• visual cortex
• VEP
• glioma
• epilepsy
• electrophysiology

In glioma patients, neural function in the affected brain areas may deteriorate with tumor progression. Neural manifestations (such as headache, sensory disturbances and seizures) often provide the first symptoms by which glioma is diagnosed. Furthermore, existing therapies to contrast glioma growth (including chemotherapy and radiotherapy) often contribute "per se" to the functional deterioration.
A pre-clinical model suited to evaluate neural functionality during glioma progression and following experimental anti-neoplastic treatment would be therefore essential, but nowadays is still missing.
In this thesis, I tried to establish a mouse glioma model in which a chronic electrode implantation allowed longitudinal recordings of neural activity in the awake animal. Visual cortex was chosen as a recording site since it can be easily activated by physiological stimuli, and for the presence of many well established parameters to evaluate its functionality.
Initially I described the properties of visual circuit in the awake animal, strongly different compared to the anesthetized condition. Temporal resolution was increased and responses were still present for stimuli with high temporal frequencies (till 12Hz). On the other hand for stimuli at lower temporal frequency several rebound oscillation succeeding the first component were present in the response. These late component can be related to the strong theta modulation present in the LFP during stimuli presentation.
A longitudinal evaluation of the responses in normal animals showed that VEP amplitudes for transient stimuli increased throughout the recording period (as a result of perceptual learning) whereas amplitudes for steady state and flash stimuli were stable. Conversely in glioma-bearing mice responses for all animals were gradually deteriorated with glioma progression. Moreover I evaluated longitudinally visual acuity, temporal resolution, and contrast threshold, and I found that visual acuity was primarily disrupted by glioma progression (rendering it a good parameter for glioma progression).
Finally I observed several epileptiform alterations in glioma bearing mice. I found both ictal and interictal events, with different typical waveforms. Notably some recordings were well resembling the spike-and-wave discharge recorded in humans during absence epilepsy.