Appraising the brain's energy budget

Raichle, Marcus E.; Gusnard, Debra A.

doi:10.1073/pnas.172399499

Cited by 666 publications

(442 citation statements)

References 35 publications

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“…Furthermore, the ability of MK-801, given alone or prior to NMDA, to significantly reduce k* for AA by 16-49%, suggests that NMDA-initiated PLA 2 activation contributes substantially to the baseline release of AA in control brain. This interpretation is consistent with evidence that glutamatergic receptors constitute about 75% of the synapses in the mammalian cortex, and that many of these synapses include NMDARs (Braitenberg and Schüz, 1998;Fonnum, 1984;Raichle and Gusnard, 2002).…”

Section: Discussionsupporting

confidence: 90%

Chronic Lithium Chloride Administration Attenuates Brain NMDA Receptor-Initiated Signaling via Arachidonic Acid in Unanesthetized Rats

Basselin

Chang

Bell

et al. 2005

Neuropsychopharmacol

106

132

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It has been proposed that lithium is effective in bipolar disorder (BD) by inhibiting glutamatergic neurotransmission, particularly via N-methyl-D-aspartate receptors (NMDARs). To test this hypothesis and to see if the neurotransmission could involve the NMDARmediated activation of phospholipase A 2 (PLA 2 ), to release arachidonic acid (AA) from membrane phospholipid, we administered subconvulsant doses of NMDA to unanesthetized rats fed a chronic control or LiCl diet. We used quantitative autoradiography following the intravenous injection of radiolabeled AA to measure regional brain incorporation coefficients k* for AA, which reflect receptormediated activation of PLA 2 . In control diet rats, NMDA (25 and 50 mg/kg i.p.) compared with i.p. saline increased k* significantly in 49 and 67 regions, respectively, of the 83 brain regions examined. The regions affected were those with reported NMDARs, including the neocortex, hippocampus, caudate-putamen, thalamus, substantia nigra, and nucleus accumbens. The increases could be blocked by pretreatment with the specific noncompetitive NMDA antagonist MK-801 ((5R,10S)-( + )-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine hydrogen maleate) (0.3 mg/kg i.p.), as well by a 6-week LiCl diet sufficient to produce plasma and brain lithium concentrations known to be effective in BD. MK-801 alone reduced baseline values for k* in many brain regions. The results show that it is possible to image NMDA signaling via PLA 2 activation and AA release in vivo, and that chronic lithium blocks this signaling, consistent with its suggested mechanism of action in BD.

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Section: Discussionsupporting

confidence: 90%

Chronic Lithium Chloride Administration Attenuates Brain NMDA Receptor-Initiated Signaling via Arachidonic Acid in Unanesthetized Rats

Basselin

Chang

Bell

et al. 2005

Neuropsychopharmacol

106

132

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“…This is consistent with a low abundance of DA synapses compared with a high (70%) abundance of glutamatergic synapses in rat brain (Fonnum, 1984;Raichle and Gusnard, 2002). Thus, baseline values of k* for AA in rat brain are decreased 20% to 50% following administration of MK-801, which blocks Ca 2 + -mediated activation of cPLA 2 via the ionotropic NMDA receptor (Basselin et al, 2005a;Dumuis et al, 1988;Weichel et al, 1999).…”

Section: Discussionsupporting

confidence: 76%

D-Amphetamine Stimulates D₂Dopamine Receptor-Mediated Brain Signaling Involving Arachidonic Acid in Unanesthetized Rats

Bhattacharjee

Chang

White

et al. 2006

J Cereb Blood Flow Metab

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In rat brain, dopaminergic D 2 -like but not D 1 -like receptors can be coupled to phospholipase A 2 (PLA 2 ) activation, to release the second messenger, arachidonic acid (AA, 20:4n-6), from membrane phospholipids. In this study, we hypothesized that D-amphetamine, a dopamine-releasing agent, could initiate such AA signaling. The incorporation coefficient, k* (brain radioactivity/integrated plasma radioactivity) for AA, a marker of the signal, was determined in 62 brain regions of unanesthetized rats that were administered i.p. saline, D-amphetamine (2.5 or 0.5 mg/kg i.p.), or the D 2 -like receptor antagonist raclopride (6 mg/kg, i.v.) before saline or 2.5 mg/kg D-amphetamine. After injecting [1-14 C]AA intravenously, k* was measured by quantitative autoradiography. Compared to saline-treated controls, D-amphetamine 2.5 mg/kg i.p. increased k* significantly in 27 brain areas rich in D 2 -like receptors. Significant increases were evident in neocortical, extrapyramidal, and limbic regions. Pretreatment with raclopride blocked the increments, but raclopride alone did not alter baseline values of k*. In independent experiments, D-amphetamine 0.5 mg/kg i.p. increased k* significantly in only seven regions, including the nucleus accumbens and layer IV neocortical regions. These results indicate that D-amphetamine can indirectly activate brain PLA 2 in the unanesthetized rat, and that activation is initiated entirely at D 2 -like receptors. D-Amphetamine's lowdose effects are consistent with other evidence that the nucleus accumbens, considered a reward center, is particularly sensitive to the drug.

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“…Since increased neural activity in the activated network would require increased rCBF and oxygen consumption (CMRO2), and since the total metabolism of the brain is approximately constant over a wide range of mental and motor activities (Raichle and Gusnard 2002), increased rCBF in the activated network might require a synchronous decrease of rCBF in adjacent regions of the brain (i.e. a hemodynamic response).…”

Section: Discussionmentioning

confidence: 99%

Common deactivation patterns during working memory and visual attention tasks: An intra‐subject fMRI study at 4 Tesla

Tomasi¹,

Ernst²,

Caparelli³

et al. 2006

Human Brain Mapping

197

143

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This parametric functional magnetic resonance imaging (fMRI) study investigates the balance of negative, and positive fMRI signals in the brain. A set of visual attention (VA) and of working memory (WM) tasks with graded levels of difficulty was used to deactivate separate, but overlapping networks that include the frontal, temporal, occipital, and limbic lobes; regions commonly associated with auditory and emotional processing. Brain activation (% signal change, and volume) was larger for VA tasks than for WM tasks, but deactivation was larger for WM tasks. BOLD responses crosscorrelated strongly in the deactivated network during VA but less so during WM. The variability of the deactivated network across different cognitive tasks supports the hypothesis that global CBF vary across different tasks, but not between conditions of the same task. The task-dependent balance of activation and deactivation might allow maximization of resources for the activated network.

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Appraising the brain's energy budget

Cited by 666 publications

References 35 publications

Chronic Lithium Chloride Administration Attenuates Brain NMDA Receptor-Initiated Signaling via Arachidonic Acid in Unanesthetized Rats

Chronic Lithium Chloride Administration Attenuates Brain NMDA Receptor-Initiated Signaling via Arachidonic Acid in Unanesthetized Rats

D-Amphetamine Stimulates D₂Dopamine Receptor-Mediated Brain Signaling Involving Arachidonic Acid in Unanesthetized Rats

Common deactivation patterns during working memory and visual attention tasks: An intra‐subject fMRI study at 4 Tesla

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Appraising the brain's energy budget

Cited by 666 publications

References 35 publications

Chronic Lithium Chloride Administration Attenuates Brain NMDA Receptor-Initiated Signaling via Arachidonic Acid in Unanesthetized Rats

Chronic Lithium Chloride Administration Attenuates Brain NMDA Receptor-Initiated Signaling via Arachidonic Acid in Unanesthetized Rats

D-Amphetamine Stimulates D2Dopamine Receptor-Mediated Brain Signaling Involving Arachidonic Acid in Unanesthetized Rats

Common deactivation patterns during working memory and visual attention tasks: An intra‐subject fMRI study at 4 Tesla

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About

D-Amphetamine Stimulates D₂Dopamine Receptor-Mediated Brain Signaling Involving Arachidonic Acid in Unanesthetized Rats