Christine Shrock: Regenerating Sight – Brevia – HCURA

Christine Shrock ‘13, a neurobiology concentrator in Pforzheimer House, views research in a unique light. For her, the time she has spent working on optic nerve regeneration in Larry Benowitz’s lab at Children’s Hospital Boston has not been about rounding out a set of extracurricular activities or getting published in a science journal before graduation. Instead, her motivation for research is her drive to apply the expertise in neurobiology she has gained from countless hours of class and problem sets to real and tangible problems. So much of being a student is about the consumption of facts and concepts; research affords the opportunity to add to the body of scientific knowledge.

Christine has always been interested in different types of brain injuries and disabilities. As a freshman, she began working in an autism research lab. The following summer, Christine travelled to China to work in an orphanage for blind children. Upon returning to Harvard, she wanted to study more about blindness and also to experience research in a “wet” laboratory, the kind of lab that deals with chemicals, organisms, and drugs.

After joining the Benowitz lab, Christine began researching the ways that eyes attempt to repair themselves after injury. For her thesis, she studied nerve regeneration in mice that had experienced blindness-inducing trauma, observing the ways in which vision was recovered. Some mice made much greater strides toward optic regeneration than others. Upon closer inspection, Christine found that an overabundance of zinc in the eye severely retarded healing and regrowth. This suggests that if the pathway for zinc entrance into the eye was blocked by a medical treatment or drug, vision recovery could be enhanced.

After she graduates this May, Christine wants to spend time as a clinical researcher working with patients before going to medical school. Her interests are varied, but she does know that she wants to keep exploring the boundaries of how we understand the brain.

Figures

Figure 1: Cross-sections of a normal, uninjured mouse retina (left), one 1 hour after optic nerve crush (ONC) (middle), and one 3 hours after ONC (right), stained with modified Timm’s silver amplification staining (black) to detect the presence of zinc. There is a dramatic elevation of zinc in the retina as early as 1 hour after injury to the optic nerve.

Figure 1: Cross-sections of a normal, uninjured mouse retina (left), one 1 hour after optic nerve crush (ONC) (middle), and one 3 hours after ONC (right), stained with modified Timm’s silver amplification staining (black) to detect the presence of zinc. There is a dramatic elevation of zinc in the retina as early as 1 hour after injury to the optic nerve.

Figure 2: Whole-mounted retinas from a normal mouse without optic nerve crush (ONC) (left), one with ONC only (middle), and one with ONC+TPEN chelator treatment to bind zinc and prevent accumulation (right). Retinal ganglion cell survival decreased significantly after injury to the optic nerve, and zinc chelator treatment promoted cell survival.

Figure 3: Longitudinal sections of a mouse optic nerve showing axons 2 weeks after optic nerve crush (ONC). ONC alone, without zinc chelator treatment, results in almost complete lack of axonal regeneration (top). However, the addition of TPEN chelator treatment to bind zinc and prevent accumulation after ONC promotes extensive regeneration of axons through the optic nerve (bottom)