Possible neurophysiological mechanisms for positive and negative BOLD contrast signals explored in rat sensory and cerebellar cortex.
Department of Clinical Neurophysiology, Glostrup Hospital and University of Copenhagen , Glostrup , Denmark .
One of the important problems in functional neuroimaging is how we translate the vascular and metabolic signals to basic neurophysiology. Not unexpectedly this relation has proven to be exceedingly complex. It appears that the positive going fMRI BOLD signals ‘the hot spots’ relate to increases in blood flow triggered by synaptic excitation of nerve cells, but low grades of stimulation may not give rise a detectable vascular signal despite of increases in activity, and excitation of inhibitory interneurons may give rise to a positive BOLD signal as well. Rises in intracellular calcium is a key co-factor for the synthesis of vasodilator substances, which produce the positive blood flow or BOLD contrast signal upon activation. It is also important to understand the basis of decreases in vascular or BOLD signals. Recent studies may suggest that increases in synaptic inhibition control the amplitude of the imaging signals by modulating the efficacy of excitatory neurotransmission, and by controlling the increases in intracellular calcium evoked by excitation. This illustrates the complexity of the physiological basis of the imaging signals. The presentation will summarize the hypothesis that brain activities, which predominantly involve deactivation or synaptic inhibition, may produce negative BOLD signals. I will discuss problems of context-sensitivity and non-linearity in transforming synaptic excitation and inhibition into a vascular and metabolic signal, and summarize the evidence which predicts that the interpretation of functional neuroimaging data in terms of basic neurophysiological function is not a simple task.