Spreading depression in the olfactory bulb of rats: Reliable initiation and boundaries of propagation

Spreading depression in the olfactory bulb of rats is an elusive phenomenon, the demonstration of which requires specific conditioning procedures. The present paper describes a simple technique for reliable initiation of bulbar spreading depression with microinjections of potassium acetate. Adult hooded rats were anesthetized with pentobarbital (50 mg/kg) and slow potential changes accompanying spreading depression were recorded with capillary microelectrodes stereotaxically inserted into the olfactory bulb and adjacent forebrain structures. KCl microinjection (0.5–1.0 μl, 0.134–0.670 mol/l) into the olfactory bulb elicited local depolarization which only exceptionally developed into a propagating spreading depression. Potassium acetate (0.5–1.0 μl, 0.15 mol/l) injected into the rostral olfactory bulb evoked a negative slow potential wave (amplitude of around 25 mV and duration 30–50 s) propagating at a rate of 3–4 mm/min through all the olfactory bulb layers. Low positive (5 mV) instead of negative waves were recorded in the superficial olfactory nerve layer with reversal in the glomerular layer (200–300 μm). The slow potential decreased in the rostrocaudal direction and expired at the caudal boundary of the olfactory bulb. Bulbar spreading depression never spread to neocortex, and cortical spreading depression never entered into the olfactory bulb but stopped in the anterior olfactory nucleus 7 mm rostral to bregma. Repeated potassium acetate injections into the olfactory bulb occasionally elicited a series of spreading depression waves recurring at regular intervals, probably reflecting reverberation of scroll-shaped waves around the rostrocaudal axis of the olfactory bulb. It is argued that the low susceptibility of the olfactory bulb to spreading depression is due to powerful GABAergic inhibition which can be weakened by (Cl −) e reduction after potassium acetate injections.