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This Article Full Text Full Text (PDF) All Versions of this Article: 102/3/1503    most recent 00289.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Thomsen, K. Articles by Lauritzen, M. PubMed PubMed Citation Articles by Thomsen, K. Articles by Lauritzen, M.

Principal Cell Spiking, Postsynaptic Excitation, and Oxygen Consumption in the Rat Cerebellar Cortex

¹Institute of Neuroscience and Pharmacology, University of Copenhagen, Copenhagen N; ²Department of Clinical Neurophysiology, Glostrup Hospital, University of Copenhagen, Glostrup, Denmark; and ³Atomic Energy Commission, Institute of Biomedical Imaging, Molecular Imaging Research Center, Fontenay-aux-Roses, France

Submitted 31 March 2009; accepted in final form 26 June 2009

Abstract

One contention within the field of neuroimaging concerns the character of the depicted activity: Does it represent neuronal action potential generation (i.e., spiking) or postsynaptic excitation? This question is related to the metabolic costs of different aspects of neurosignaling. The cerebellar cortex is well suited for addressing this problem because synaptic input to and spiking of the principal cell, the Purkinje cell (PC), are spatially segregated. Also, PCs are pacemakers, able to generate spikes endogenously. We examined the contributions to cerebellar cortical oxygen consumption (CMRO₂) of postsynaptic excitation and PC spiking during evoked and ongoing neuronal activity in the rat. By inhibiting excitatory synaptic input using ionotropic glutamate receptor blockers, we found that the increase in CMRO₂ evoked by parallel fiber (PF) stimulation depended entirely on postsynaptic excitation. In contrast, PC spiking was largely responsible for the increase in CMRO₂ when ongoing neuronal activity was increased by -aminobutyric acid type A receptor blockade. In this case, CMRO₂ increased equally during PC spiking with excitatory synaptic activity as during PC pacemaker spiking without excitatory synaptic input. Subsequent inhibition of action potential propagation and neurotransmission by blocking voltage-gated Na⁺-channels eliminated the increases in CMRO₂ due to PF stimulation and increased PC spiking, but left a large fraction of CMRO₂, i.e., basal CMRO₂, intact. In conclusion, whereas basal CMRO₂ in anesthetized animals did not seem to be related to neurosignaling, increases in CMRO₂ could be induced by all aspects of neurosignaling. Our findings imply that CMRO₂ responses cannot a priori be assigned to specific neuronal activities.