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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.
