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The Journal of Neuroscience, June 13, 2007, 27(24):6452-6460; doi:10.1523/JNEUROSCI.3141-06.2007

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Cellular/Molecular
The Relationship between Blood Flow and Neuronal Activity in the Rodent Olfactory Bulb

Emmanuelle Chaigneau,^1,2 Pascale Tiret,^1,2 * Jérôme Lecoq,^1,2 * Mathieu Ducros,^1,2 Thomas Knöpfel,³ and Serge Charpak^1,2

¹Institut National de la Santé et de la Recherche Médicale U603, 75006 Paris, France, ²Laboratory of Neurophysiology, Université Paris Descartes, 75006 Paris, France, and ³Laboratory for Neural Circuit Dynamics, Riken Brain Science Institute, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan

Correspondence should be addressed to Serge Charpak, Institut National de la Santé et de la Recherche Médicale U603, Laboratory of Neurophysiology, 45 rue des St Pères, 75006 Paris, France. Email: serge.charpak{at}univ-paris5.fr

In the brain, neuronal activation triggers an increase in cerebral blood flow (CBF). Here, we use two animal models and several techniques (two-photon imaging of CBF and neuronal calcium dynamics, intracellular and extracellular recordings, local pharmacology) to analyze the relationship between neuronal activity and local CBF during odor stimulation in the rodent olfactory bulb. Application of glutamate receptor antagonists or tetrodotoxin directly into single rat olfactory glomeruli blocked postsynaptic responses but did not affect the local odor-evoked CBF increases. This suggests that in our experimental conditions, odor always activates more than one glomerulus and that silencing one of a few clustered glomeruli does not affect the vascular response. To block synaptic transmission more widely, we then superfused glutamate antagonists over the surface of the olfactory bulb in transgenic G-CaMP2 mice. This was for two reasons: (1) mice have a thin olfactory nerve layer compared to rats and this will favor drug access to the glomerular layer, and (2) transgenic G-CaMP2 mice express the fluorescent calcium sensor protein G-CaMP2 in mitral cells. In G-CaMP2 mice, odor-evoked, odor-specific, and concentration-dependent calcium increases in glomeruli. Superfusion of glutamate receptor antagonists blocked odor-evoked postsynaptic calcium signals and CBF responses. We conclude that activation of postsynaptic glutamate receptors and rises in dendritic calcium are major steps for neurovascular coupling in olfactory bulb glomeruli.

Key words: two-photon microscopy; olfactory bulb; neurovascular coupling; field potential; mitral cell; blood flow

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Received July 24, 2006; revised May 2, 2007; accepted May 4, 2007.

Correspondence should be addressed to Serge Charpak, Institut National de la Santé et de la Recherche Médicale U603, Laboratory of Neurophysiology, 45 rue des St Pères, 75006 Paris, France. Email: serge.charpak{at}univ-paris5.fr

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