Arab, R. | bioRxiv Science

bioRxiv2026

From Functional Organization to Vascular Structure in the Primate Visual Cortex Using Ultrasound Imaging

The primary visual cortex (V1) provides an exceptional structure to assess information encoding in the cortex thanks to its highly controlled visual input. However, optical measures and electrophysiology are limited to very superficial layers while fMRI provides low spatial resolution. Taking advantages of functional ultrasound imaging (fUSi), we examined large volumes of V1 in two awake non-human primates. We showed the conservation of retinotopic maps within deep sulcal regions and across cortical layers. We then assessed the cortical point image and compared it to its vasculature distribution through ultrasound localization microscopy (ULM). We further identified the smallest vascular compartment underlying the signal. Together, these results establish fUSi, complemented by ULM, as a minimally invasive mesoscale approach for resolving functional organization of the cortex in deep sulci.

neuroscience↗

bioRxiv2022

Failed remyelination of the non-human primate optic nerve leads to axon degeneration, retinal damages and visual dysfunction.

White matter disorders of the CNS such as MS, lead to failure of nerve conduction and long-lasting neurological disabilities affecting a variety of sensory and motor systems including vision. While most disease-modifying therapies target the immune and inflammatory response, the promotion of remyelination has become a new therapeutic avenue, to prevent neuronal degeneration and promote recovery. Most of these strategies are developed in short-lived rodent models of demyelination, which spontaneously repair and do not reflect the size, organization, and biology of the human CNS. Thus, well-defined non-human primate models are required to efficiently advance therapeutic approaches for patients. Here, we followed the consequence of long-term toxin-induced demyelination of the macaque optic nerve on remyelination and axon preservation, as well as its impact on visual functions. Findings from oculo-motor behavior, ophthalmic examination, electrophysiology, and retinal imaging indicate visual impairment involving the optic nerve and retina. These visual dysfunctions fully correlated at the anatomical level, with sustained optic nerve demyelination, axonal degeneration, and alterations of the inner retinal layers. This non-human primate model of chronic optic nerve demyelination associated with axonal degeneration and visual dysfunction, recapitulates several key features of MS lesions and should be instrumental in providing the missing link to translate emerging repair pro-myelinating/neuroprotective therapies to the clinic for myelin disorders such as MS. Significance StatementPromotion of remyelination has become a new therapeutic avenue, to prevent neuronal degeneration and promote recovery in white matter diseases such as MS. To date most of these strategies are developed in short-lived rodent models of demyelination, which spontaneously repair. Well-defined non-human primate models closer to man would allow to efficiently advance therapeutic approaches. Here we present a non-human primate model of optic nerve demyelination that recapitulates several features of MS lesions. The model leads to failed remyelination, associated with progressive axonal degeneration and visual dysfunction, thus providing the missing link to translate emerging pre-clinical therapies to the clinic for myelin disorders such as MS.

neuroscience↗