@article {46525, title = {Age-dependent changes in intrinsic neuronal excitability in subiculum after status epilepticus.}, journal = {PLoS One}, volume = {10}, year = {2015}, month = {2015 Mar 16}, pages = {e0119411}, abstract = {

Kainic acid-induced status epilepticus (KA-SE) in mature rats results in the development of spontaneous recurrent seizures and a pattern of cell death resembling hippocampal sclerosis in patients with temporal lobe epilepsy. In contrast, KA-SE in young animals before postnatal day (P) 18 is less likely to cause cell death or epilepsy. To investigate whether changes in neuronal excitability occur in the subiculum after KA-SE, we examined the age-dependent effects of SE on the bursting neurons of subiculum, the major output region of the hippocampus. Patch-clamp recordings were used to monitor bursting in pyramidal neurons in the subiculum of rat hippocampal slices. Neurons were studied either one or 2-3 weeks following injection of KA or saline (control) in immature (P15) or more mature (P30) rats, which differ in their sensitivity to KA as well as the long-term sequelae of the KA-SE. A significantly greater proportion of subicular pyramidal neurons from P15 rats were strong-bursting neurons and showed increased frequency-dependent bursting compared to P30 animals. Frequency-dependent burst firing was enhanced in P30, but not in P15 rats following KA-SE. The enhancement of bursting induced by KA-SE in more mature rats suggests that the frequency-dependent limitation of repetitive burst firing, which normally occurs in the subiculum, is compromised following SE. These changes could facilitate the initiation of spontaneous recurrent seizures or their spread from the hippocampus to other parts of the brain.

}, issn = {1932-6203}, doi = {10.1371/journal.pone.0119411}, author = {Chung, Sungkwon and Spruston, Nelson and Koh, Sookyong} } @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 {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} }