title: Persistent activity in layer 5 pyramidal neurons following cholinergic activation of mouse primary cortices.
abstract: Persistent spiking activity is thought to be a cellular process involved in working memory. We have been interested in whether persistent activity also exists in cortical areas which are not involved in this memory process. To study the possible presence and the mechanisms of persistent activity in layer 5 pyramidal cells of the mouse primary somatosensory, visual and motor cortices, we used patch-clamp and calcium imaging techniques. A combination of cholinergic receptor activation and suprathreshold depolarization or sufficient extracellular stimulation leads to either a subthreshold afterdepolarization or suprathreshold persistent activity in these cortices. There is a continuum of response amplitudes depending on depolarization size. To initiate persistent activity, spikes have to be induced at a frequency of at least 20 Hz, if tested for 1 s. Acetylcholine muscarinic, but not nicotinic, receptors are important for initiating persistent activity. Persistent activity is an intrinsic cellular, not a network, phenomenon as it persists under blockade of ionotropic glutamate and GABA receptors. A rise in intracellular calcium concentration through voltage-gated calcium channels is needed for persistent activity initiation, while intracellular calcium stores are not crucial. The increased intracellular calcium concentration leads to the activation of calcium-sensitive nonspecific cationic channels. This study for the first time describes the presence and the underlying mechanisms of persistent activity in pyramidal cells of three primary sensory and motor cortex areas. These results thereby suggest that persistent activity may be a general capability of deep layer cortical pyramidal cells.
authors.affiliation: Institute of Physiology and Pathophysiology, University Medical Center of the Johannes Gutenberg University of Mainz, Mainz, Germany.
authors.forename: Jamilur
authors.initials: J
authors.lastname: Rahman
authors.forename: Thomas
authors.initials: T
authors.lastname: Berger
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology*; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002217:Carbachol / Q000494:pharmacology; D002540:Cerebral Cortex / Q000166:cytology*; D018679:Cholinergic Agonists / Q000494:pharmacology; D005439:Flufenamic Acid / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D018721:Muscarinic Agonists / Q000494:pharmacology; D018727:Muscarinic Antagonists / Q000494:pharmacology; D018722:Nicotinic Agonists / Q000494:pharmacology; D018733:Nicotinic Antagonists / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D017966:Pyramidal Cells / Q000187:drug effects* / Q000502:physiology*; D011976:Receptors, Muscarinic / Q000378:metabolism; D011978:Receptors, Nicotinic / Q000378:metabolism; D013569:Synapses / Q000187:drug effects / Q000502:physiology
chemical_list: D000893:Anti-Inflammatory Agents; D018679:Cholinergic Agonists; D018721:Muscarinic Agonists; D018727:Muscarinic Antagonists; D018722:Nicotinic Agonists; D018733:Nicotinic Antagonists; D011976:Receptors, Muscarinic; D011978:Receptors, Nicotinic; D005439:Flufenamic Acid; D002217:Carbachol; D000109:Acetylcholine; D002118:Calcium