GABA-ergic Modulation of Prefrontal Spatio-temporal Activation Pattern during Emotional Processing: A Combined fMRI/MEG Study with Placebo and Lorazepam

Abstract

Various prefrontal cortical regions have been shown to be activated during emotional stimulation, whereas neurochemical mechanisms underlying emotional processing in the prefrontal cortex remain unclear. We therefore investigated the influence of the GABA-A potentiator lorazepam on prefrontal cortical emotional-motor spatio-temporal activation pattern in a combined functional magnetic resonance imaging/magnetoencephalography study. Lorazepam led to the reversal in orbito-frontal activation pattern, a shift of the early magnetic field dipole from the orbito-frontal to medial prefrontal cortex, and alterations in premotor/motor cortical function during negative and positive emotional stimulation. It is concluded that negative emotional processing in the orbito-frontal cortex may be modulated either directly or indirectly by GABA-A receptors. Such a modulation of orbito-frontal cortical emotional function by lorazepam has to be distinguished from its effects on cortical motor function as being independent from the kind of processing either emotional or nonemotional.

Modulation of human risky decision making by flunitrazepam

“…Deakin et al (2004) demonstrated that compared to a placebo group, 20 mg diazepam produced an increase in the amount wagered on the riskiest trial type (e.g., lower chance to win, but higher payoff, thus having the greatest risk/benefit conflict). Northoff et al (2002) showed that administration of lorazepam modulated activity in the orbitofrontal cortex during processing of negative emotional stimuli. Several studies have shown alcohol-induced changes in risky decision making (George et al 2005;Lane et al 2004;Roehrs et al 2004;Stoner et al 2006).…”

Reciprocal modulation and attenuation in the prefrontal cortex: An fMRI study on emotional–cognitive interaction

“…Neural correlates and functional mechanisms underlying these interactions remain unclear. Lesion and functional imaging studies have predominantly related emotional processing to medial prefrontal cortical regions, such as the ventro-and dorsomedial prefrontal cortex (VMPFC, DMPFC) as well as the medial orbitofrontal cortex (MOFC) [Damasio, 1999;Davidson and Irwin, 1999;Northoff et al, 2000Northoff et al, , 2002Phan et al, 2002]. In contrast, cognitive tasks have been implicated in the activation of lateral prefrontal cortical regions, such as the ventro-and dorsolateral prefrontal cortex (VLPFC, DLPFC) and adjacent lateral prefrontal cortical regions [see Duncan and Owen, 2000 for an overview].…”

How Does Our Brain Constitute Defense Mechanisms? First-Person Neuroscience and Psychoanalysis

“…Finally neurochemical challenge studies during emotional stimulation, for example with lorazepam that relieves the acute catatonic state [61, 62], might also be of interest. This is especially so given the fact that lorazepam in healthy subjects modulates neural activity in those regions (the orbitofontal cortex) [74] that are altered in catatonia.…”

“…In other studies right hemispheric dysfunction in the lateral parietal cortex was observed to correlate with spatial deficits [105]. The exact relationship between the midline and the right lateral parietal cortical changes, however, remains unclear [74.] What is ultimately needed are studies that link the different subjective experiences and their different individual contents in catatonic and hysterical conversion to different though probably overlapping neural networks with specific patterns of increased and decreased functional connectivity.…”