Sponsor: Theanne Griffith, Ph.D. MED: Physiology & Membrane Bio The NaV 1.2 voltage-gated sodium channel is known to play an important role in neuronal excitability in the brain. Mutations in NaV1.2 are highly correlated with neurodevelopmental disorders, which are also accompanied by somatosensory abnormalities. However, a role for NaV1.2 in somatosensation has not been investigated. Here, we investigated whether NaV1.2 mutations also result in abnormal spinal cord innervation by different subtypes of somatosensory neurons. We collected spinal cord sections from two mutant mouse models (Y84x and R1627x) harboring NaV1.2 premature stop codon mutations found in human patients with severe neurodevelopmental abnormalities. Spinal cord sections were labeled with antibodies against vesicular glutamate transporter 1 (VGlut1), which identifies touch sensitive somatosensory neurons, as well as isolectin B4 (IB4) and calcitonin gene-related peptide (CGRP), which mark two different classes of pain sensing somatosensory neurons. Following confocal microscope imaging, quantification found a significant reduction in the size of the termination zone of CGRP-expressing neurons in Y84x mutant females, but not Y84X mutant males or in R1627x mice of either sex and genotype. Analyses of the other markers are ongoing. Our results demonstrate that mutations in NaV1.2 can result in reduced sensory innervation of the spinal cord. Does Socioeconomic Status Predict Cognitive Exhaustion? Examining Effort Depletion Under Sustained Task Demands Using Pupillometric Measures

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