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This study describes the synaptogenic function of an ErbB2-interacting protein called Erbin, particularly its function in the formation of excitatory synapses on interneurons and its regulation of AMPA-type glutamate receptors through its interaction with the auxiliary AMPA receptor protein TARP γ-2.
The authors show that fear conditioning induces potentiation of excitatory synapses onto somatostatin-positive inhibitory neurons in the lateral division of the central amygdala. Preventing this synaptic potentiation impairs the formation of fear memories, and activation of these neurons is necessary and sufficient for expression of fear memories.
Age-related cognitive decline is paralleled by two other prominent brain changes: structural atrophy prominent in medial prefrontal cortex (mPFC) and disrupted non-rapid eye movement (NREM) slow-wave sleep (SWS). This study establishes an interaction between these factors, demonstrating that the extent of mPFC atrophy predicts the degree of impaired NREM SWS quality, thereby compromising hippocampal-dependent memory consolidation in the aging human brain.
Previous evidence has suggested that hippocampal place fields in rodents arise from the summation of input from entorhinal grid cells. Here the authors show that perturbing excitatory backprojections from the hippocampus to the entorhinal cortex causes a gradual firing rate–dependent loss of grid pattern and an emergence of head-directional tuning in grid cells of the medial entorhinal cortex.
Using paired recordings from rat entorhinal stellate cells and computational modeling, this study shows that stellate cells in the medial entorhinal cortex (MEC) are almost exclusively connected to each other via inhibitory interneurons in an all-or-none style and that stable grid firing can arise from this recurrent inhibitory circuitry within the MEC.
In this Resource study, the authors used high-resolution mass spectrometry to elucidate the precise proteomic complement of the inner ear hair bundle. Many of the proteins that are enriched in the hair bundles are encoded by known deafness-associated genes.
This study describes the transcriptional programming of yolk sac–derived microglia specification in the brain, in which c-kit–positive erythromyeloid cells are further modified into three developmental subpools of microglia progenitors and their microglia differentiation is mediated by the transcription factors Pu.1 and IRF8.
In this study, the authors show that velocity-dependent lag normalization in the retina is accomplished via a subset of adjacent directionally selective ganglion cells that are electrically coupled, allowing each activated cell to prime its neighbor.
The authors report that calcium channels with a mutation associated with Timothy syndrome cause activity-dependent dendrite retraction in rodent neurons and in induced pluripotent stem cell–derived neurons from individuals with Timothy syndrome. This retraction was independent of Ca permeation but was associated with activation of RhoA signaling.
Here the authors derive the mathematical relationship among the key ingredients of the standard neural decision-making model: choice probabilities, read-out weights and correlated variability. This allows them to infer decoding strategies from experimentally measurable quantities and to test whether the organism is using an optimal decoding strategy for a given task, even without knowing the underlying correlations.
This study uses optogenetics in vivo in mice to provide causal evidence for the distinct roles played by different cortical layers in the regulation of intrinsic oscillations.
Using simultaneous quadruple-to-octuple whole-cell recordings in rat sensorimotor cortex and testing over 14,000 putative synaptic connections between over 8,000 cells, Jiang and colleagues identify two new multi-layer disynaptic interneuronal circuits. Functionally, these two circuits either inhibit or disinhibit the initiation of complex spikes in the apical dendrite of layer 5 pyramidal cells.
Treatment of pain with morphine leads to paradoxical hyperalgesia. The authors provide evidence that morphine-induced hyperalgesia is a result of downregulation of the chloride transporter KCC2 in spinal lamina I neurons. Microglial expression of P2X4 receptors and release of BDNF may underlie this change in neuronal chloride homeostasis and morphine-induced hyperalgesia.
The accessory olfactory bulb consists of anterior (aAOB) and posterior (pAOB) portions that control distinct aspects of social behavior. In this study, the authors show that, unlike their aAOB counterparts, pAOB neurons arise at the diencephalon-telencephalon border and migrate rostrally. A similar migration is seen in the Xenopus AOB.
Tuning of neurons in higher visual cortices is less diverse than in primary visual cortex (V1), but the mechanisms underlying this specialization are unknown. In this paper, Glickfeld and colleagues used two-photon imaging in awake mice to measure the visual responses of boutons from V1 projection neurons in the higher visual areas and found that bouton tunings matched the preference of their target areas. These findings suggest that inter-areal visual stimulus feature segregation occurs via the target-specific routing of visual information as it ascends the cortical hierarchy.
Thalamocortical axonal inputs to the neocortex terminate in the cortical layer 4, whereas corticobulbar and corticospinal output from the cortex mostly originate from layer 5B pyramidal neurons. This study utilizes a novel in vivo gene expression system in postmitotic neurons and demonstrates the reprogramming of layer 4 input-receiver neurons in postnatal mice into layer 5B–like cortical output neurons using the expression of the transcription factor Fezf2.
This study shows that a non-clustered protocadherin, NFPC, is locally translated in retinal axons in response to Sema3A and demonstrates that NFPC-mediated homophilic adhesion helps guide retinal axons in the optic tract, thus revealing a new mechanism for axon guidance by linking a diffusible cue to adhesion-based navigation.