Publications by authors named "Micah Feri"

Article Synopsis
  • * Using an EAE mouse model, researchers tracked the progression of visual impairment during different disease stages, finding significant demyelination and axon damage over time.
  • * Analysis showed that untreated early inflammation can lead to severe, lasting damage to the optic nerves, providing insights into the worsening visual dysfunction experienced in MS.
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Although over 20 disease modifying therapies are approved to treat Multiple Sclerosis (MS), these do not increase remyelination of demyelinated axons or mitigate axon damage. Previous studies showed that lanthionine ketenamine ethyl ester (LKE) reduces clinical signs in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS and increased maturation of oligodendrocyte (OL) progenitor cells (OPCs) . In the current study, we used the cuprizone (CPZ) demyelination model of MS to test if LKE could increase remyelination.

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Neural circuits in female rats are exposed to sequential estradiol and progesterone to regulate the release of luteinizing hormone (LH) and ultimately ovulation. Estradiol induces progesterone receptors (PGRs) in anteroventral periventricular nucleus (AVPV) kisspeptin neurons, and as estradiol reaches peak concentrations, neuroprogesterone (neuroP) synthesis is induced in hypothalamic astrocytes. This local neuroP signals to PGRs expressed in kisspeptin neurons to trigger the LH surge.

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Visual deficits are among the most prevalent symptoms in patients with multiple sclerosis (MS). To understand deficits in the visual pathway during MS and potential treatment effects, we used experimental autoimmune encephalomyelitis (EAE), the most commonly used animal model of MS. The afferent visual pathway was assessed in vivo using optical coherence tomography (OCT), electroretinography (ERG), and visually evoked cortical potentials (VEPs).

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In estradiol-primed nonreceptive ovariectomized rats, activation of G protein-coupled estrogen receptor 1 (GPER) in the arcuate nucleus of the hypothalamus (ARH) rapidly facilitates sexual receptivity (lordosis). Estradiol priming activates ARH β-endorphin (β-END) neurons that then activate medial preoptic (MPN) μ-opioid receptors (MOP) to inhibit lordosis. ARH infusion of non-esterified 17β-estradiol (E2) 47.

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