INTRODUCTION: Over the past decade, we and other groups have shown that ketamine and other NMDA receptor antagonists evoke high‑frequency oscillations (HFO; 130‑180 Hz) in a variety of rodent cortical and subcortical regions. AIM(S): Our recent studies show that the olfactory bulb (OB) appears to be particularly important for the generation of this activity. To date, this activity has mainly been recorded in awake rats; however, there is some evidence that fast oscillation can be recorded in the OB of rodents under ketamine xylazine anesthesia. METHOD(S): LFPs in the OB were recorded using twisted stainless-steel electrodes in rats under ketamine 100 mg/kg + xylazine 10 mg/kg anesthesia (KX) or a subanesthetic dose of ketamine 20 mg/kg. In a second study, rats were implanted with thermocouples for simultaneous recording of nasal respiration and LFPs in the OB. In a third study, 32 channel silicon probes were used to record LFPs under KX. KX was associated with the emergence of a fast oscillations, around 120 Hz (which we termed KX-HFO) that occurred in bursts nested on slower oscillations. This is similar to HFO that occurs in awake rats following subanesthetic doses of ketamine. KX‑HFO were attenuated by unilateral naris blockade and reversed phase close to the mitral layer – also similar to the awake state. RESULTS: Simultaneous recordings from the nasal cavity (with thermocouples) and LFPs showed that KX-HFO was tightly coupled to nasal respiration, around 2 Hz. Spatial profile of LFPs recorded across the OB revealed strong HFO current sources close to the mitral layer that was preceded by a large current sink (around 2 Hz) more ventrally (in the extraplexiform/glomerular layers). CONCLUSIONS: Nasal respiration drives afferent input to the OB that produces corresponding large current sinks (local depolarization) in the OB which under KX anesthesia (and more generally NMDAR blockade) leads to the emergence of HFO by stimulating mitral/ tufted neurons at their apical dendrites.
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