Spectroscopic measurement of cortical nitric oxide release induced by ascending activation

- We report in vivo changes on nitric oxide (NO) dynamics in the cat cortex.
- The stimulation of ascendant systems, BS and BF, increments cortical NO levels.
- The systemic blockade of NO production abolished the observed responses to BS.
- Responses to BF stimulation are less affected by blockade of NO production.
- These findings suggest that NO collaborates in the modulation of cortical activity.

The transition from sleep to the awake state is regulated by the activation of subcortical nuclei of the brainstem (BS) and basal forebrain (BF), releasing acetylcholine and glutamate throughout the cortex and inducing a tonic state of neural activity. It has been suggested that such activation is also mediated by the massive and diffuse cortical release of nitric oxide (NO). In this work we have combined the spectroscopic measurement of NO levels in the somatosensory cortex of the cat through its marker methemoglobin, as well as two other hemodynamic markers (oxyhemoglobin - oxyHb - and deoxyhemoglobin - deoxyHb), together with the electrical stimulation of BS and BF - to induce an experimental transition from a sleep-like state to an awake-like mode. The results show an increase of NO levels either after BS or BF activation. The response induced by BS stimulation was biphasic in the three studied markers, and lasted for up to 30 s. The changes induced by BF were monophasic lasting for up to 20 s. The systemic blockade of NO production abolished the observed responses to BS whereas responses to BF stimulation were much less affected. These results indicate a crucial role for NO in the neuronal activation induced by the ascending systems.