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The anterior cingulate cortex (ACC), a limbic region associated with pain-related working memory and memory acquisition, receives a dense cholinergic innervation. To further understand the role of acetylcholine in ACC, we characterized the firing properties of pyramidal neurons following muscarinic receptor activation. Using whole-cell patch clamp recordings in acute brain slices, we report long-lasting nonsynaptic plateau potentials and persistent firing induced by carbachol (CCh) in pyramidal neurons in layers II/III of rat ACC. CCh responses were abolished by the muscarinic receptor antagonist atropine or by inhibitors of G proteins and phospholipase C. Inhibiting L-type calcium channels with nifedipine, removing extracellular calcium or chelating intracellular calcium with BAPTA also abolished plateau potentials and persistent firing. Blockade of nonselective cation channels with flufenamic acid, 2-aminoethyl diphenylborinate or SKF-96365 suppressed CCh responses and voltage-clamp recordings of CCh-sensitive currents revealed a transient receptor potential canonical-like cationic conductance. The group I metabotropic glutamate receptor (mGluR) agonist (S)-3,5-dihydroxyphenylglycine hydrate induced plateau potentials and persistent firing that were mediated by mGluR5. Our data demonstrate that receptor-operated channels drive calcium-dependent plateau potentials and persistent firing in layers II/III of ACC. Therefore, acetylcholine- and glutamate-evoked persistent activity in ACC may play a mnemonic role by allowing transient storage of information during pain processing.

Metabotropic Induction of Persistent Activity in Layers II/III of Anterior Cingulate Cortex