Abstract
Unambiguously identifying an epileptic focus with high spatial resolution is a challenge, especially when no anatomic abnormality can be detected. Neurovascular coupling (NVC)-based brain mapping techniques are often applied in the clinic despite a poor understanding of ictal NVC mechanisms, derived primarily from recordings in anesthetized animals with limited spatial sampling of the ictal core. In this study, we used simultaneous wide-field mesoscopic imaging of GCamp6f and intrinsic optical signals (IOS) to record the neuronal and hemodynamic changes during acute ictal events in awake, behaving mice. Similar signals in isoflurane-anesthetized mice were compared to highlight the unique characteristics of the awake condition. In awake animals, seizures were more focal at the onset but more likely to propagate to the contralateral hemisphere. The HbT signal, derived from an increase in cerebral blood volume (CBV), was more intense in awake mice. As a result, the “epileptic dip” in hemoglobin oxygenation became inconsistent and unreliable as a mapping signal. Our data indicate that CBV-based imaging techniques should be more accurate than blood oxygen level dependent (BOLD)-based imaging techniques for seizure mapping in awake behaving animals.
Highlights
Neurovascular coupling (NVC) describes the intimate relationship between neuronal activation and the resulting rise in cerebral blood flow (Kocharyan et al, 2008)
Ictal events were recorded with local field potential (LFP) electrodes from both awake and isoflurane-anesthetized mice and the waveforms were similar in morphology (Figure 1)
The initial spike showed a rapid increase in calcium amplitude, which reached its peak at 0.318 ± 0.081 s (Figure 1A)
Summary
Neurovascular coupling (NVC) describes the intimate relationship between neuronal activation and the resulting rise in cerebral blood flow (Kocharyan et al, 2008). In epilepsy patients, NVC can break down or be altered as a result of chronic structural, chemical, or metabolic alteration in brain tissue A detailed understanding of NVC during seizure activity requires techniques that can simultaneously measure both electrical and hemodynamic activity with high spatiotemporal resolution and widespread spatial sampling. Such a combination does not yet exist in clinical practice. Current knowledge of NVC during seizure activity derives predominantly from animal models recorded under general anesthesia
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