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Long, K. H.

Publications and source records attributed to Long, K. H..

3 recordsLinked to original sources

Texture Coding In Higher Order Somatosensory Cortices

AO_SCPLOWBSTRACTC_SCPLOWOur sense of touch confers to us the ability to perceive textural features over a broad range of spatial scales and material properties, giving rise to a complex sensory experience. To understand the neural basis of texture perception requires that the responses of somatosensory neurons be probed with stimuli that tile the space of spatial scales and material properties experienced during everyday interactions with objects. We have previously shown that neurons in early stages of somatosensory processing - the nerves and somatosensory cortex (S1) - are highly sensitive to texture and carry a representation of texture that is highly informative about the surface but also predicts the evoked sensory experience. In contrast, the texture signals in higher order areas - secondary somatosensory cortex (S2) and the parietal ventral area (PV) - have never been investigated with a rich and naturalistic textural set. To fill this gap, we recorded single-unit activity in S2/PV of macaques while they performed a texture discrimination task. We then characterized the neural responses to texture and compared these to their counterparts in somatosensory cortex (S1). We found that the representation of texture in S2/PV differs markedly from its counterpart in S1. In particular, S2/PV neurons carry a much sparser representation of texture identity and also information about task variables, including the animals eventual perceptual decision. S2/PV thus seems to carry a labile representation of texture that reflects task demands rather than faithfully encoding the stimulus.

neuroscience↗

Texture is encoded in precise temporal spiking patterns in primate somatosensory cortex

AO_SCPLOWBSTRACTC_SCPLOWWe are exquisitely sensitive to the microstructure and material properties of surfaces. In the peripheral nerves, two separate mechanisms convey texture information: coarse textural features are encoded in spatial patterns of activation that reflect their spatial layout and fine features are encoded in highly repeatable, texture specific temporal spiking patterns evoked as the skin moves across the surface. In the present study, we examined whether this temporal code is preserved in the responses of neurons in somatosensory cortex. To this end, we scanned a diverse set of everyday textures across the fingertip of awake macaques while recording the responses evoked in individual cortical neurons. We found that temporal spiking patterns are highly repeatable across multiple presentations of the same texture, with millisecond precision. As a result, texture identity can be reliably decoded from the temporal patterns themselves, even after information carried in the spike rates is eliminated. However, the combination of rate and timing does is more informative than either code in isolation. The temporal precision of the texture response is heterogenous across cortical neurons and depends on the submodality composition of their input and on their location along the somatosensory neuraxis. Furthermore, temporal spiking patterns in cortex dilate and contract with decreases and increases in scanning speed and this systematic relationship between speed and patterning may contribute to the observed perceptual invariance to speed. Finally, we find that the quality of a texture percept can be better predicted when these temporal patterns are taken into consideration. We conclude that high-precision spike timing complements rate-based signals to encode texture in somatosensory cortex.

neuroscience↗

Genetic mapping in Diversity Outbred mice identifies a Trpa1 variant influencing late phase formalin response

Identification of genetic variants that influence susceptibility to chronic pain is key to identifying molecular mechanisms and targets for effective and safe therapeutic alternatives to opioids. To identify genes and variants associated with chronic pain, we measured late phase response to formalin injection in 275 male and female Diversity Outbred (DO) mice genotyped for over 70 thousand SNPs. One quantitative trait locus (QTL) reached genome-wide significance on chromosome 1 with a support interval of 3.1 Mb. This locus, Nociq4 (nociceptive sensitivity inflammatory QTL 4; MGI:5661503), harbors the well-known pain gene Trpa1 (transient receptor potential cation channel, subfamily A, member 1). Trpa1 is a cation channel known to play an important role in acute and chronic pain in both humans and mice. Analysis of DO founder strain allele effects revealed a significant effect of the CAST/EiJ allele at Trpa1, with CAST/EiJ carrier mice showing an early, but not late, response to formalin relative to carriers of the seven other inbred founder alleles (A/J, C57BL/6J, 129S1/SvImJ, NOD/ShiLtJ, NZO/HlLtJ, PWK/PhJ, and WSB/EiJ). We characterized possible functional consequences of sequence variants in Trpa1 by assessing channel conductance, Trpa1/Trpv1 interactions, and isoform expression. The phenotypic differences observed in CAST/EiJ relative to C57BL/6J carriers were best explained by Trpa1 isoform expression differences, implicating a splice junction variant as the causal functional variant. This study demonstrates the utility of advanced, high-precision genetic mapping populations in resolving specific molecular mechanisms of variation in pain sensitivity.

bioinformatics↗