Plasma level-dependent effects of methylphenidate on task-related functional magnetic resonance imaging signal changes

2005 ◽  
Vol 180 (4) ◽  
pp. 624-633 ◽  
Author(s):  
Ulrich Müller ◽  
J. Suckling ◽  
F. Zelaya ◽  
G. Honey ◽  
H. Faessel ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Plasma Level ◽  
Functional Magnetic Resonance Imaging ◽  
Functional Magnetic Resonance ◽  
Resonance Imaging ◽  
Magnetic Resonance Imaging Signal ◽  
Signal Changes

scholarly journals Contributions of structural connectivity and cerebrovascular parameters to functional magnetic resonance imaging signals in mice at rest and during sensory paw stimulation

2016 ◽  
Vol 37 (7) ◽  
pp. 2368-2382 ◽  
Author(s):  
Aileen Schroeter ◽  
Joanes Grandjean ◽  
Felix Schlegel ◽  
Bechara J Saab ◽  
Markus Rudin
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Functional Connectivity ◽  
Functional Magnetic Resonance Imaging ◽  
Diffusion Tensor ◽  
Structural Connectivity ◽  
Blood Oxygenation ◽  
Functional Magnetic Resonance ◽  
Resonance Imaging ◽  
Signal Changes

Previously, we reported widespread bilateral increases in stimulus-evoked functional magnetic resonance imaging signals in mouse brain to unilateral sensory paw stimulation. We attributed the pattern to arousal-related cardiovascular changes overruling cerebral autoregulation thereby masking specific signal changes elicited by local neuronal activity. To rule out the possibility that interhemispheric neuronal communication might contribute to bilateral functional magnetic resonance imaging responses, we compared stimulus-evoked functional magnetic resonance imaging responses to unilateral hindpaw stimulation in acallosal I/LnJ, C57BL/6, and BALB/c mice. We found bilateral blood-oxygenation-level dependent signal changes in all three strains, ruling out a dominant contribution of transcallosal communication as reason for bilaterality. Analysis of functional connectivity derived from resting-state functional magnetic resonance imaging, revealed that bilateral cortical functional connectivity is largely abolished in I/LnJ animals. Cortical functional connectivity in all strains correlated with structural connectivity in corpus callosum as revealed by diffusion tensor imaging. Given the profound influence of systemic hemodynamics on stimulus-evoked functional magnetic resonance imaging outcomes, we evaluated whether functional connectivity data might be affected by cerebrovascular parameters, i.e. baseline cerebral blood volume, vascular reactivity, and reserve. We found that effects of cerebral hemodynamics on functional connectivity are largely outweighed by dominating contributions of structural connectivity. In contrast, contributions of transcallosal interhemispheric communication to the occurrence of ipsilateral functional magnetic resonance imaging response of equal amplitude to unilateral stimuli seem negligible.

scholarly journals Effects of Hypoglycemia on Functional Magnetic Resonance Imaging Response to Median Nerve Stimulation in the Rat Brain

2000 ◽  
Vol 20 (9) ◽  
pp. 1352-1359 ◽  
Author(s):  
Richard P. Kennan ◽  
Ralph J. Jacob ◽  
Robert S. Sherwin ◽  
John C. Gore
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Functional Magnetic Resonance Imaging ◽  
Median Nerve ◽  
Nerve Stimulation ◽  
Plasma Glucose ◽  
Functional Magnetic Resonance ◽  
Resonance Imaging ◽  
Median Nerve Stimulation ◽  
Signal Changes

The authors studied the effects of a standardized mild-moderate hypoglycemic stimulus (glucose clamp) on brain functional magnetic resonance imaging (fMRI) responses to median nerve stimulation in anesthetized rats. In the baseline period (plasma glucose 6.6 ± 0.3 mmol/L), the MR signal changes induced by median nerve activation were determined within a fixed region of the somatosensory cortex from preinfusion activation maps. Subsequently, insulin and a variable glucose infusion were administered to decrease plasma glucose. The goal was to produce a stable hypoglycemic plateau (2.8 ± 0.2 mmol/L) for 30 minutes. Thereafter, plasma glucose was restored to euglycemic levels (6.0 ± 0.3 mmol/L). In the early phase of insulin infusion (15 to 30 minutes), before hypoglycemia was reached (4.7 ± 0.3 mmol/L), the activation signal was unchanged. However, once the hypoglycemic plateau was achieved, the activation signal was significantly decreased to 57 ± 6% of the preinfusion value. Control regions in the brain that were not activated showed no significant changes in MR signal intensity. Upon return to euglycemia, the activation signal change increased to within 10% of the original level. No significant activation changes were noted during euglycemic hyperinsulinemic clamp experiments. The authors concluded that fMRI can detect alterations in cerebral function because of insulin-induced hypoglycemia. The signal changes observed in fMRI activation experiments were sensitive to blood glucose levels and might reflect increases in brain metabolism that are limited by substrate deprivation during hypoglycemia.

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