Using proton magnetic resonance imaging and spectroscopy to understand brain "activation"  

Oleh:

Baslow, Morris H. ; Guilfoyle, David N.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Brain and Language (Full Text) vol. 102 no. 2 (2007), page 153-164.
Topik: Cognition; Hyperemia; Metabotropic glutamate receptor 3; NAAG peptidase; N-Acetylaspartate: N-Acetylaspartylglutamate
Fulltext: 102_02_Baslow.pdf (256.9KB)

Isi artikel

Upon stimulation, areas of the brain associated with specific cognitive processing tasks may undergo observable physiological changes, and measures of such changes have been used to create brain maps for visualization of stimulated areas in task-related brain ‘‘activation’’ studies. These perturbations usually continue throughout the period of the stimulating event, and then subside when the event is terminated. In this communication, we consider the nature and meaning of these task-related brain activations. Since stimulation usually results in an increase in the frequency of neuron depolarizations or ‘‘spikes’’, an energy expensive activity that requires ATP for restoration of ionic gradients, additional energy supplies must be rapidly deployed to the stimulated areas or rates of re-polarization could be decreased, and refractory periods between spikes increased. As a result, maximum spiking rates may be decreased and some frequency-encoded information lost. The energy available to brain cells to re-synthesize ATP from ADP is a function of levels of glucose and oxygen in blood, and their availability to stimulated neurons is a function of the rate at which focal blood supplies can be increased (hyperemia). In this review we explore how neurons transmit meaningful encoded information; how the integrity of that information is dependent on a continuous supply of energy, and how proton magnetic imaging and spectroscopy may aid in understanding the process. Finally, evidence is presented that the neuropeptide, N-acetylaspartylglutamate, is a neuronal astrocyte-vascular feedback signal that regulates activation induced focal hyperemic responses.

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