Spreading depression (SD) is a concerted, massive neuronal/glial depolarization propagating within the gray matter. Being associated with cerebropathology such as cerebral ischemia or hemorrhage, epilepsy, and migraine, it is well studied in cortex and hippocampus. Less is known, however, about the susceptibility of the brainstem to hypoxia-induced spreading depression (HSD), which could critically interfere with cardio-respiratory control. In rat brainstem slices, severe hypoxia triggered HSD episodes within minutes. The sudden extracellular DC potential shift of approximately -20 mV showed the typical profile known from other brain regions and was accompanied by an intrinsic optical signal (IOS). Spatiotemporal IOS analyses revealed that in infant brainstem, HSD was preferably ignited within the spinal trigeminal nucleus and spread out mostly medially invading the hypoglossal nucleus, the nucleus of the solitary tract (NTS), and occasionally also the ventral respiratory group (VRG). The neuronal hypoxic depolarizations underlying the generation of HSD were massive, but incomplete, and the propagation velocity of HSD and the associated extracellular K⁺ rise were less marked than in other brain regions. In adult brainstem, HSD was mostly confined to the NTS; its occurrence was facilitated by hypotonic solutions, but not by glial poisoning or block of GABAergic and glycinergic synapses.

Supported by the Deutsche Forschungsgemeinschaft (CMPB) and BCCN.