Introduction The optic nerve, part of the central nervous system (CNS), connects the eye to the brain. In anamniotes when the optic nerve is injured, it regenerates and restores the axonal connections. The molecular mechanisms underlying this phenomenon are only partially understood. This makes members of the anamniotes a useful group in which to study these mechanisms (Sperry, ). The South African claw-toed frog, has been the model organism of choice to Xenopus laevis study optic nerve regeneration for many years (Gaze, ). CNS regeneration is an area of interest because in amniotes, damage to the axons of the optic nerve is permanent. The CNS axons of amniotes, including mammals, do not regenerate after damage. In non-regenerative axons, the portion of the injured neuron that is part of the greater cell body makes the axon retract. The retracting region of axon is the retraction bulb, which inhibits axonal outgrowth. A glial scar forms a physical barrier to regeneration and the local glia express growth inhibitory compounds (Vajn et al., 2013). In after sustaining damage to the optic nerve, retinal ganglion cells (RGCs) begin X. laevis, generating new axons at 3 days (Zhao and Szaro, 1994). The axons grow along the periphery of the optic tract until they reach the brain approximately 18 days after the nerve injury. The process ends after several months, when normal vision has been restored (Szaro et al., 1985). Previous experiments have implicated Suppressor of Cytokine Signaling 2 (SOCS2) as part of the CNS axonal regeneration process in tadpoles (Gibbs et al., 2011). SOCS2 is one of the eight members of the SOCS protein family (Hilton et al., 1998). Its expression in the cell is induced by stimulation from hormones and other cytokines. SOCS2,
Introduction The optic nerve, part of the central nervous system (CNS), connects the eye to the brain. In anamniotes when the optic nerve is injured, it regenerates and restores the axonal connections. The molecular mechanisms underlying this phenomenon are only partially understood. This makes members of the anamniotes a useful group in which to study these mechanisms (Sperry, ). The South African claw-toed frog, Xenopus laevis has been the model organism of choice to study optic nerve regeneration for many years (Gaze, ). CNS regeneration is an area of interest because in amniotes, damage to the axons of the optic nerve is permanent. The CNS axons of amniotes, including mammals, do not regenerate after damage. In non-regenerative axons, the portion of the injured neuron that is part of the greater cell body makes the axon retract. The retracting region of axon is the retraction bulb, which inhibits axonal outgrowth. A glial scar forms a physical barrier to regeneration and the local glia express growth inhibitory compounds (Vajn et al., 2013). In X. laevis, after sustaining damage to the optic nerve, retinal ganglion cells (RGCs) begin generating new axons at 3 days (Zhao and Szaro, 1994). The axons grow along the periphery of the optic tract until they reach the brain approximately 18 days after the nerve injury. The process ends after several months, when normal vision has been restored (Szaro et al., 1985). Previous experiments have implicated Suppressor of Cytokine Signaling 2 (SOCS2) as part of the CNS axonal regeneration process in tadpoles (Gibbs et al., 2011). SOCS2 is one of the eight members of the SOCS protein family (Hilton et al., 1998). Its expression in the cell is induced by stimulation from hormones and other cytokines. SOCS2,
Gura_Honors_Thesis.docx