Browse our latest Neuroscience articles

High mortality following traumatic brain injury in mice carrying a human mutation for familial hemiplegic migraine type 1 (FHM1) is caused by a decreased threshold for cortical spreading depolarizations (CSDs) and subsequent brain edema formation.

Many V1 double-opponent cells integrate light information across their receptive fields as linearly as simple cells do.

Electrophysiology, optogenetics, and imaging in a mouse model of Dravet syndrome reveals dentate gyrus circuit dysfunction driven by hyperexcitability of the perforant path input from entorhinal cortex that can be modulated by recruitment of parvalbumin-expressing inhibitory interneurons.

Axon degeneration due to loss of mitochondria is suppressed by CaMKII activity and MAP kinase signaling.

TADR (torn and diminished rhabdomeres)-dependent histidine transporting is required for de novo synthesis of histamine and for maintaining synaptic transmission of photoreceptor neurons in Drosophila.

Stimulus-induced causal interactions in the gamma range can flow in direction opposite to the canonical microcircuit, violating the notion that they are signatures of feedforward communication.

When oligodendrocytes lack expression of the low-abundant myelin protein CMTM5, central nervous system axons are myelinated normally but subsequently degenerate involving a Wallerian-like pathomechanism.

Humans perseverate on previously instructed goals in a novel multigoal reinforcement learning task, and do this to a greater extent for punishment avoidance goals.

The m⁶A reader YTHDF2 negatively regulates retinal ganglion cell dendrite branching through destabilizing its m⁶A-modified target mRNAs which control dendrite development and maintenance, and Ythdf2 conditional knockout in retina improves visual acuity and alleviates acute ocular hypertension-induced glaucoma in mice.

Optical recordings from L5 cortical pyramidal neurons expressing mitochondria-targeted Ca²⁺ indicator, mitoGCaMP6m, reveal compartment-specific mitochondrial responses to spike firing and synaptic activity.