Palaeontological data of extinct groups often sheds light on the evolutionary sequences leading to extant groups, but has failed to resolve the basal metazoan phylogeny including the origin of the Cnidaria. Here we report the occurrence of a stem-group cnidarian, Cambroctoconus orientalis gen. et sp. nov., from the mid-Cambrian of China, which is a colonial organism with calcareous octagonal conical cup-shaped skeletons. It bears cnidarian features including longitudinal septa arranged in octoradial symmetry and colonial occurrence, but lacks a jelly-like mesenchyme. Such morphological characteristics suggest that the colonial occurrence with polyps of octoradial symmetry is the plesiomorphic condition of the Cnidaria and appeared earlier than the jelly-like mesenchyme during the course of evolution.

BackgroundHomeostatic intrinsic plasticity encompasses the mechanisms by which neurons stabilize their excitability in response to prolonged and destabilizing changes in global activity. However, the milieu of molecular players responsible for these regulatory mechanisms is largely unknown.ResultsUsing whole-cell patch clamp recording and unbiased gene expression profiling in rat dissociated hippocampal neurons cultured at high density, we demonstrate here that chronic activity blockade induced by the sodium channel blocker tetrodotoxin leads to a homeostatic increase in action potential firing and down-regulation of potassium channel genes. In addition, chronic activity blockade reduces total potassium current, as well as protein expression and current of voltage-gated Kv1 and Kv7 potassium channels, which are critical regulators of action potential firing. Importantly, inhibition of N-Methyl-D-Aspartate receptors alone mimics the effects of tetrodotoxin, including the elevation in firing frequency and reduction of potassium channel gene expression and current driven by activity blockade, whereas inhibition of L-type voltage-gated calcium channels has no effect.ConclusionsCollectively, our data suggest that homeostatic intrinsic plasticity induced by chronic activity blockade is accomplished in part by decreased calcium influx through N-Methyl-D-Aspartate receptors and subsequent transcriptional down-regulation of potassium channel genes.Electronic supplementary materialThe online version of this article (doi:10.1186/s13041-015-0094-1) contains supplementary material, which is available to authorized users.

BackgroundSustained changes in network activity cause homeostatic synaptic plasticity in part by altering the postsynaptic accumulation of N-methyl-D-aspartate receptors (NMDAR) and α-amino-3-hydroxyle-5-methyl-4-isoxazolepropionic acid receptors (AMPAR), which are primary mediators of excitatory synaptic transmission. A key trafficking modulator of NMDAR and AMPAR is STriatal-Enriched protein tyrosine Phosphatase (STEP61) that opposes synaptic strengthening through dephosphorylation of NMDAR subunit GluN2B and AMPAR subunit GluA2. However, the role of STEP61 in homeostatic synaptic plasticity is unknown.FindingsWe demonstrate here that prolonged activity blockade leads to synaptic scaling, and a concurrent decrease in STEP61 level and activity in rat dissociated hippocampal cultured neurons. Consistent with STEP61 reduction, prolonged activity blockade enhances the tyrosine phosphorylation of GluN2B and GluA2 whereas increasing STEP61 activity blocks this regulation and synaptic scaling. Conversely, prolonged activity enhancement increases STEP61 level and activity, and reduces the tyrosine phosphorylation and level of GluN2B as well as GluA2 expression in a STEP61–dependent manner.ConclusionsGiven that STEP61-mediated dephosphorylation of GluN2B and GluA2 leads to their internalization, our results collectively suggest that activity-dependent regulation of STEP61 and its substrates GluN2B and GluA2 may contribute to homeostatic stabilization of excitatory synapses.Electronic supplementary materialThe online version of this article (doi:10.1186/s13041-015-0148-4) contains supplementary material, which is available to authorized users.

The Cambrian succession in the North China Platform comprises a mixed carbonate-siliciclastic sequence, superbly exposed in the southern part of Shandong Province, China. In order to refine the lithostratigraphy of the Cambrian succession, this paper presents detailed sedimentary logs of outcrop sections in the Jinan, Laiwu, Jining, and Linyi areas. The entire succession consists of six lithologic units: Liguan, Zhushadong, Mantou, Zhangxia, Gushan, and Chaomidian formations in ascending order. The upper boundary of the Zhushadong Formation is refined as the base of the first purple mudstone bed of the Mantou Formation. The Mantou Formation is, in turn, bounded at the top by a thick oolitic grainstone bed of the Zhangxia Formation. The upper boundary of the Gushan Formation is placed at the base of a distinct bioclastic grainstone bed of the Chaomidian Formation. The constituent members of the Zhushadong, Mantou, and Chaomidian formations are also refined. Seventeen trilobite biozones are recognized, representing the Cambrian Series 2 to the Furongian.

A modified Pierce circuit topology has been used to first demonstrate a 9.75 MHz µmechanical resonator reference oscillator, then to assess the ultimate frequency stability of such an oscillator via accurate measurement of its close-to-carrier phase noise, which seems to exhibit an unexpected 1/f 3 dependence that limits the phase noise to −80 dBc at a 1 kHz offset from the carrier-a value that must be improved before use in most communications applications. Through theoretical analysis, this 1/f 3 dependence seems to derive from aliasing of active circuit 1/f noise onto the carrier caused by nonlinearity in the capacitive transducer of the µmechanical resonator.