关键词：
Neurosciences
Pharmacology
摘要：
The mammalian olfactory bulb (OB) generates gamma (40 – 100 Hz) and beta (15 – 30 Hz) oscillations of the local field potential (LFP). Beta oscillations occur in response to odorants in learning or odor sensitization paradigms, but their generation mechanism is still poorly understood. When centrifugal inputs to the OB are blocked, beta oscillations disappear, but gamma oscillations persist. These inputs primarily target GABAergic granule cells (GC) in the GC layer (GCL) and regulate their excitability. This leads us to the central question motivating this work: What role does GC excitability play in generating beta oscillations? To answer this question we first developed a computational model incorporating the biophysical properties of the reciprocal dendrodendritic synapses between glutamatergic mitral cells (MC) and GCs. The model predicted that beta oscillations emerge only when inhibition of MCs, due to heightened GC excitability, and the excitation of MCs due to sensory input is sufficiently balanced. Because of this balance of excitation and inhibition, the model predicted that beta oscillations could also be supported in the absence of heightened GC excitability provided that the input strength was also low. The model also predicted that beta oscillations are sustained by voltage dependent calcium channel (VDCC) mediated GABA release, independently of NMDA channels. We tested the predictions of this model using pharmacology in the OBs of rats. Infusion of scopolamine, a muscarinic antagonist known to decrease GC excitability, decreased or completely suppressed odor-evoked beta in response to a strong stimulus, but increased beta power in response to a weak stimulus, as predicted by our model. APV, an NMDA receptor antagonist, suppressed gamma oscillations selectively (in OB and PC), lending support to the model’s prediction that beta oscillations can be supported by VDCC currents. In another set of experiments we recorded extracellular potentials in the GCL
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