Synaptic Plasticity at Intrathalamic Connections via CaV3.3 T-type Ca2+ Channels and GluN2B-Containing NMDA Receptors.

The T-type Ca(2+) channels encoded by the Ca(V)3 genes are well established electrogenic drivers for burst discharge. Here, using Ca(V)3.3(-/-) mice we found that Ca(V)3.3 channels trigger synaptic plasticity in reticular thalamic neurons. Burst discharge via Ca(V)3.3 channels induced long-term potentiation at thalamoreticular inputs when coactivated with GluN2B-containing NMDA receptors, which are the dominant subtype at these synapses. Notably, oscillatory burst discharge of reticular neurons is typical for sleep-related rhythms, suggesting that sleep contributes to strengthening intrathalamic circuits

Manipulating sleep spindles - expanding views on sleep, memory, and disease.

Sleep spindles are distinctive electroencephalographic (EEG) oscillations emerging during non-rapid-eye-movement sleep (NREMS) that have been implicated in multiple brain functions, including sleep quality, sensory gating, learning, and memory. Despite considerable knowledge about the mechanisms underlying these neuronal rhythms, their function remains poorly understood and current views are largely based on correlational evidence. Here, we review recent studies in humans and rodents that have begun to broaden our understanding of the role of spindles in the normal and disordered brain. We show that newly identified molecular substrates of spindle oscillations, in combination with evolving technological progress, offer novel targets and tools to selectively manipulate spindles and dissect their role in sleep-dependent processes

ESR Modes in CsCuCl3 in Pulsed Magnetic Fields

We present ESR results for 35-134GHz in the antiferromagnet CsCuCl3 at T=1.5K. The external field is applied perpendicular to the hexagonal c-axis. With our pulsed field facility we reach 50T an unprecedented field for low temperature ESR. We observe strong resonances up to fields close to the ferromagnetic region of ~30T. These results are discussed in a model for antiferromagnetic modes in a two-dimensional frustrated triangular spin system.Comment: 3 pages, RevTeX, 3 figures. to be published in Solid State Communication

Acoustic Faraday effect in Tb3_3Ga5_5O12_{12}

The transverse acoustic wave propagating along the [100] axis of the cubic Tb$_3$Ga$_5$O$_{12}$ (acoustic $c_{44}$ mode) is doubly degenerate. A magnetic field applied in the direction of propagation lifts this degeneracy and leads to the rotation of the polarization vector - the magneto-acoustic Faraday rotation. Here, we report on the observation and analysis of the magneto-acoustic Faraday-effect in Tb$_3$Ga$_5$O$_{12}$ in static and pulsed magnetic fields. We present also a theoretical model based on magnetoelastic coupling of 4$f$ electrons to both, acoustic and optical phonons and an effective coupling between them. This model explains the observed linear frequency dependence of the Faraday rotation angle

Suppression of Sleep Spindle Rhythmogenesis in Mice with Deletion of CaV3.2 and CaV3.3 T-type Ca(2+) Channels.

STUDY OBJECTIVES: Low-threshold voltage-gated T-type Ca(2+) channels (T-channels or CaV3 channels) sustain oscillatory discharges of thalamocortical (TC) and nucleus Reticularis thalami (nRt) cells. The CaV3.3 subtype dominates nRt rhythmic bursting and mediates a substantial fraction of spindle power in the NREM sleep EEG. CaV3.2 channels are also found in nRt, but whether these contribute to nRt-dependent spindle generation is unexplored. We investigated thalamic rhythmogenesis in mice lacking this subtype in isolation (CaV3.2KO mice) or in concomitance with CaV3.3 deletion (CaV3.double-knockout (DKO) mice). METHODS: We examined discharge characteristics of thalamic cells and intrathalamic evoked synaptic transmission in brain slices from wild-type, CaV3.2KO and CaV3.DKO mice through patch-clamp recordings. The sleep profile of freely behaving CaV3.2KO and CaV3.DKO mice was assessed by polysomnographic recordings. RESULTS: CaV3.2 channel deficiency left nRt discharge properties largely unaltered, but additional deletion of CaV3.3 channels fully abolished low-threshold whole-cell Ca(2+) currents and bursting, and suppressed burst-mediated inhibitory responses in TC cells. CaV3.DKO mice had more fragmented sleep, with shorter NREM sleep episodes and more frequent microarousals. The NREM sleep EEG power spectrum displayed a relative suppression of the σ frequency band (10-15 Hz), which was accompanied by an increase in the δ band (1-4 Hz). CONCLUSIONS: Consistent with previous findings, CaV3.3 channels dominate nRt rhythmogenesis, but the lack of CaV3.2 channels further aggravates neuronal, synaptic, and EEG deficits. Therefore, CaV3.2 channels can boost intrathalamic synaptic transmission, and might play a modulatory role adjusting the relative presence of NREM sleep EEG rhythms

SNSF Career Tracker Cohorts (CTC) Newsletter 2022/1

This newsletter shows the first results of a longitudinal analysis of the CTC-18 cohort, which consists of people who applied for Early Postdoc.Mobility and Postdoc.Mobility in fall 2018. The following results are preliminary as the data preparation has not been completed ye