Cellular and subcellular localization of γ-aminobutyric acidB receptors in the rat olfactory bulb
Section snippets
Acknowledgements
We thank Dr. Jean-Marc Fritschy (University of Zürich) for his comments on the manuscript. This work was supported by the Italian M.U.R.S.T.
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Aversive Learning Increases Release Probability of Olfactory Sensory Neurons
2020, Current BiologyCitation Excerpt :To test this possibility, future experiments would require activating adjacent glomeruli individually while recording from their postsynaptic cells. Although the immunostaining experiments shown in Figure 5 do not differentiate GABAB receptors on the pre- or postsynaptic cells, previous studies using immuno-electron microscopy demonstrate that GABAB-positive neuropils within glomeruli are predominantly axon terminals of the olfactory nerve [35, 36]. These GABAB receptors mediate presynaptic inhibition and suppress glutamate release from OSNs, supported by ex vivo as well as in vivo pharmacological studies [12–17].
Carbonic anhydrase I, II, and VI, blood plasma, erythrocyte and saliva zinc and copper increase after repetitive transcranial magnetic stimulation
2010, American Journal of the Medical SciencesPhysiology of the Main Olfactory Bulb
2008, The Senses: A Comprehensive ReferenceAn argument for an olfactory thalamus
2007, Trends in NeurosciencesSensory-Evoked Intrinsic Optical Signals in the Olfactory Bulb Are Coupled to Glutamate Release and Uptake
2006, NeuronCitation Excerpt :To our knowledge, our data, together with reports from Wachowiak et al. (2005) and Vucinic et al. (2006), are some of the first direct evidence that GABA-B receptors are activated by normal sensory-evoked activity in the olfactory bulb and that these receptors serve to limit transmission of sensory signals. We believe GABA-B and DA agonists to be acting presynaptically on ORN terminals because glomeruli express D2 and GABA-B receptors presynaptically (McLean and Shipley, 1988; Coronas et al., 1997; Duchamp-Viret et al., 1997; Bonino et al., 1999; Koster et al., 1999; Gutierrez-Mecinas et al., 2005). It remains possible that the small component that was not suppressed by these agonists reflects a release-independent component of the IOS (e.g., one due to some other mechanism of coupling of presynaptic action potentials).
Coding and synaptic processing of sensory information in the glomerular layer of the olfactory bulb
2006, Seminars in Cell and Developmental Biology