Search

The anorexigenic gastrointestinal hormone Peptide YY plays an important role in the communication between the gastrointestinal tract and the central nervous system. PYY has been shown to modulate brain activity in regions implicated in reward and food related behavior. Its effects on brain structure however, remain unknown. Voxel-based morphometry was used to investigate the relationship between fasting and postprandial plasma PYY concentrations and regional gray matter volume (GMV). For this analysis twenty adult, non diabetic Caucasians were included (18F/2M, age 31±9 y, percentage of body fat [PFAT] 32±8%) who had volumetric brain magnetic resonance images and underwent H(2)(15)O positron emission tomographic (PET) measurements of regional cerebral blood flow (rCBF), a marker of local neuronal activity, and measurements of plasma total PYY, prior to (fasting) and following a satiating liquid meal. Voxel-wise analysis revealed a regional positive association between postprandial PYY and gray matter volume bilaterally in the caudate nuclei. These associations remained significant (p<0.05) after small volume correction for multiple comparisons. Based on these findings we investigated whether postprandial PYY is associated with PET measured rCBF of the caudate nucleus. We found a significant negative association between average postprandial caudate rCBF and postprandial plasma PYY concentrations (r=-0.60, p<0.02, age, sex and PFAT adjusted). Average postprandial caudate rCBF was also negatively associated with rCBF in the right medial orbitofrontal cortex and the right hippocampal formation (p<0.05, corrected for multiple comparisons). Total PYY is positively associated with gray matter but negatively with postprandial activity in the caudate nuclei while caudate activity is negatively associated with rCBF in prefrontal and paralimbic regions implicated in reward behavior. Thus, PYY may act centrally to modulate eating behavior via striatal networks., (Published by Elsevier Inc.)

We have studied a number of long-term meditators in previous studies. The purpose of this study was to determine if there are differences in baseline brain function of experienced meditators compared to non-meditators. All subjects were recruited as part of an ongoing study of different meditation practices. We evaluated 12 advanced meditators and 14 non-meditators with cerebral blood flow (CBF) SPECT imaging at rest. Images were analyzed with both region of interest and statistical parametric mapping. The CBF of long-term meditators was significantly higher (p<.05) compared to non-meditators in the prefrontal cortex, parietal cortex, thalamus, putamen, caudate, and midbrain. There was also a significant difference in the thalamic laterality with long-term meditators having greater asymmetry. The observed changes associated with long-term meditation appear in structures that underlie the attention network and also those that relate to emotion and autonomic function., (Copyright © 2010 Elsevier Inc. All rights reserved.)

We report five cases with caudate infarction due to Heubner's recurring artery occlusion, in which we conducted detailed memory examinations in terms of explicit memory and implicit memory. We performed the auditory verbal learning test as explicit memory tasks, and motor and cognitive procedural memory tasks, developed by Komori, as implicit memory tasks. Comparing normal control subjects with patients with left caudate infarction due to Heubner's recurring artery occlusion demonstrated lower scores on both declarative and motor procedural memory tasks. These results suggest that the left caudate nucleus may be related with both declarative memory and procedural memory.

Focal cerebral ischemia was produced in monkeys by transorbital occlusion of the right middle cerebral artery. Following this, in one group of animals the total microvasculature, including both perfused and nonperfused vessels of the opposite caudate nucleus and insula, was examined by alkaline phosphatase staining of the endothelium. In another group, the patency of the microvascular bed was visualized by india ink perfusion. The number, diameter, and length of visualized vessels were measured by means of a Wild ASBA image analysis system. The perfused patient microvascular bed was significantly reduced in both insula and caudate nucleus in the supposedly normal left side, although the total microvascular volume showed an increase at 4 and 12 hr in the insula and at 48 hr in the caudate nucleus. Reduced perfusion in the hemisphere opposite to the occluded middle cerebral artery provides an anatomical substrate for the phenomenon of "diaschisis."

Microvasculature of the right caudate nucleus and insular cortex of monkeys with their right middle cerebral artery occluded was morphometrically measured with an image analysis system at 1/2, 4, 12, 24, and 48 hr and 2 weeks. A biphasic change in the microvasculature was observed. In the first phase up to 12 hr an increase in the number and length of the total microvasculature, visualized by alkaline phosphatase staining, along with a reduction in the number and length of the perfused part of the microvasculature, visualized by India ink perfusion, was observed. In the second phase after 48 hr, the number and length of the total microvascular bed as well as the perfused functional bed were significantly reduced.

The ability of the nonglucocorticoid 21-aminosteroid U74006F, a potent inhibitor of iron-dependent lipid peroxidation, to antagonize acute progressive cerebral hypoperfusion following experimental subarachnoid hemorrhage (SAH) was examined in chloralose-anesthetized cats. The SAH was produced by injection of 0.5 ml/kg of unheparinized autologous blood into the cisterna magna after prior withdrawal of an equivalent volume of cerebrospinal fluid. In untreated animals the SAH caused a progressive decline in caudate nuclear blood flow (CNBF) (-51.4% by 3 h) and an increase in intracranial pressure (ICP) (+18.5 mm Hg by 3 h). In comparison, in cats that received a 1 mg/kg iv dose of U74006F at 30 min after SAH, there was a complete prevention of the fall in CNBF and a significant attenuation of the rise in ICP. Furthermore, the drug reduced a concomitant fall in the mean arterial blood pressure and cerebral perfusion pressure. While not as effective as the 1 mg/kg dose, a 0.1 mg/kg dose also significantly attenuated the post-SAH fall in CNBF. These results support a role of lipid peroxidation in the acute pathophysiology of SAH and suggest that U74006F may be useful in the early treatment of this disorder.