During the next four days, massive cell death in the dLGN ensues, with many injured dLGN projection neurons displaying cytoplasmic vacuoles, disrupted membranes and nuclear condensation. Many trophic factors, such as nerve growth factor, fibroblast growth factor-2, brain-derived Orbifloxacin neurotrophic factor, ciliary neurotrophic factor and glial cellderived neurotrophic factor, have been demonstrated to mitigate the severity of neuronal loss after injury or disease. Some of these factors have been used to mitigate axotomyinduced cell death in the rat dLGN, and among them CNTF and FGF2 have been shown to be effective. A single administration of FGF2 at the time of axotomy increased the number of surviving dLGN neurons 3 months after axotomy up to 110% compared to controls. FGF2, a member of a family of proteins that bind heparin and heparan sulfate, is involved in a large number of biological activities and plays a crucial role in the maintenance, survival and selective vulnerability of various neuronal populations in the normal, injured, or diseased brain. An injury in the CNS may trigger FGF2 gene expression and promote reactive astrocytes and injured neurons to synthesize increased amounts of FGF2, which in turn protects injured neurons from death and stimulates neuronal plasticity and tissue repair. These known trophic functions of FGF2 indicate that its administration soon after a neuronal injury may prevent or mitigate the early stages of neuronal degeneration and contribute to the survival or slow the death of injured neurons. Cell soma atrophy, the condensation of nuclear chromatin, and subsequent DNA fragmentation are generally believed to indicate that an injured neuron is undergoing apoptotic cell death. Neurons undergoing apoptosis also can be distinguished by the activation of cysteine proteases, commonly known as caspases. Typically, these proteases exist as inactive pro-caspases in healthy cells, but under various pathological conditions, procaspases are cleaved, and the resulting active caspases trigger a cascade of events that leads to apoptotic cell death. Thus, caspase activation is thought to play a central role in apoptosis. In the caspase family, caspase-3 is one of the major members implicated in neurons undergoing apoptotic cell death. Currently, caspase-3 activation has been observed in neurons after various forms of injury and is considered to be a key mediator of apoptosis. We investigated caspase-3 activity in axotomized dLGN projection neurons immediately following injury using an antibody raised against fractin, a 32 kDa N-terminal actin fragment that results exclusively from the cleavage of beta actin by activated caspase-3. Thus while other proteases such as calpain may be involved in the death of axotomized dLGN neurons, the presence of fractin confirms the involvement of caspase-3. The present results demonstrate that the majority of axotomized dLGN projection neurons undergo apoptotic cell death, and they provide details about the initiation, duration, and cytological distribution of activated caspase-3 activity in injured dLGN projection neurons. All BDA-labeled neurons were examined with a brightfield microscope at a magnification of 1000X. Since the BDA labeling quality varied significantly among individual dLGN projection neurons, structural analysis was restricted to projection neurons that appeared to be completely labeled. Using the same criteria as described previously, the cell soma and dendrites of a neuron considered to be completely labeled 
with BDA and contained within a single 75 mm Albaspidin-AA section on a clean background without interference from other labeled neuronal profiles were analyzed. Observing these constraints stringently, completely labeled projection neurons in the dLGN were traced with the aid of a camera lucida drawing tube attachment.