Figure 6.

Proposed mechanism underlying the O₂ responses recorded after electrical stimulation of the ventral noradrenergic bundle (VNB). Temporal (upper) and spatial (lower) models are provided. Stimulation of the VNB induces norepinephrine release from noradrenergic cells originating in the nucleus of the solitary tract (NST) and A1 cell groups. Non-noradrenergic cell populations coursing near the coordinates of the stimulating electrode are also excited, leading to simultaneous release of other neurotransmitters within the ventral bed nucleus of the stria terminalis (vBNST). This overflow of norepinephrine and other vasoactive neurotransmitters causes dilation of local microvessels and a subsequent influx of O₂. The noradrenergic contribution to this response is mediated through activation of β-adrenoceptors either indirectly, by modulating local cell activity, or directly, by relaxation of vascular smooth muscle. Local O₂ concentrations continue to rise shortly after the stimulation ceases. Thereafter, a signaling cascade initiated by the synergistic activation of adrenoceptors on astrocytes results in the release of secondary messengers from astrocytic endfeet. These messengers act upon vessels to cause their constriction, and in turn, provide an active termination of the hyperemic response. As a result, O₂ levels transiently decrease before returning to baseline concentrations.