization-induced suppression of inhibition enhanced bAP-induced dendritic calcium transients. Taken together, these results point to a potentially important role for the eCB system in regulating dendritic backpropagation in layer 2/3 PNs.
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