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Brain O2 Levels

Glutamate is ubiquitous throughout the brain and serves as the primary excitatory neurotransmitter. Neurons require energy to fire, and energetic substrates, such as O2 and glucose, are renewed via cerebral blood flow, CBF, to maintain metabolic homeostasis.

Magnetic resonance brain functionality studies rely on the assumption that CBF and neuronal activity are coupled consistently throughout the brain. However, the origin of neuronal activity does not always coincide with signals indicative of energy consumption, for example O2 decreases, at high spatial resolutions. Therefore, relationships between excitatory neurotransmission and energy use must be evaluated at higher resolutions.

In a study published in ACS Chemical Neuroscience, researchers in the Wightman Group show that both endogenously released and exogenously ejected glutamate decrease local tissue O2 concentrations, but whether hyperemic O2 restoration followed depended on the stimulus method. Electrically stimulating the glutamatergic corticostriatal pathway evoked biphasic O2 responses at striatal terminals. First O2 decreased, then concentrations increased above baseline. Using iontophoresis to locally eject ionotropic glutamate receptor antagonists revealed that these receptors only influenced the O2 decrease.

The group members compared electrical stimulation to iontophoretic glutamate stimulation, and measured concurrent single-unit activity and O2 to limit both stimulation and recordings to <50 ┬Ám radius from our sensor. Similarly, iontophoretic glutamate delivery elicited monophasic O2 decreases without subsequent increases. This technique serves as a starting point for investigating spatially targeted cerebrovascular coupling as it relates to glutamate elicited neurotransmission and O2 responses.