Cellular mechanisms of long-term depression induced by noradrenaline in rat 
prefrontal neurons prefrontal neurons

Marzo, A; Bai, J; Caboche, J; Vanhoutte, P; Otani, S

doi:10.1016/j.neuroscience.2010.04.046

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Cellular mechanisms of long-term depression induced by noradrenaline in rat prefrontal neurons prefrontal neurons

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https://www.sciencedirect.com/science/article/pii/S0306452210006135
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Citation

Marzo, A., Bai, J., Caboche, J., Vanhoutte, P., & Otani, S. (2010). Cellular mechanisms of long-term depression induced by noradrenaline in rat prefrontal neurons prefrontal neurons. Neuroscience, 169(11), 74-86. doi:10.1016/j.neuroscience.2010.04.046.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0013-BE9C-5

Abstract

Noradrenaline (NA) is released in the prefrontal cortex (PFC) during salient behavioral phases
and thought to modulate PFC-mediated cognitive functions. However, cellular actions of NA
in PFC neurons are still not well understood. In the present study, we investigated long-term
effects of bath-applied NA (12.5 min) on glutamatergic synaptic transmission in rat PFC
pyramidal neurons maintained in vitro. We found that NA concentration-dependently (5 956;M-20 956;M) induces long-term depression (LTD) of layer I-II to layer V pyramidal neuron
glutamatergic synapses. NA acts through alpha1- and alpha2- adrenoceptors, but not beta-adrenoceptors,
to induce LTD. This NA-induced LTD depends on concurrent single synaptic activations of
N-methyl-D-aspartate (NMDA) receptors and requires the activation of protein kinase C and
postsynaptic Extracellular signal-Regulated Kinases (ERK1/2). Western blot analyses showed
that NA (20 956;M for 12.5 min) indeed induces transient increases of ERK1/2 phosphorylation
in PFC neurons, which is dependent at least in part on the activation of NMDA receptors and
alpha1-adrenoceptors. Together, these results demonstrate that NA can lastingly depress
glutamatergic synapses in rat PFC neurons through mechanisms involving alpha-adrenoceptors,
NMDA receptors, and the activation of postsynaptic ERK1/2.