Research Highlights

CLEGR2+ neurons immediately before 43% of IPSPs driven by claustrum tones considerably reduced auditory activation were probably mediated population responses. by NPY neurons, whereas 35% in brief In the other study, Jackson et al. were mediated by FS neurons and used a retrograde virus approach to 22% by co-innervation​ by FS and SPATIAL NAVIGATION specifically target claustral neurons NPY neurons. Pharmacogenetic Planning a path projecting to the prefrontal cortex silencing of PV+ neurons (including (PFC) in mice (CL PFC neurons). FS neurons) or NPY neurons greatly Spatial navigation involves co-ordination between action → planning by the prefrontal cortex and spatial representation Optogenetic stimulation of these reduced the inhibitory responses of the environment in the hippocampus. In this study, when CL → PFC afferents led to a strong of pyramidal cells to claustral rats performed an alternating arm choice task in a T maze, the overall inhibition of pyramidal stimulation. Notably, when NPY coordination of the timing of spikes between neurons in neurons and inhibitory neurons in neurons were silenced, claustral the medial prefrontal cortex (mPFC), the thalamic nucleus the PFC. In acute slices, claustrum-​ stimulation even led to excitation reuniens (NR) and the hippocampal CA1 was found to increase; stimulated inhibitory responses of pyramidal cells, suggesting co-ordinated firing between supramammillary nucleus (SUM) and CA1 neurons also increased. Silencing of SUM neurons of prefrontal pyramidal cells were that claustrocortical excitation of decreased spike-time coordination in the mPFC-NR-CA1 blocked by glutamate receptor pyramidal cells is usually prevented circuit and impaired representations of the trajectory of antagonists, suggesting that the by NPY cell-mediated​ inhibition. travel in NR and CA1, suggesting that SUM modulates the claustrum inhibits pyramidal cells Together, these studies show that communication of action planning information from the mPFC through inhibitory interneurons. the claustrum provides inhibition to downstream targets. In line with this notion, fast-spiking​ to the PFC and auditory cortex, Original article Ito, H. T. et al. Supramammillary nucleus modulates spike-time + coordination in the prefrontal-thalamo-hippocampal circuit during navigation. Neuron 99, parvalbumin-expressing​ (PV ) thus shedding light on how the 576–587 (2018) interneurons (FS neurons) and claustrum may regulate cortical neuropeptide Y-expressing​ function. TECHNIQUES interneurons (NPY neurons) were Natasha Bray strongly depolarized following Catching waves photostimulation of CL → PFC Original articles Atlan, G. et al. The claustrum Measurement of changes in intra-axonal​ calcium with afferents. supports resilience to distraction. Curr. Biol. https:// high temporal and spatial resolution has been technically doi.org/10.1016/j.cub.2018.06.068 (2018) | difficult. Now, a technique has been developed that enables By analysing pyramidal cell Jackson, J. et al. Inhibitory control of prefrontal the genetically encoded calcium indicator GCaMP6 to inhibitory postsynaptic potentials cortex by the claustrum. Neuron https:// doi.org/10.1016/j.neuron.2018.07.031 (2018) be transported into axons, where calcium fluctuations can be (IPSPs), Jackson et al. deduced that monitored with high signal-to-noise​ ratio, brightness and stability. This approach was used to measure layer-specific​ axon activity in mouse cortex at deeper cortical levels than replaced by homomeric GluA1 AMPARs. effects on AMPARs by incorporating was previously possible. Sequential confocal microscopy of GluA1 homomers. Together, these Original article Broussard, G. J. et al. In vivo measurement of afferent activity with anti-GluA2​ IgG pretreated hippocampal findings again indicate that axon-​specific calcium imaging. Nat. Neurosci. 21, 1272–1280 (2018) neurons revealed decreased surface anti-GluA2​ IgG treatment affects expression of GluA2, which was blocked AMPAR properties in a way that NEURODEGENERATIVE DISEASE by inhibiting endocytosis during is consistent with a decrease in Untangling tau structure pretreatment. This indicates that GluA2-containing and rise in anti-GluA2​ IgG induces GluA2-containing non-​GluA2-containing receptors. The human form of tau exists in isoforms that contain either three (3R) or four (4R) microtubule-binding​ repeats. Tau can AMPAR internalization. The authors next examined also form filamentous aggregates, which are a hallmark of The authors examined whether long-​term potentiation (LTP) in the Alzheimer disease and Pick disease. In this study, cryo-electron​ human anti-​GluA2 IgG also affected Schaffer collateral–CA1 hippocampal microscopy was used to investigate tau structure in these AMPAR signalling in brain tissue pathway after treatment, as LTP aggregates. The folded structure of tau that aggregates in by delivering this fraction into mice by is thought to be a key mechanism patients with Pick disease was found to be distinct from that intrahippocampal injection. Confocal underlying hippocampal-​dependent found in patients with Alzheimer disease, which might contribute microscopy of hippocampal slices from memory. IgG fraction treatment to the distinct neuropathological phenotypes of these disorders. these animals revealed downregulation impaired a postsynaptic component Original article Falcon, B. et al. Structures of filaments from Pick’s disease reveal a of synaptic GluA2 after injection. of LTP. Mice that received anti-GluA2​ novel tau protein fold. Nature 561, 137–140 (2018) Although the treatment did not affect IgG by passive transfer into the brain the peak amplitude of electrically also showed deficits in memory in an NEURONAL CELL BIOLOGY evoked EPSCs in granule cells of the object recognition task. Novel inhibition dentate gyrus, there was a decrease Together, these data indicate Recent technological advances have enabled ever more in the number of single channels and that autoantibodies against GluA2 detailed characterizations of neuronal subtypes. Here, a rise in the conductance of these induce changes in AMPAR subunit immunohistochemistry and unbiased single-nucleus​ RNA channels. In addition, when slices from composition, which may alter receptor sequencing was used to identify several human cortical injected mice were treated with a properties, and impair LTP and memory. GABAergic neuronal subtypes that possess distinct molecular non-GluA2-containing​ AMPAR inhibitor, Darran Yates signatures and transcriptomes. One notable subtype had there was a decrease in mEPSC ‘rosehip’-like axonal boutons and inhibited backpropagating Original article Haselmann, H. et al. Human amplitudes. A similar decrease was autoantibodies against the AMPA receptor action potentials in pyramidal neuron dendrites; these neurons also observed in slices from anti-GluA2​ subunit GluA2 induce receptor reorganization are thus likely to be involved in local regulation of dendritic IgG-treated​ GluA1 knockout mice, and memory dysfunction. Neuron https://doi.org/ computation. 10.1016/j.neuron.2018.07.048 (2018) which could not compensate for any Original article Boldog, E. et al. Transcriptomic and morphophysiological evidence for a specialized human cortical GABAergic cell type. Nat. Neurosci. 21, 1185–1195 (2018)

nATuRe RevIewS | Neuroscience volume 19 | OCTOBER 2018 | 581