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. 2013 Jun 13;8(6):e66122. doi: 10.1371/journal.pone.0066122

Figure 9. Molecular components involved in NE-induced persistent firing in superficial pyramidal neurons of prefrontal cortex.

Figure 9

NE released from noradrenergic varicosities in the prefrontal cortex binds to pre- and postsynaptic α1 adrenoceptors. Activation of presynaptic α1 adrenoceptors facilitates glutamate release. Glutamate activates postsynaptic mGluR5 and induces persistent neuronal firing. Postsynaptic α2 adrenoceptors and HCN channels colocalize on dendritic spines [44]. Activation of postsynaptic α2 adrenoceptors by NE inhibits cAMP signaling and blocks HCN channels thereby increasing membrane input resistance, cell excitability and the efficacy of synaptic transmission. Cholinergic inputs induce persistent neuronal firing driven by M1 muscarinic receptors via TRPC channel-dependent mechanisms [24]. α2 adrenoceptor-mediated inhibition of HCN channels underlies NE-mediated modulation of cholinergic persistent firing. Ach: acetylcholine; Glu: glutamate.