@article {6780, title = {A post-burst after depolarization is mediated by group i metabotropic glutamate receptor-dependent upregulation of Ca(v)2.3 R-type calcium channels in CA1 pyramidal neurons.}, journal = {PLoS Biology}, volume = {8}, year = {2010}, month = {2010}, pages = {e1000534}, abstract = {

Activation of group I metabotropic glutamate receptors (subtypes mGluR1 and mGluR5) regulates neural activity in a variety of ways. In CA1 pyramidal neurons, activation of group I mGluRs eliminates the post-burst afterhyperpolarization (AHP) and produces an afterdepolarization (ADP) in its place. Here we show that upregulation of Ca(v)2.3 R-type calcium channels is responsible for a component of the ADP lasting several hundred milliseconds. This medium-duration ADP is rapidly and reversibly induced by activation of mGluR5 and requires activation of phospholipase C (PLC) and release of calcium from internal stores. Effects of mGluR activation on subthreshold membrane potential changes are negligible but are large following action potential firing. Furthermore, the medium ADP exhibits a biphasic activity dependence consisting of short-term facilitation and longer-term inhibition. These findings suggest that mGluRs may dramatically alter the firing of CA1 pyramidal neurons via a complex, activity-dependent modulation of Ca(v)2.3 R-type channels that are activated during spiking at physiologically relevant rates and patterns.

}, keywords = {Action Potentials, Animals, Calcium Channels, Cation Transport Proteins, Female, Inbred C57BL, Ion Channel Gating, Male, Metabotropic Glutamate, Methoxyhydroxyphenylglycol, Mice, Neurons, Patch-Clamp Techniques, Pyramidal Cells, R-Type, Rats, Receptors, Up-Regulation, Wistar, Xenopus}, issn = {1545-7885}, doi = {10.1371/journal.pbio.1000534}, author = {Park, Jin-Yong and Remy, Stefan and Varela, Juan and Cooper, Donald C and Chung, Sungkwon and Kang, Ho-Won and Lee, Jung-Ha and Spruston, Nelson} } @article {45911, title = {Plasticity of burst firing induced by synergistic activation of metabotropic glutamate and acetylcholine receptors.}, journal = {Neuron}, volume = {61}, year = {2009}, month = {2009 Jan 29}, pages = {287-300}, abstract = {

Subiculum, the primary efferent pathway of hippocampus, participates in memory for spatial tasks, relapse to drug abuse, and temporal lobe seizures. Subicular pyramidal neurons exhibit low-threshold burst firing driven by a spike afterdepolarization. Here we report that burst firing can be regulated by stimulation of afferent projections to subiculum. Unlike synaptic plasticity, burst plasticity did not require synaptic depolarization, activation of AMPA or NMDA receptors, or action potential firing. Rather, enhancement of burst firing required synergistic activation of group I, subtype 1 metabotropic glutamate receptors (mGluRs) and muscarinic acetylcholine receptors (mAChR). When either of these receptors was blocked, a suppression of bursting was revealed, which in turn was blocked by antagonists of group I, subtype 5 mGluRs. These results indicate that the output of subiculum can be strongly and bidirectionally regulated by activation of glutamatergic inputs within the hippocampus and cholinergic afferents from the medial septum.

}, keywords = {Acetylcholine, Action Potentials, Afferent Pathways, Animals, Cholinergic Fibers, Electric Stimulation, Excitatory Amino Acid Antagonists, Glutamic Acid, Hippocampus, Male, Neuronal Plasticity, Pyramidal Cells, Rats, Rats, Wistar, Receptors, Cholinergic, Receptors, Metabotropic Glutamate, Receptors, Muscarinic, Septal Nuclei, Synaptic Transmission, Theta Rhythm}, issn = {1097-4199}, doi = {10.1016/j.neuron.2008.12.013}, author = {Moore, Shannon J and Cooper, Donald C and Spruston, Nelson} } @article {45901, title = {Output-mode transitions are controlled by prolonged inactivation of sodium channels in pyramidal neurons of subiculum.}, journal = {PLoS Biol}, volume = {3}, year = {2005}, month = {2005 Jun}, pages = {e175}, abstract = {

Transitions between different behavioral states, such as sleep or wakefulness, quiescence or attentiveness, occur in part through transitions from action potential bursting to single spiking. Cortical activity, for example, is determined in large part by the spike output mode from the thalamus, which is controlled by the gating of low-voltage-activated calcium channels. In the subiculum--the major output of the hippocampus--transitions occur from bursting in the delta-frequency band to single spiking in the theta-frequency band. We show here that these transitions are influenced strongly by the inactivation kinetics of voltage-gated sodium channels. Prolonged inactivation of sodium channels is responsible for an activity-dependent switch from bursting to single spiking, constituting a novel mechanism through which network dynamics are controlled by ion channel gating.

}, keywords = {Adenosine Diphosphate, Animals, Cognition, Evoked Potentials, Hippocampus, In Vitro Techniques, Membrane Potentials, Pyramidal Cells, Rats, Sodium Channels}, issn = {1545-7885}, doi = {10.1371/journal.pbio.0030175}, author = {Cooper, Donald C and Chung, Sungkwon and Spruston, Nelson} }