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000163678 0247_ $$2doi$$a10.1016/j.neuroimage.2021.118769
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000163678 037__ $$aDZNE-2022-00424
000163678 041__ $$aEnglish
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000163678 1001_ $$0P:(DE-2719)2811871$$aArboit, Alberto$$b0$$eFirst author$$udzne
000163678 245__ $$aBrief neuronal afterdischarges in the rat hippocampus lead to transient changes in oscillatory activity and to a very long-lasting decline in BOLD signals without inducing a hypoxic state.
000163678 260__ $$aOrlando, Fla.$$bAcademic Press$$c2021
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000163678 520__ $$aThe effects of hippocampal neuronal afterdischarges (nAD) on hemodynamic parameters, such as blood-oxygen-level-dependent (BOLD) signals) and local cerebral blood volume (CBV) changes, as well as neuronal activity and metabolic parameters in the dentate gyrus, was investigated in rats by combining in vivo electrophysiology with functional magnetic resonance imaging (fMRI) or 1H-nuclear magnetic resonance spectroscopy (1H-NMRS). Brief electrical high-frequency pulse-burst stimulation of the right perforant pathway triggered nAD, a seizure-like activity, in the right dentate gyrus with a high incidence, a phenomenon that in turn caused a sustained decrease in BOLD signals for more than 30 min. The decrease was associated with a reduction in CBV but not with signs of hypoxic metabolism. nAD also triggered transient changes mainly in the low gamma frequency band that recovered within 20 min, so that the longer-lasting altered hemodynamics reflected a switch in blood supply rather than transient changes in ongoing neuronal activity. Even in the presence of reduced baseline BOLD signals, neurovascular coupling mechanisms remained intact, making long-lasting vasospasm unlikely. Subsequently generated nAD did not further alter the baseline BOLD signals. Similarly, nAD did not alter baseline BOLD signals when acetaminophen was previously administered, because acetaminophen alone had already caused a similar decrease in baseline BOLD signals as observed after the first nAD. Thus, at least two different blood supply states exist for the hippocampus, one low and one high, with both states allowing similar neuronal activity. Both acetaminophen and nAD switch from the high to the low blood supply state. As a result, the hemodynamic response function to an identical stimulus differed after nAD or acetaminophen, although the triggered neuronal activity was similar.
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000163678 650_7 $$2Other$$a1H-NMR spectroscopy
000163678 650_7 $$2Other$$aElectrophysiology
000163678 650_7 $$2Other$$aGamma oscillations
000163678 650_7 $$2Other$$aNegative BOLD
000163678 650_7 $$2Other$$aPostictal state
000163678 650_2 $$2MeSH$$aAnimals
000163678 650_2 $$2MeSH$$aBrain Waves: drug effects
000163678 650_2 $$2MeSH$$aBrain Waves: physiology
000163678 650_2 $$2MeSH$$aDisease Models, Animal
000163678 650_2 $$2MeSH$$aElectrocorticography
000163678 650_2 $$2MeSH$$aHippocampus: drug effects
000163678 650_2 $$2MeSH$$aHippocampus: physiology
000163678 650_2 $$2MeSH$$aMagnetic Resonance Imaging
000163678 650_2 $$2MeSH$$aMale
000163678 650_2 $$2MeSH$$aNeuroimaging
000163678 650_2 $$2MeSH$$aNeurovascular Coupling: drug effects
000163678 650_2 $$2MeSH$$aNeurovascular Coupling: physiology
000163678 650_2 $$2MeSH$$aProton Magnetic Resonance Spectroscopy
000163678 650_2 $$2MeSH$$aRats
000163678 650_2 $$2MeSH$$aRats, Wistar
000163678 650_2 $$2MeSH$$aSeizures: metabolism
000163678 650_2 $$2MeSH$$aSeizures: physiopathology
000163678 7001_ $$aKu, Shih-Pi$$b1
000163678 7001_ $$0P:(DE-2719)2278716$$aKrautwald, Karla$$b2$$udzne
000163678 7001_ $$0P:(DE-2719)2810456$$aAngenstein, Frank$$b3$$eLast author$$udzne
000163678 773__ $$0PERI:(DE-600)1471418-8$$a10.1016/j.neuroimage.2021.118769$$gVol. 245, p. 118769 -$$p118769$$tNeuroImage$$v245$$x1053-8119$$y2021
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