Myelination, the insulating ensheathment of axons by oligodendrocytes, is thought to both optimize signal propagation and provide metabolic support. Despite the well-established physiological importance of myelination to neuronal function, relatively little is known about the myelination of GABAergic interneurons in the cerebral cortex. Here, we report that a large fraction of myelin in mouse cerebral cortex ensheaths GABAergic interneurons, reaching up to 80% in hippocampal subregions. Moreover, we find that a very high proportion of neocortical and hippocampal parvalbumin (PV) interneurons exhibit axonal myelination. Using a combination of intracellular recordings and biocytin labeling of ex vivo human neocortex, we also confirm that axons of fast-spiking PV interneurons are extensively myelinated in the human brain. PV interneuron myelination in both mice and humans exhibits a stereotyped topography with a bias towards proximal axonal segments and relatively short internodes (~27 μm) interspersed with branch points. Interestingly, myelin-deficient Shiverer mice exhibit an increased density and more proximal location of en passant boutons, suggesting that myelination might function in part to regulate synapse formation along PV interneuron axons. Taken together, fast-spiking interneuron myelination is likely to have broad implications for cerebral cortex function in health and disease.

Memories are encoded within sparsely distributed neuronal ensembles. However, the defining cellular properties of neurons within a memory trace remain incompletely understood. Using a fluorescence-based Arc reporter, we were able to visually identify the distinct subset of lateral amygdala (LA) neurons activated during auditory fear conditioning. We found that Arc-expressing neurons have enhanced intrinsic excitability and are preferentially recruited into newly encoded memory traces. Furthermore, synaptic potentiation of thalamic inputs to the LA during fear conditioning is learning-specific, postsynaptically mediated and highly localized to Arc-expressing neurons. Taken together, our findings validate the immediate-early gene Arc as a molecular marker for the LA neuronal ensemble recruited during fear learning. Moreover, these results establish a model of fear memory formation in which intrinsic excitability determines neuronal selection, whereas learning-related encoding is governed by synaptic plasticity.

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The present study investigated how gaze following eye movements are affected by stimulus contrast and spatial frequency and by aberrations in central visual acuity due to refractive errors. We measured 30 healthy subjects with a range of visual acuities but without any refractive correction. Visual acuity was tested using a Landolt-C chart. Subjects were divided into three groups with low, intermediate, or good visual acuity. Gaze following responses (GFR) to moving Gabor patches were recorded by video-oculography. In each trial, the subjects were presented with a single Gabor patch with a specific spatial frequency and luminance contrast that moved sinusoidally in the horizontal plane. We observed that GFR gain decreased with increasing spatial frequency and decreasing contrast and was correlated with visual acuity. GFR gain was lower and decreased more for subjects with lower visual acuity; this was especially so for lower stimulus contrasts that are not tested in standard acuity tests. The largest differences between the groups were observed at spatial frequencies around 4 cpd and at contrasts up to 10%. Aberrations in central visual acuity due to refractive errors affect the GFR response depending on the contrast and spatial frequency of the moving stimulus. Measuring this effect may contribute to a better estimate of changes in visual function as a result of aging, disease, or treatments meant to improve vision.