Background: Experimental studies have yielded a wealth of information related to the pathological mechanism of optic nerve injury. However, there is no suitable animal model to study intracranial optic nerve injury.
Aim: To establish an experimental model of acute optic nerve injury.
Material and methods: We established an animal model of acute intracranial optic nerve injury using the classic pterional approach in cats and investigated electrophysiological and ultrastructural changes. We applied immunohistochemical staining to examine the expression of glial fibrillary acid protein, neurofilament protein, myelin basic protein pre- and post-injury.
Results: We successfully established an animal model of acute intracranial optic nerve injury.
Conclusion: The pathological processes of acute optic nerve injury may involve the following series of steps. Direct mechanical injury of the optic nerve leads to the death of oligodendrocytes in the optic nerve, which consequently results in optic nerve demyelination. Following optic nerve injury, the astrocytes in the injured area die and produce excitatory amino acids, which have an adverse effect on neurons, resulting in the proliferation and activation of astrocytes. The astrocytes can absorb the glutamic acid and transform it into atoxic glutamine. The glutamic acid can then injure retinal ganglion cells, resulting in the reduction of neurofilament proteins in the axons. We believe that the application of the pterional approach to establish optic nerve injury animal models has both a clinical and theoretical basis.