Involvement of the inferior frontal junction in cognitive control: meta-analyses of switching and Stroop studies

There is growing evidence that a specific region in the posterior frontolateral cortex is involved intimately in cognitive control processes. This region, located in the vicinity of the junction of the inferior frontal sulcus and the inferior precentral sulcus, was termed the inferior frontal junction (IFJ). The IFJ was shown to be involved in the updating of task representations and to be activated commonly in a within-subject investigation of a task-switching paradigm, the Stroop task, and a verbal n-back task. Here, we investigate the involvement of the IFJ in cognitive control by employing a meta-analytic approach. Two quantitative meta-analyses of functional magnetic resonance imaging (fMRI) studies were conducted. One meta-analysis included frontal activations from task-switching, set-shifting, and stimulus-response (S-R) reversal studies, the other included frontal activations from color-word Stroop studies. Results showed highly significant clustering of activations in the IFJ in both analyses. These results provide strong evidence for the consistent involvement of the IFJ in both switching and Stroop paradigms. Furthermore, they support our concept of areal specialization in the frontolateral cortex, which posits that it is not only the middorsolateral part that plays an important role in cognitive control, but also the IFJ. Finally, our results demonstrate how quantitative meta-analyses can be used to test hypotheses about the involvement of specific brain regions in cognitive control.     

Internally generated and directly cued task sets: an investigation with fMRI

It is widely acknowledged that the prefrontal cortex (PFC) plays a major role for goal-directed behaviour. In this context it is usually necessary to coordinate environmental information and internally represented intentions. Such goal-directed "endogenous control processes" can be investigated with the task-switching paradigm in which participants are required to alternate between different tasks. In the present study, we aimed at investigating different degrees of endogenous control by introducing two cue types with varying directness of the cue-task association. The "transition cues" informed the participants about repeating or switching the task but not about the task identity. Contrary to that, the "task cues" were directly associated with the upcoming task set. Since the transition cues are not directly associated with the task set they should require a higher demand of endogenous control than the task cues. The comparison of both cue types revealed frontolateral as well as frontomedian activations for the transition cue. We assume that the frontolateral activation reflects the coordination of information within working memory (WM) and the frontomedian cortex reflects the higher demand for endogenous control. Furthermore, regions of interest (ROIs) analyses indicate an important role for anterior regions along the left inferior frontal sulcus and frontomedian wall. This is suggested to reflect a functional gradient in anterior-posterior direction which is linked to the relative degree of required endogenous control.     

Middle cerebral artery blood velocity and cerebral blood flow in sickle cell disease

To understand better the relationship between blood velocity measured by transcranial Doppler and cerebral blood flow measured by the 133Xe inhalation method, we examined 23 patients undergoing evaluation in the Comprehensive Sickle Cell Center at Columbia University. Blood velocity in the middle cerebral artery was directly related to cerebral flow (r = 0.77; p less than 0.05). A multivariate analysis in this sample made it possible to improve this correlation to account for more than 90% of the variability in cerebral blood flow by the use of transcranial Doppler measures of velocity and pulsatility along with the patient's age and hematocrit (r = 0.95; p less than 0.001). It is likely that the combination of Doppler and clinical or demographic variables in other diseases will similarly improve the quantitative estimation of cerebral blood flow.     

Effect of clofibrate treatment on hepatic prostaglandin catabolism and action

Prostaglandins (PG) modulate hepatocyte glucose and lipid metabolism. Hepatocytes rapidly metabolize PG via beta-oxidation, terminating PG action. Clofibrate induces hepatic peroxisomal beta-oxidative activity, for which PG are substrates. To determine the effect of clofibrate-treatment on liver PG metabolism and action, hepatocytes were isolated from rats maintained on a control or clofibrate-supplemented (0.5%) diet for 7 to 9 days. Rates of PG catabolism were determined by high performance liquid chromatography resolution of [3H]PG from [3H]metabolites. Clofibrate treatment enhanced the rates of PGE2, PGF2, and PGD2 degradation by 85%, 278% and 137%, respectively. Rates of PG degradation were correlated with hepatocyte carnitine acetyltransferase activity, a marker of peroxisomal proliferation. Further evidence of enhanced hepatocyte peroxisomal beta-oxidation of PG after clofibrate-treatment was obtained by confirming loss of the 1-position carbon from [1-14C]PGE2 during PGE2 metabolism and failure of the carnitine acyltransferase inhibitor acetyl-DL-aminocarnitine to inhibit PGE2 metabolism. Associated with the faster degradation of PGE2 by hepatocytes from clofibrate-treated rats was loss of inhibition of hepatocyte glucagon-stimulated glycogenolysis by exogenous PGE2. Thus, clofibrate's induction of peroxisomal beta-oxidation is associated with accelerated catabolism of PG and decreased PG action. Alterations in PG breakdown provide a mechanism for modulating hepatic PG effects.