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1
Zhang, Zengli, Zhi Ma, Wangyuan Zou, Hang Guo, Min Liu, Yulong Ma, and Lixia Zhang. "The Appropriate Marker for Astrocytes: Comparing the Distribution and Expression of Three Astrocytic Markers in Different Mouse Cerebral Regions." BioMed Research International 2019 (June 24, 2019): 1–15. http://dx.doi.org/10.1155/2019/9605265.
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Astrocytes possess different morphological characteristics depending on the cerebral region in which they are found. However, none of the current astrocytic markers can label all subpopulations successfully. Thus, identifying the appropriate marker for a specific scientific investigation is critical. Here, we compared the distribution and protein expression of three astrocyte markers: NDRG2, GFAP, and S100β, in the cortex, hippocampus, and thalamus. NDRG2- and S100β-positive astrocytes were distributed more uniformly than GFAP-positive astrocytes throughout the whole cerebrum. NDRG2 and S100βimmunoreactivities were the strongest in the dorsal cortex and thalamus, while GFAP immunoreactivity was the strongest in the hippocampus. Moreover, protein expression levels of NDRG2, GFAP, and S100βin adult mice were the highest in the cortex, hippocampus, and thalamus, respectively. We also detected astrocyte morphology and found that, in the corpus callosum and cerebral peduncle, GFAP-positive astrocytes were found with more numerous and longer processes than NDRG2- and S100β-positive astrocytes. These results demonstrate that NDRG2 and S100βare more suitably used to visualize the overall distribution and changes in the number of astrocytes, as well as label astrocytes in the cortex and thalamus. GFAP, however, is more appropriately used to label astrocytes in the corpus callosum, cerebral peduncle, and the hippocampus. These results help to guide researchers in the choice of appropriate astrocyte marker and suggest differences in immunological qualities of astrocytes based on the tissue in which they are found.
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Zhang, Dongyang, Abraham Z. Snyder, Michael D. Fox, Mark W. Sansbury, Joshua S. Shimony, and Marcus E. Raichle. "Intrinsic Functional Relations Between Human Cerebral Cortex and Thalamus." Journal of Neurophysiology 100, no. 4 (October 2008): 1740–48. http://dx.doi.org/10.1152/jn.90463.2008.
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The brain is active even in the absence of explicit stimuli or overt responses. This activity is highly correlated within specific networks of the cerebral cortex when assessed with resting-state functional magnetic resonance imaging (fMRI) blood oxygen level–dependent (BOLD) imaging. The role of the thalamus in this intrinsic activity is unknown despite its critical role in the function of the cerebral cortex. Here we mapped correlations in resting-state activity between the human thalamus and the cerebral cortex in adult humans using fMRI BOLD imaging. Based on this functional measure of intrinsic brain activity we partitioned the thalamus into nuclear groups that correspond well with postmortem human histology and connectional anatomy inferred from nonhuman primates. This structure/function correspondence in resting-state activity was strongest between each cerebral hemisphere and its ipsilateral thalamus. However, each hemisphere was also strongly correlated with the contralateral thalamus, a pattern that is not attributable to known thalamocortical monosynaptic connections. These results extend our understanding of the intrinsic network organization of the human brain to the thalamus and highlight the potential of resting-state fMRI BOLD imaging to elucidate thalamocortical relationships.
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Fujikawa, D. G., B. E. Dwyer, R. R. Lake, and C. G. Wasterlain. "Local cerebral glucose utilization during status epilepticus in newborn primates." American Journal of Physiology-Cell Physiology 256, no. 6 (June 1, 1989): C1160—C1167. http://dx.doi.org/10.1152/ajpcell.1989.256.6.c1160.
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The effect of bicuculline-induced status epilepticus (SE) on local cerebral metabolic rates for glucose (LCMRglc) was studied in 2-wk-old ketamine-anesthetized marmoset monkeys, using the 2-[14C]-deoxy-D-glucose autoradiographical technique. To estimate LCMRglc in cerebral cortex and thalamus during SE, the lumped constant (LC) for 2-deoxy-D-glucose (2-DG) and the rate constants for 2-DG and glucose were calculated for these regions. The control LC was 0.43 in frontoparietal cortex, 0.51 in temporal cortex, and 0.50 in thalamus; it increased to 1.07 in frontoparietal cortex, 1.13 in temporal cortex, and 1.25 in thalamus after 30 min of seizures. With control LC values, LCMRglc in frontoparietal cortex, temporal cortex, and dorsomedial thalamus appeared to increase four to sixfold. With seizure LC values, LCMRglc increased 1.5- to 2-fold and only in cortex. During 45-min seizures, LCMRglc in cortex and thalamus probably increases 4- to 6-fold initially and later falls to the 1.5- to 2-fold level as tissue glucose concentrations decrease. Together with our previous results demonstrating depletion of high-energy phosphates and glucose in these regions, the data suggest that energy demands exceed glucose supply. The long-term effects of these metabolic changes on the developing brain remain to be determined.
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Hiroki, Masahiko, Takeshi Uema, Naofumi Kajimura, Kenichi Ogawa, Masami Nishikawa, Masaaki Kato, Tsuyoshi Watanabe, et al. "Cerebral white matter blood flow is constant during human non-rapid eye movement sleep: a positron emission tomographic study." Journal of Applied Physiology 98, no. 5 (May 2005): 1846–54. http://dx.doi.org/10.1152/japplphysiol.00653.2004.
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This study aimed to identify brain regions with the least decreased cerebral blood flow (CBF) and their relationship to physiological parameters during human non-rapid eye movement (NREM) sleep. Using [15O]H2O positron emission tomography, CBF was measured for nine normal young adults during nighttime. As NREM sleep progressed, mean arterial blood pressure and whole brain mean CBF decreased significantly; arterial partial pressure of CO2 and, selectively, relative CBF of the cerebral white matter increased significantly. Absolute CBF remained constant in the cerebral white matter, registering 25.9 ± 3.8 during wakefulness, 25.8 ± 3.3 during light NREM sleep, and 26.9 ± 3.0 (ml·100 g−1·min−1) during deep NREM sleep ( P = 0.592), and in the occipital cortex ( P = 0.611). The regression slope of the absolute CBF significantly differed with respect to arterial partial pressure of CO2 between the cerebral white matter (slope 0.054, R = − 0.04) and frontoparietal association cortex (slope − 0.776, R = − 0.31) ( P = 0.005) or thalamus (slope − 1.933, R = − 0.47) ( P = 0.004) and between the occipital cortex (slope 0.084, R = 0.06) and frontoparietal association cortex ( P = 0.021) or thalamus ( P < 0.001), and, with respect to mean arterial blood pressure, between the cerebral white matter (slope − 0.067, R = − 0.10) and thalamus (slope 0.637, R = 0.31) ( P = 0.044). The cerebral white matter CBF keeps constant during NREM sleep as well as the occipital cortical CBF, and may be specifically regulated by both CO2 vasoreactivity and pressure autoregulation.
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RamaRao, G., CK Waghmare, Nalini Srivastava, and BK Bhattacharya. "Regional alterations of JNK3 and CaMKIIα subunit expression in the rat brain after soman poisoning." Human & Experimental Toxicology 30, no. 6 (November 1, 2010): 448–59. http://dx.doi.org/10.1177/0960327110386814.
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Calcium/calmodulin-dependent protein kinase II (CaMKII) and c-Jun N-terminal kinases (JNKs) exert numerous and diverse functions in the brain. However, their role in nerve agent poisoning is poorly understood. In the present study, rats were exposed to soman (80 µg/kg) subcutaneously to study the changes in the protein levels of calcium/calmodulin-dependent protein kinase II alpha subunit (CaMKIIα) and JNK3 and activities of acetylcholinestarase (AChE) and CaMKII in the rat brain. Western blot analysis revealed that significant changes were found in both the protein kinases expression. Immunoreactivity levels of neural specific JNK3 isoform increased from 2.5 hours to 30 days after soman exposure in cerebral cortex, hippocampus, striatum and thalamus regions and decreased in the case of cerebellum. CaMKIIα expression levels were also increased from 2.5 hours to 30 days after soman exposure in cerebral cortex, hippocampus, thalamus and down regulated in cerebellum. AChE activity remained inhibited in plasma and brain up to 3 days post exposure. CaMKII activity was increased in cerebrum and decreased in cerebellum. Results suggest that altered expression of both the protein kinases play a role in nerve agent-induced long-term neurotoxic effects.
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Nwokolo, Munachiso, Stephanie A. Amiel, Owen O'Daly, Megan L. Byrne, Bula M. Wilson, Andrew Pernet, Sally M. Cordon, Ian A. Macdonald, Fernando O. Zelaya, and Pratik Choudhary. "Hypoglycemic thalamic activation in type 1 diabetes is associated with preserved symptoms despite reduced epinephrine." Journal of Cerebral Blood Flow & Metabolism 40, no. 4 (April 20, 2019): 787–98. http://dx.doi.org/10.1177/0271678x19842680.
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Brain responses to low plasma glucose may be key to understanding the behaviors that prevent severe hypoglycemia in type 1 diabetes. This study investigated the impact of long duration, hypoglycemia aware type 1 diabetes on cerebral blood flow responses to hypoglycemia. Three-dimensional pseudo-continuous arterial spin labeling magnetic resonance imaging was performed in 15 individuals with type 1 diabetes and 15 non-diabetic controls during a two-step hyperinsulinemic glucose clamp. Symptom, hormone, global cerebral blood flow and regional cerebral blood flow responses to hypoglycemia were measured. Epinephrine release during hypoglycemia was attenuated in type 1 diabetes, but symptom score rose comparably in both groups. A rise in global cerebral blood flow did not differ between groups. Regional cerebral blood flow increased in the thalamus and fell in the hippocampus and temporal cortex in both groups. Type 1 diabetes demonstrated lesser anterior cingulate cortex activation; however, this difference did not survive correction for multiple comparisons. Thalamic cerebral blood flow change correlated with autonomic symptoms, and anterior cingulate cortex cerebral blood flow change correlated with epinephrine response across groups. The thalamus may thus be involved in symptom responses to hypoglycemia, independent of epinephrine action, while anterior cingulate cortex activation may be linked to counterregulation. Activation of these regions may have a role in hypoglycemia awareness and avoidance of problematic hypoglycemia.
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kakou, Medard, Fulbert Kouakou, Dominique Nâdri Oka, Alban Slim Mbende, Johann Peltier, and Stéphane Velut. "Microanatomy of Thalamic Radiations." International Journal of Human Anatomy 1, no. 1 (December 20, 2017): 28–37. http://dx.doi.org/10.14302/issn.2577-2279.ijha-17-1719.
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Background Thalamic radiations also known as thalamocortical pathways are reciprocal myelinated nerve fibers, arranged in a fanning pattern, grouped into tracts or fasciculi; and connecting the thalamus to the cerebral cortex. Detailed in vitro study of these tracts is seldom reported in the literature. Objective We sought to describe the microanatomy of thalamic radiations by means of the fiber-dissection technique to discuss challenges in dissection techniques and anatomic nomenclature, and follow through with a literature review. Methods Twenty formalin-fixed normal human hemispheres were dissected according to Klinglerâs fiber-dissection technique under operative microscope. Results Thalamic radiations are reciprocal myelinated nerve fibers connecting the thalamus to the cerebral cortex and are referred to as corticothalamic and thalamocortical tracts. They are the most medial fibers of the internal capsule and consist of anterior (thalamofrontal), superior (thalamo-fronto-parietal or thalamoparietal), posterior (thalamooccipital) and inferior (thalamotemporal) thalamic fasciculi. Conclusion From the cerebral cortex, thalamic radiation fibers fan out into the thalamus and are the most medial fibers of the internal capsule. There is a great deal of controversy surrounding the distinction between anterior and superior thalamic radiations, sub-ependymal stratum and the fronto-occipital fasciculus.
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McCormick, David A. "Neurotransmitter Actions in the Thalamus and Cerebral Cortex." Journal of Clinical Neurophysiology 9, no. 2 (April 1992): 212–23. http://dx.doi.org/10.1097/00004691-199204010-00004.
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Swanson, Larry W., Olaf Sporns, and Joel D. Hahn. "The network organization of rat intrathalamic macroconnections and a comparison with other forebrain divisions." Proceedings of the National Academy of Sciences 116, no. 27 (June 18, 2019): 13661–69. http://dx.doi.org/10.1073/pnas.1905961116.
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The thalamus is 1 of 4 major divisions of the forebrain and is usually subdivided into epithalamus, dorsal thalamus, and ventral thalamus. The 39 gray matter regions comprising the large dorsal thalamus project topographically to the cerebral cortex, whereas the much smaller epithalamus (2 regions) and ventral thalamus (5 regions) characteristically project subcortically. Before analyzing extrinsic inputs and outputs of the thalamus, here, the intrinsic connections among all 46 gray matter regions of the rat thalamus on each side of the brain were expertly collated and subjected to network analysis. Experimental axonal pathway-tracing evidence was found in the neuroanatomical literature for the presence or absence of 99% of 2,070 possible ipsilateral connections and 97% of 2,116 possible contralateral connections; the connection density of ipsilateral connections was 17%, and that of contralateral connections 5%. One hub, the reticular thalamic nucleus (of the ventral thalamus), was found in this network, whereas no high-degree rich club or clear small-world features were detected. The reticular thalamic nucleus was found to be primarily responsible for conferring the property of complete connectedness to the intrathalamic network in the sense that there is, at least, one path of finite length between any 2 regions or nodes in the network. Direct comparison with previous investigations using the same methodology shows that each division of the forebrain (cerebral cortex, cerebral nuclei, thalamus, hypothalamus) has distinct intrinsic network topological organization. A future goal is to analyze the network organization of connections within and among these 4 divisions of the forebrain.
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Benzi, G., O. Pastoris, F. Marzatico, and R. F. Villa. "Cerebral Enzyme Antioxidant System. Influence of Aging and Phosphatidylcholine." Journal of Cerebral Blood Flow & Metabolism 9, no. 3 (June 1989): 373–80. http://dx.doi.org/10.1038/jcbfm.1989.56.
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To obtain a comprehensive profile of the age-related changes of the antioxidant enzyme system in discrete brain regions (cortex, caudate-putamen, substantia nigra, thalamus), the present study involved practically the total life span of male Wistar rats (from 5 to 35 months of age). The activities of both glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase increase from 5 to 25 months of life and remain relatively constant or decrease scantily thereafter. In thalamus, the activity of total superoxide dismutase (SOD) increases from 5 to 20 months of rat life and decreases thereafter. Conversely, in both substantia nigra and caudate-putamen, enzyme activity declines steadily with age, while in parietotemporal cortex enzyme activity deteriorates from the 25th month onward. In both caudate-putamen and parietotemporal cortex, the activity of glutathione peroxidase increases from 5 to 20 months of life and remains relatively constant thereafter, while in substantia nigra the enzyme activity is practically unmodified during the life span. Furthermore, the activity of glutathione reductase in parietotemporal cortex declines from the 20th month onward, while in caudate-putamen and thalamus, enzyme activity deteriorates after an increase from 5 to 20 months of life. The interference of phosphatidylcholine and/or its metabolite(s) with the cerebral enzyme antioxidant system shows a characteristic specificity as regards both the time of onset and the enzyme activities involved, namely, SOD and glutathione reductase. The interference with SOD is related to the cytosolic form of the enzyme and affects the cortex only of 5-month-old animals and also extends to the thalamus of 15-month-old rats and all regions in 25-month-old ones. The interference of phosphatidylcholine and/or its metabolite(s) with glutathione reductase is found in the brain of 25-month-old rats.
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Toulmin, Hilary, Christian F. Beckmann, Jonathan O'Muircheartaigh, Gareth Ball, Pumza Nongena, Antonios Makropoulos, Ashraf Ederies, et al. "Specialization and integration of functional thalamocortical connectivity in the human infant." Proceedings of the National Academy of Sciences 112, no. 20 (May 4, 2015): 6485–90. http://dx.doi.org/10.1073/pnas.1422638112.
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Connections between the thalamus and cortex develop rapidly before birth, and aberrant cerebral maturation during this period may underlie a number of neurodevelopmental disorders. To define functional thalamocortical connectivity at the normal time of birth, we used functional MRI (fMRI) to measure blood oxygen level-dependent (BOLD) signals in 66 infants, 47 of whom were at high risk of neurocognitive impairment because of birth before 33 wk of gestation and 19 of whom were term infants. We segmented the thalamus based on correlation with functionally defined cortical components using independent component analysis (ICA) and seed-based correlations. After parcellating the cortex using ICA and segmenting the thalamus based on dominant connections with cortical parcellations, we observed a near-facsimile of the adult functional parcellation. Additional analysis revealed that BOLD signal in heteromodal association cortex typically had more widespread and overlapping thalamic representations than primary sensory cortex. Notably, more extreme prematurity was associated with increased functional connectivity between thalamus and lateral primary sensory cortex but reduced connectivity between thalamus and cortex in the prefrontal, insular and anterior cingulate regions. This work suggests that, in early infancy, functional integration through thalamocortical connections depends on significant functional overlap in the topographic organization of the thalamus and that the experience of premature extrauterine life modulates network development, altering the maturation of networks thought to support salience, executive, integrative, and cognitive functions.
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Tanaka, Akira, Shinya Yoshinaga, and Masato Kimura. "Xenon-enhanced Computed Tomographic Measurement of Cerebral Blood Flow in Patients with Chronic Subdural Hematomas." Neurosurgery 27, no. 4 (October 1, 1990): 554–61. http://dx.doi.org/10.1227/00006123-199010000-00009.
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Abstract We compared clinical symptoms with extent of brain shift on computed tomographic (CT) scans and quantitative and three-dimensional measurements of cerebral blood flow (CBF) on xenon-enhanced CT scans in 10 patients with chronic subdural hematomas. Five patients had only headache and minimal or no brain shift on a CT scan. The other five had hemiparesis and/or mental disturbance in addition to headache and moderate or severe brain shift on a CT scan. The mean hemispheric CBF decreased about 7% in patients with headache and about 35% in patients with hemiparesis and/or mental disturbance. It decreased also on the side without the hematoma. The CBF reduction was always more pronounced in the putamen and thalamus than in the cortex. On the contrary, the cortex CBF was mostly preserved or even elevated in both groups of patients. We speculate that CBF reduction in patients with a chronic subdural hematoma occurs initially in central cerebral areas like the basal ganglia and thalamus, and then extends to the entire hemisphere including the cortex as brain compression and displacement progress. Central cerebral area involvement might be more responsible for clinical symptoms than the cortex.
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Hayward, Nick MEA, Pavel Yanev, Annakaisa Haapasalo, Riitta Miettinen, Mikko Hiltunen, Olli Gröhn, and Jukka Jolkkonen. "Chronic Hyperperfusion and Angiogenesis Follow Subacute Hypoperfusion in the Thalamus of Rats with Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 31, no. 4 (November 17, 2010): 1119–32. http://dx.doi.org/10.1038/jcbfm.2010.202.
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Cerebral blood flow (CBF) is disrupted after focal ischemia in rats. We examined long-term hemodynamic and cerebrovascular changes in the rat thalamus after focal cerebral ischemia. Cerebral blood flow quantified by arterial spin labeling magnetic resonance imaging was decreased in the ipsilateral and contralateral thalamus 2 days after cerebral ischemia. Partial thalamic CBF recovery occurred by day 7, then the ipsilateral thalamus was chronically hyperperfused at 30 days and 3 months compared with its contralateral side. This contrasted with permanent hypoperfusion in the ipsilateral cortex. Angiogenesis was indicated by endothelial cell (RECA-1) immunohistochemistry that showed increased blood vessel branching in the ipsilateral thalamus at the end of the 3-month follow-up. Only transient thalamic IgG extravasation was observed, indicating that the blood–brain barrier was intact after day 2. Angiogenesis was preceded by transiently altered expression levels of cadherin family adhesion molecules, cadherin-7, protocadherin-1, and protocadherin-17. In conclusion, thalamic pathology after focal cerebral ischemia involved long-term hemodynamic changes and angiogenesis preceded by altered expression of vascular adhesion factors. Postischemic angiogenesis in the thalamus represents a novel type of remote plasticity, which may support removal of necrotic brain tissue and aid functional recovery.
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Cui, Shaoyang, Mingzhu Xu, Jianting Huang, Qing Mei Wang, Xinsheng Lai, Binbin Nie, Baoci Shan, Xun Luo, John Wong, and Chunzhi Tang. "Cerebral Responses to Acupuncture at GV24 and Bilateral GB13 in Rat Models of Alzheimer’s Disease." Behavioural Neurology 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/8740284.
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Acupuncture has been widely used in China to treat neurological diseases including Alzheimer’s disease (AD). However, its mechanism remains unclear. In the present study, eighty healthy Wistar rats were divided into a normal control group (n=15) and premodel group (n=65). Forty-five rats that met the criteria for the AD model were then randomly divided into the model group (MG), the nonacupoint group (NG), and the acupoint group (AG). All rats received positron emission tomography (PET) scanning, and the images were analyzed with Statistical Parametric Mapping 8.0. MG exhibited hypometabolism in the olfactory bulb, insular cortex, orbital cortex, prelimbic cortex, striatum, parietal association cortex, visual cortex, cingulate gyrus, and retrosplenial cortex. AG exhibited prominent and extensive hypermetabolism in the thalamus, hypothalamus, bed nucleus of the stria terminalis, cerebral peduncle, midbrain tegmentum, and pontine tegmentum compared to NG. These results demonstrated that acupuncturing at GV24 and bilateral GB13 acupoints may improve the learning and memory abilities of the AD rats, probably via altering cerebral glucose metabolism (CGM) in the hypothalamus, thalamus, and brain stem. The observed effects of acupuncture may be caused by regulating the distribution of certain kinds of neurotransmitters and enhancing synaptic plasticity.
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Guillery, R. W. "Branching Thalamic Afferents Link Action and Perception." Journal of Neurophysiology 90, no. 2 (August 2003): 539–48. http://dx.doi.org/10.1152/jn.00337.2003.
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Recent observations of single axons and review of older literature show that axons afferent to the thalamus commonly branch, sending one branch to the thalamus and another to a motor or premotor center of the brain stem. That is, the messages that the thalamus relays to the cerebral cortex can be regarded as copies of motor instructions. This pattern of axonal branching is reviewed, particularly for the somatosensory and the visual pathways. The extent to which this anatomical evidence relates to views that link action to perception is explored. Most pathways going through the thalamus to the cortex are already involved in motor mechanisms. These motor links occur before and during activity in the parallel and hierarchical corticocortical circuitry that currently forms the focus of many studies of perceptual processing.
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Shirotani, Toshiki, Katsuji Shima, Miwako Iwata, Hideyuki Kita, and Hiroo Chigasaki. "Calcium Accumulation following Middle Cerebral Artery Occlusion in Stroke-Prone Spontaneously Hypertensive Rats." Journal of Cerebral Blood Flow & Metabolism 14, no. 5 (September 1994): 831–36. http://dx.doi.org/10.1038/jcbfm.1994.104.
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Delayed neuronal damage in the ischemic region of the rat brain following middle cerebral artery (MCA) occlusion in stroke-prone spontaneously hypertensive rats was studied. The distribution of neuronal damage was determined by 45Ca autoradiography. Accumulation of 45Ca was observed in the corpus callosum and ipsilateral cerebral cortex immediately following MCA occlusion. After 3 days of occlusion, 45Ca had accumulated in the ipsilateral pyramidal tract, the ventral posterior nucleus of the thalamus, and the lateral portion of the striatum. Significant accumulation of 45Ca was observed in the same areas after 7 and 14 days of occlusion. Next the effect of MK-801 on accumulation of 45Ca after MCA occlusion was examined using the same technique. MK-801 (0.5–10 mg/kg i.v.) or saline was administered 15 min before MCA occlusion, and volumes of accumulation of 45Ca were calculated 1 week after ischemic insults. MK-801 significantly reduced 45Ca uptake in the cortex, striatum, and thalamus. Furthermore, there was a strong statistical correlation between the volume of accumulation of 45Ca in the cortex and that in the thalamus ( r = 0.8974; p < 0.001; n = 25). We speculate that delayed neuronal damage in the corpus callosum, ipsilateral pyramidal tract, and thalamus may be caused by secondary neuronal degeneration. However, neuronal damage in the striatum, a segment not supplied by the MCA, may be related to excessive release of glutamate.
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Ito, Masaki, Satoshi Kuroda, Tohru Shiga, Nagara Tamaki, and Yoshinobu Iwasaki. "Motor Cortex Stimulation Improves Local Cerebral Glucose Metabolism in the Ipsilateral Thalamus in Patients With Poststroke Pain: Case Report." Neurosurgery 69, no. 2 (March 30, 2011): E462—E469. http://dx.doi.org/10.1227/neu.0b013e318218cfa0.
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Abstract BACKGROUND AND IMPORTANCE: Motor cortex stimulation (MCS) is documented as an effective therapeutic option for patients with poststroke pain. However, its underlying mechanism is still unclear. This study aimed to evaluate local cerebral glucose metabolism before and after MCS in patients with poststroke pain. CLINICAL PRESENTATION: Using 18F-fluorodeoxyglucose positron emission tomography, cerebral metabolic rate for glucose (CMRGlu) was measured in 6 patients with poststroke pain before MCS. Their lesions were located in the corona radiata, internal capsule, and thalamus. An epidural electrode was implanted under the monitoring of intraoperative neuronavigation and somatosensory evoked/motor evoked potentials. 18F-fluorodeoxyglucose positron emission tomography was repeated in 4 patients (67%) who underwent successful MCS. Asymmetry of CMRGlu was semiquantitatively analyzed using an automated region of interest setting method. Before MCS, the ratio of CMRGlu in the ipsilateral to contralateral thalamus was 0.81 ± 0.13 (n = 6), (range, 0.63-0.97). However, there was no significant asymmetry of CMRGlu in other regions. Successful MCS significantly improved the asymmetry of CMRGlu in the ipsilateral thalamus from 0.81 ± 0.14 to 0.89 ± 0.17 (P < .01, n = 4). The therapeutic effect was proportional to the improvement of CMRGlu asymmetry (R = 0.79, P = 0.28; single regression analysis). CONCLUSION: Poststroke pain is closely related to the reduced glucose use in the thalamus contralateral to the painful area. Successful MCS significantly improves glucose use in the thalamus ipsilateral to MCS, suggesting that electrical stimulation of the motor cortex may activate the corticothalamic connection from the motor cortex.
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Edelman, David B. "Consciousness without corticocentrism: Beating an evolutionary path." Behavioral and Brain Sciences 30, no. 1 (February 2007): 91–92. http://dx.doi.org/10.1017/s0140525x07000994.
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Merker's approach allows the formulation of an evolutionary view of consciousness that abandons a dependence on structural homology – in this case, the presence of a cerebral cortex – in favor of functional concordance. In contrast to Merker, though, I maintain that the emergence of complex, dynamic interactions, such as those which occur between thalamus and cortex, was central to the appearance of consciousness.
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Wünschmann, Arno, Robert Lopez-Astacio, Aníbal G. Armién, Leslie Reed, and Colin R. Parrish. "Parvovirus-induced encephalitis in a juvenile raccoon." Journal of Veterinary Diagnostic Investigation 33, no. 1 (October 26, 2020): 140–43. http://dx.doi.org/10.1177/1040638720967381.
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A juvenile raccoon was euthanized because of severe neurologic signs. At postmortem examination, no significant gross lesions were present. Histologic evaluation demonstrated nonsuppurative encephalitis in thalamus, brainstem, and hippocampus, cerebellar Purkinje cell loss, as well as poliomyelitis and demyelination of the spinal cord. Parvovirus antigen–specific immunohistochemistry revealed immunopositive neurons in the brainstem, cerebral cortex, and hippocampus. A few Purkinje cells were also immunopositive. DNA extracted from formalin-fixed, paraffin-embedded brain tissue (thalamus, hippocampus, cerebral cortex) yielded a positive signal using PCR targeting both feline and canine parvovirus. Sequencing analyses from a fragment of the NS1 gene and a portion of the VP2 gene confirmed the presence of DNA of a recent canine parvovirus variant (CPV-2a–like virus) in the cerebellum. Our case provides evidence that a recent canine parvovirus (CPV) strain ( Carnivore protoparvovirus 1) can infect cerebral and diencephalic neurons and cause encephalitis in an otherwise healthy raccoon. Parvovirus-induced encephalitis is a differential diagnosis of rabies and canine distemper in raccoons with neurologic signs.
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Bucher, Stefan F., Marianne Dieterich, Klaus C. Seelos, and Thomas Brandt. "Sensorimotor cerebral activation during optokinetic nystagmus." Neurology 49, no. 5 (November 1997): 1370–77. http://dx.doi.org/10.1212/wnl.49.5.1370.
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Self-motion or object motion can elicit optokinetic nystagmus (OKN), which is an integral part of dynamic spatial orientation. We used functional MR imaging during horizontal OKN to study cerebral activation patterns in sensory and ocular motor areas in 10 subjects. We found activation bilaterally in the primary visual cortex, the motion-sensitive areas in the occipitotemporal cortex (the middle temporal and medial superior temporal areas), and in areas known to control several types of saccades such as the precentral and posterior median frontal gyrus, the posterior parietal cortex, and the medial part of the superior frontal gyrus (frontal, parietal, and supplementary eye fields). Additionally, we observed cortical activation in the anterior and posterior parts of the insula and in the prefrontal cortex. Bilateral activation of subcortical structures such as the putamen, globus pallidus, caudate nucleus, and the thalamus traced the efferent pathways of OKN down to the brainstem. Functional MRI during OKN revealed a complex cerebral network of sensorimotor cortical and subcortical activation.
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Agarwal, Shyam Lal, Mrinalkanti Ghosh, Shadab Afroze, Anirbaan Palit, Aniruddha Ghosh, and Kaustav Nayek. "Neuroimaging evaluation of pattern of brain involvement in Japanese encephalitis and other viral encephalitis in paediatric age group." International Journal of Biomedical Research 9, no. 4 (May 1, 2018): 132. http://dx.doi.org/10.7439/ijbr.v9i4.4694.
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Introduction: Japanese encephalitis virus, a flavivirus is a significant cause of arboviral encephalitis worldwide. The virus is transmitted to humans via the bite of infected Culex mosquitoes especially C. tritaeniorhynchus, they prefer to bite outdoors and are extremely active and are extremely active in the evening and night. Neuroimaging reveals by MRI and CT scan of patients of Japanese encephalitis shows characteristic lesions particularly in the thalami, substantia nigra, basal ganglia, cerebral cortex, cerebellum, brainstem and white matter.Material & Method: A total of 50 patients divided in 25 anti JE antibody positive patients and another 25 in anti JE antibody negative group. A cross sectional observational analytical study was performed in the time period of January 2015 to August 2016, the patients was studied using IgM capture ELISA and 1.5T MRI machine.Result Analysis: The results were analysed using chi square test and p values. It was found that gray matter structures were the most commonly affected, the thalamus, basal ganglia but white matter lesions were also noted. The thalamus was the most commonly involved structure, followed by the brainstem and cerebral cortex. Haemorrhagic lesions were noted in the cortex, midbrain and cerebellum.Conclusion: Involvement of the thalamus showed the most significant difference between JE and non JE patients with 64% of the JE patients showed thalamic involvement. No other part of the brain showed such significant difference.
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Yin, Y., and Y. Yuan. "The Dopaminergic Polymorphisms in Psychomotor Retardation of Depression: A Pathway-based Imaging Genetics Association Study." European Psychiatry 41, S1 (April 2017): S145—S146. http://dx.doi.org/10.1016/j.eurpsy.2017.01.1989.
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IntroductionSeveral lines of evidence implicate dopamine is involved in the psychomotor retardation (PMR) in major depressive disorder (MDD). Besides, abnormal cerebral blood flow (CBF) of PMR was also found in the cortico-basal ganglia-thalamo-cortical (CBTC) circuitry. We hypothesize that the polymorphisms of the dopaminergic pathway should be associated the abnormal CBF in the CBTC circuitry.ObjectiveTo investigate the association of the polymorphisms throughout the dopaminergic pathway with the cerebral blood flow (CBF) of PMR in MDD.MethodsThe blood sample of 63 patients (23 PMR, 40 NPMR) were collected for genotyping the dopaminergic polymorphisms (92 SNPs from10 genes). After quality controlling, 15 SNPs in 8 candidate genes were entered into the mass univariate modeling analysis. For the statistical analysis, patients with unqualified fMRI image and unmatched demographic data were ruled out. Consequently 56 patients (23 PMR, 33 NPMR) were taken into the statistical analysis.ResultsGenotype-by PMR associations with the CBF differences predominately distributed in bilateral prefrontal cortex (PFC), temporal cortex, and striatum, the left thalamus, the right primary motor cortex, insular cortex, fusiform gyri, and lingual gyri. There were significant negative correlation between the CBF of the PFC and the PMR severity. However, the CBF of the striatum and the thalamus were positively correlated with the PMR severity.ConclusionsThe polymorphisms of dopaminergic pathway are associated with not only CSTC circuitry, but also some other brain regions involving in cognition and emotion controlling. While the increased CBF of PFC might suppress PMR, the increased CBF of striatum and thalamus adversely aggravate PMR.
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Svensson, Peter, Satoshi Minoshima, Ahmad Beydoun, Thomas J. Morrow, and Kenneth L. Casey. "Cerebral Processing of Acute Skin and Muscle Pain in Humans." Journal of Neurophysiology 78, no. 1 (July 1, 1997): 450–60. http://dx.doi.org/10.1152/jn.1997.78.1.450.
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Svensson, Peter, Satoshi Minoshima, Ahmad Beydoun, Thomas J. Morrow, and Kenneth L. Casey. Cerebral processing of acute skin and muscle pain in humans. J. Neurophysiol. 78: 450–460, 1997. The human cerebral processing of noxious input from skin and muscle was compared with the use of positron emission tomography with intravenous H2 15O to detect changes in regional cerebral blood flow (rCBF) as an indicator of neuronal activity. During each of eight scans, 11 normal subjects rated the intensity of stimuli delivered to the nondominant (left) forearm on a scale ranging from 0 to 100 with 70 as pain threshold. Cutaneous pain was produced with a high-energy CO2 laser stimulator. Muscle pain was elicited with high-intensity intramuscular electrical stimulation. The mean ratings of perceived intensity for innocuous and noxious stimulation were32.6 ± 4.5 (SE) and 78.4 ± 1.7 for cutaneous stimulation and 15.4 ± 4.2 and 73.5 ± 1.4 for intramuscular stimulation. The pain intensity ratings and the differences between noxious and innocuous ratings were similar for cutaneous and intramuscular stimuli ( P > 0.05). After stereotactic registration, statistical pixel-by-pixel summation ( Z score) and volumes-of-interest (VOI) analyses of subtraction images were performed. Significant increases in rCBF to both noxious cutaneous and intramuscular stimulation were found in the contralateral secondary somatosensory cortex (SII) and inferior parietal lobule [Brodmann area (BA) 40]. Comparable levels of rCBF increase were found in the contralateral anterior insular cortex, thalamus, and ipsilateral cerebellum. Noxious cutaneous stimulation caused significant activation in the contralateral lateral prefrontal cortex (BA 10/46) and ipsilateral premotor cortex (BA 4/6). Noxious intramuscular stimulation evoked rCBF increases in the contralateral anterior cingulate cortex (BA 24) and subsignificant responses in the contralateral primary sensorimotor cortex (MI/SI) and lenticular nucleus. These activated cerebral structures may represent those recruited early in nociceptive processing because both forms of stimuli were near pain threshold. Correlation analyses showed a negative relationship between changes in rCBF for thalamus and MI/SI for cutaneous stimulation, and positive relationships between thalamus and anterior insula for both stimulus modalities. Direct statistical comparisons between innocuous cutaneous and intramuscular stimulation with the use of Z scores and VOI analyses showed no reliable differences between these two forms of noxious stimulation, indicating a substantial overlap in brain activation pattern. The comparison of noxious cutaneous and intramuscular stimulation indicated more activation in the premotor cortex, SII, and prefrontal cortex with cutaneous stimulation, but these differences did not reach statistical significance. The similar cerebral activation patterns suggest that the perceived differences between acute skin and muscle pain are mediated by differences in the intensity and temporospatial pattern of neuronal activity within similar sets of forebrain structures.
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Liu, Qi, Peihai Zhang, Junjie Pan, Zhengjie Li, Jixin Liu, Guangsen Li, Wei Qin, et al. "Cerebral Activity Changes in Different Traditional Chinese Medicine Patterns of Psychogenic Erectile Dysfunction Patients." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/503536.
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Background.Pattern differentiation is the foundation of traditional Chinese medicine (TCM) treatment for erectile dysfunction (ED). This study aims to investigate the differences in cerebral activity in ED patients with different TCM patterns.Methods.27 psychogenic ED patients and 27 healthy subjects (HS) were enrolled in this study. Each participant underwent an fMRI scan in resting state. The fractional amplitude of low-frequency fluctuation (fALFF) was used to detect the brain activity changes in ED patients with different patterns.Results.Compared to HS, ED patients showed an increased cerebral activity in bilateral cerebellum, insula, globus pallidus, parahippocampal gyrus, orbitofrontal cortex (OFC), and middle cingulate cortex (MCC). Compared to the patients with liver-qi stagnation and spleen deficiency pattern (LSSDP), the patients with kidney-yang deficiency pattern (KDP) showed an increased activity in bilateral brainstem, cerebellum, hippocampus, and the right insula, thalamus, MCC, and a decreased activity in bilateral putamen, medial frontal gyrus, temporal pole, and the right caudate nucleus, OFC, anterior cingulate cortex, and posterior cingulate cortex (P<0.005).Conclusions.The ED patients with different TCM patterns showed different brain activities. The differences in cerebral activity between LSSDP and KDP were mainly in the emotion-related regions, including prefrontal cortex and cingulated cortex.
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Hsieh, Ching-Liang, Qwang-Yuen Chang, I.-hsin Lin, Jaung-Geng Lin, Chung-Hsiang Liu, Nou-Ying Tang, and Hsien-Yuan Lane. "The Study of Electroacupuncture on Cerebral Blood Flow in Rats With and Without Cerebral Ischemia." American Journal of Chinese Medicine 34, no. 02 (January 2006): 351–61. http://dx.doi.org/10.1142/s0192415x06003886.
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Electroacupuncture (EA) is widely used to treat disorders of the nervous system, such as stroke. The aim of the present study was to investigate the effect of EA on cerebral blood flow (CBF) in cerebral ischemic rats. We developed an animal model of cerebral ischemia (CI) by occluding the blood flow of both common carotid arteries in Sprague-Dawley (SD) rats; 2 or 15 Hz EA was applied to both Zusanli acupoints. The levels of nitric oxide (NO) in the peripheral blood and amounts of calcitonin gene-related peptide (CGRP) in the cerebral cortex and thalamus were measured. In addition, L-N (G)-nitro arginine methyl ester (L-NAME) was used to measure the changes in CBF induced by EA in rats with and without CI. The results indicated that both 2 and 15 Hz EA increase the mean CBF in rats with and without CI. However, neither 2 nor 15 Hz EA induced changes in levels of NO in peripheral blood or changes in CGRP levels in cerebral cortex and thalamus. In addition, L-NAME did not change the increase in CBF. We concluded that both 2 and 15 Hz EA at both Zusanli acupoints induced the increase of CBF in rats with and without CI. Whether the effect of EA is related to NO or CGRP will be investigated in a future study.
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Guell, Xavier, Anila M. D’Mello, Nicholas A. Hubbard, Rachel R. Romeo, John D. E. Gabrieli, Susan Whitfield-Gabrieli, Jeremy D. Schmahmann, and Sheeba Arnold Anteraper. "Functional Territories of Human Dentate Nucleus." Cerebral Cortex 30, no. 4 (November 7, 2019): 2401–17. http://dx.doi.org/10.1093/cercor/bhz247.
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Abstract Anatomical connections link the cerebellar cortex with multiple sensory, motor, association, and paralimbic cerebral areas. The majority of fibers that exit cerebellar cortex synapse in dentate nuclei (DN) before reaching extracerebellar structures such as cerebral cortex, but the functional neuroanatomy of human DN remains largely unmapped. Neuroimaging research has redefined broad categories of functional division in the human brain showing that primary processing, attentional (task positive) processing, and default-mode (task negative) processing are three central poles of neural macroscale functional organization. This broad spectrum of human neural processing categories is represented not only in the cerebral cortex, but also in the thalamus, striatum, and cerebellar cortex. Whether functional organization in DN obeys a similar set of macroscale divisions, and whether DN are yet another compartment of representation of a broad spectrum of human neural processing categories, remains unknown. Here, we show for the first time that human DN are optimally divided into three functional territories as indexed by high spatio-temporal resolution resting-state MRI in 77 healthy humans, and that these three distinct territories contribute uniquely to default-mode, salience-motor, and visual cerebral cortical networks. Our findings provide a systems neuroscience substrate for cerebellar output to influence multiple broad categories of neural control.
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Blinkenberg, Morten, Christian Bonde, Søren Holm, Claus Svarer, Jimmy Andersen, Olaf B. Paulson, and Ian Law. "Rate Dependence of Regional Cerebral Activation during Performance of a Repetitive Motor Task: A PET Study." Journal of Cerebral Blood Flow & Metabolism 16, no. 5 (September 1996): 794–803. http://dx.doi.org/10.1097/00004647-199609000-00004.
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Using repeated positron emission tomography (PET) measures of regional cerebral counts, we investigated the regional cortical activations induced in eight normal subjects performing eight different frequencies of fingertapping (0.5–4 Hz) with the right index finger. The task was auditorially cued and the performance recorded during the scanning procedure. Performance evaluation showed increased error rates, during fingertapping, of high and low frequencies, and the best tapping performance was measured in the midrange of frequencies. Significantly activated areas ( p < 0.05) of normalized cerebral counts were located in the left sensorimotor cortex (M1S1), right motor cortex, left thalamus, right insula, supplementary motor area (SMA), and bilaterally in the primary auditory cortex and the cerebellum. Statistical evaluation showed a significant ( p < 0.01) and positive dependence of cerebral activation upon movement rate in the contralateral M1S1. There was no significant rate dependence of cerebral activation in other activated motor areas. The SMA and the right cerebellar hemisphere showed a more uniform activation throughout the tapping frequency range. Furthermore, we found a stimulus rate dependence of cerebral activation in the primary auditory cortex. We believe that the present data provide useful information for the preparation and interpretation of future motor activation studies of normal human subjects and may serve as reference points for studies of pathological conditions.
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Abdallah, Majd, Nicolas Farrugia, Valentine Chirokoff, and Sandra Chanraud. "Static and dynamic aspects of cerebro-cerebellar functional connectivity are associated with self-reported measures of impulsivity: A resting-state fMRI study." Network Neuroscience 4, no. 3 (January 2020): 891–909. http://dx.doi.org/10.1162/netn_a_00149.
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Human and animal brain studies bring converging evidence of a possible role for the cerebellum and the cerebro-cerebellar system in impulsivity. However, the precise nature of the relation between cerebro-cerebellar coupling and impulsivity is far from understood. Characterizing functional connectivity (FC) patterns between large-scale brain networks that mediate different forms of impulsivity, and the cerebellum may improve our understanding of this relation. Here, we analyzed static and dynamic features of cerebro-cerebellar FC using a highly sampled resting-state functional magnetic resonance imaging (rs-fMRI) dataset and tested their association with two widely used self-reports of impulsivity: the UPPS-P impulsive behavior scale and the behavioral inhibition/approach systems (BIS/BAS) in a large group of healthy subjects ( N = 134, ≈ 1 hr of rs-fMRI/subject). We employed robust data-driven techniques to identify cerebral and cerebellar resting-state networks and extract descriptive summary measures of static and dynamic cerebro-cerebellar FC. We observed evidence linking BIS, BAS, sensation seeking, and lack of premeditation to the total strength and temporal variability of FC within networks connecting regions of the prefrontal cortex, precuneus, posterior cingulate cortex, basal ganglia, and thalamus with the cerebellum. Overall, our findings improve the existing knowledge of the neural correlates of impulsivity and the behavioral correlates of the cerebro-cerebellar system.
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Yamamoto, Kazumi, Fumiharu Akai, Toshiki Yoshimine, and Takehiko Yanagihara. "Immunohistochemical investigation of cerebral ischemia after middle cerebral artery occlusion in gerbils." Journal of Neurosurgery 67, no. 3 (September 1987): 414–20. http://dx.doi.org/10.3171/jns.1987.67.3.0414.
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✓ Progression and recovery of ischemic and postischemic damage after occlusion of the middle cerebral artery and subsequent reperfusion were investigated in the gerbil. This study was performed by immunohistochemical reaction testing for tubulin and creatine kinase BB-isoenzyme to visualize the neuronal structure and by immunohistochemical reaction testing for astroprotein (an astrocyte-specific protein) to visualize reactive astrocytes. The earliest ischemic lesion became visible in the frontoparietal cortex after 7 minutes of ischemia as a laminar loss of the reaction for tubulin involving the neuropil, neuronal perikarya, and dendrites. The earliest lesion in the caudoputamen evolved after 30 minutes of ischemia. After reestablishment of cerebral circulation, the immunohistochemical ischemic lesions in the neuronal structure disappeared if the ischemic period was 10 minutes or less and partially disappeared even after ischemia for 15 minutes in the cerebral cortex, while the postischemic lesion in the caudoputamen disappeared even after ischemia for 15 minutes. Reactive astrocytes were detected in the cerebral cortex and caudoputamen as early as 24 hours after reperfusion, both in the areas with and without the neuronal lesions. No lesion was identified in the hippocampus or thalamus. This experimental model is suitable for investigation of rapidly progressive regional ischemia in the cerebral cortex and for comparison with other regional or global cerebral ischemia in the gerbil or other animal species.
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Li, Jing, Chong Peng, Dongjian Lai, Kejie He, Yumei Wang, Gaochuan Zhang, Yuwen Wu, et al. "Changes in cerebral glucose metabolism after acupuncture at KI3 in spontaneously hypertensive rats: a positron emission tomography study." Acupuncture in Medicine 37, no. 2 (March 11, 2019): 107–15. http://dx.doi.org/10.1177/0964528419828733.
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Objective: The aim of this study was to explore the effect of acupuncture stimulation at KI3 on brain glucose metabolism in spontaneously hypertensive rats (SHRs). Methods: Brain glucose metabolism in SHRs after acupuncture stimulation at KI3 was detected using 18F-2-fluorodeoxy-D-glucose positron emission tomography (18F-FDG-PET). SHRs were randomly divided into three groups: no treatment (SHR group); acupuncture at KI3 (KI3 group); and sham acupuncture (Sham group). Wistar Kyoto (WKY) rats were used as a normal blood pressure (BP) control group. Rats were subjected to 10 min of acupuncture once a day for 7 days. BP and positron emission tomography–computed tomography (PET-CT) were measured after the first acupuncture session and after 7 days of treatment. Results: The results showed that BP was lower in the KI3 group than in the SHR group, both 30–60 min after the first acupuncture session and 24–48 h after the 7-day treatment. Compared with the WKY group, the SHR group had lower glucose metabolism in the motor cortex, sensory cortex, basal ganglia, corpus callosum, caudate putamen, and visual cortex. Compared with the untreated/sham-treated SHR control groups, cerebral glucose metabolism was lower in the medulla oblongata, thalamus, dorsal thalamus, orbital cortex, and hypothalamus after acupuncture at KI3, while it was higher in the olfactory cortex and inferior phrenic muscle. Conclusion: Our results show that, in SHRs, needling at KI3 reduces high BP, most likely by altering the activation of cerebral regions.
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Dasdelen, Dervis, Rasim Mogulkoc, and Abdülkerim Kasim Baltaci. "Aquaporins and Roles in Brain Health and Brain Injury." Mini-Reviews in Medicinal Chemistry 20, no. 6 (May 11, 2020): 498–512. http://dx.doi.org/10.2174/1389557519666191018142007.
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In the literature screening, aquaporins were found in the cerebral structures including the pia mater, choroid plexus, ependyma, piriform cortex, hippocampus, dorsal thalamus, supraoptic and suprachiasmatic nuclei, white matter and subcortical organ. Among these, the most common are AQP1, AQP4, and AQP9. The roles of aquaporins have been demonstrated in several diseases such as cerebral edema, various central nervous system tumors, Alzheimer’s Disease and epilepsy. In this review, the relationship between brain/brain-injury and aquaporin, has been reviewed.
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Yoshimine, Toshiki, Kazuyoshi Morimoto, Joan M. Brengman, Henry A. Homburger, Heitaro Mogami, and Takehiko Yanagihara. "Immunohistochemical investigation of cerebral ischemia during recirculation." Journal of Neurosurgery 63, no. 6 (December 1985): 922–28. http://dx.doi.org/10.3171/jns.1985.63.6.0922.
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✓ Immunohistochemical methods for the determination of tubulin, creatine kinase BB-isoenzyme, and astroprotein-glial fibrillary acidic protein were used to investigate recovery of the ischemic lesion after temporary occlusion of a common carotid artery in the gerbil and the evolution of the postischemic lesion following reperfusion. One group of gerbils was followed from 15 minutes to one month after an ischemic period of 30 minutes, and another group was examined after 7 days following an ischemic period of 5 to 30 minutes. It was found that the postischemic lesion, visualized as loss of the immunohistochemical reaction for tubulin and creatine kinase BB-isoenzyme, evolved within 60 minutes after reperfusion in the hippocampus and cerebral cortex and within 3 hours in the caudoputamen and thalamus. Resolution of the preexisting ischemic lesion was possible only after an ischemic period of less than 10 minutes in the cerebral cortex and caudoputamen and less than 15 minutes in the thalamus. In the CA1-CA2 region of the hippocampus, the ischemic lesion already existed after an ischemic period of 5 minutes and was mostly irreversible. The immunohistochemical method of testing for different cellular and subcellular components was very useful for investigation of cerebral ischemia and may also be advantageous for investigation of other pathophysiological conditions of the nervous system.
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Hofbauer, Robert K., Pierre Fiset, Gilles Plourde, Steven B. Backman, and M. Catherine Bushnell. "Dose-dependent Effects of Propofol on the Central Processing of Thermal Pain." Anesthesiology 100, no. 2 (February 1, 2004): 386–94. http://dx.doi.org/10.1097/00000542-200402000-00031.
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Background Anatomic and physiologic data show that multiple regions of the forebrain are activated by pain. However, the effect of anesthetic level on nociceptive input to these regions is not well understood. Methods The authors used positron emission tomography to measure the effect of various concentrations of propofol on pain-evoked changes in regional cerebral blood flow. Fifteen volunteers were scanned while warm and painful heat stimuli were presented to the volar forearm using a contact thermode during administration of target propofol concentrations of 0.0 microg/ml (alert control), 0.5 microg/ml (mild sedation), 1.5 microg/ml (moderate sedation), and 3.5 microg/ml (unconsciousness). Results During the 0.5-microg/ml target propofol concentration (mild sedation), the subjects' pain ratings increased relative to the alert control condition; correspondingly, pain-evoked regional cerebral blood flow increased in the thalamus and the anterior cingulate cortex. In contrast, when subjects lost consciousness (3.5 microg/ml), pain-evoked responses in the thalamus and the anterior cingulate cortex were no longer observed, whereas significant pain-evoked activation remained in the insular cortex. Conclusion These data show that propofol has a dose-dependent effect on thalamocortical transfer of nociceptive information but that some pain-evoked cortical activity remains after loss of consciousness.
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McGuire, P. K., C. J. Bench, C. D. Frith, I. M. Marks, R. S. J. Frackowiak, and R. J. Dolan. "Functional Anatomy of Obsessive–Compulsive Phenomena." British Journal of Psychiatry 164, no. 4 (April 1994): 459–68. http://dx.doi.org/10.1192/bjp.164.4.459.
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Regional cerebral blood flow was measured with H215O positron emission tomography in four patients with obsessive–compulsive disorder. Patients were scanned on 12 occasions in the same session, with each scan paired with brief exposure to one of a hierarchy of contaminants that elicited increasingly intense urges to ritualise. The relationship between symptom intensity and regional cerebral blood flow (rCBF; an index of neural activity) was subsequently examined in the group and in individual patients. The group showed significant positive correlations between symptom intensity and blood flow in the right inferior frontal gyrus, caudate nucleus, putamen, globus pallidus and thalamus, and the left hippocampus and posterior cingulate gyrus. Negative correlations were evident in the right superior prefrontal cortex, and the temporoparietal junction, particularly on the right side. The pattern in single subjects was broadly similar, although individual differences in neural response were also observed. A graded relationship between symptom intensity and regional brain activity can thus be identified in obsessive–compulsive disorder. It is hypothesised that the increases in rCBF in the orbitofrontal cortex, neostriatum, global pallidus and thalamus were related to urges to perform compulsive movements, while those in the hippocampus and posterior cingulate cortex corresponded to the anxiety that accompanied them.
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Ross, Douglas T., and David I. Graham. "Selective Loss and Selective Sparing of Neurons in the Thalamic Reticular Nucleus following Human Cardiac Arrest." Journal of Cerebral Blood Flow & Metabolism 13, no. 4 (July 1993): 558–67. http://dx.doi.org/10.1038/jcbfm.1993.73.
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Neurons in the portion of the human thalamic reticular nucleus (RT) associated with the prefrontal cortex and mediodorsal thalamic nuclei were found to be selectively vulnerable to ischemic neuronal damage following relatively short (≤5-min) duration cardiac arrest. In contrast, selective sparing of these RT neurons occurred in cases with longer (>10-min) duration of arrest that was sufficient to produce extensive ischemic neuronal damage throughout the cerebral cortex and thalamic relay nuclei. The selective degeneration of RT neurons appears to require the sustained activity of corticothalamic or thalamocortical projections to the RT following the ischemic insult. Loss of RT neurons associated with the frontal cortex and mediodorsal thalamus may be the biological basis of some types of persisting cognitive deficits in attentional processing experienced by patients following cardiac arrest, open heart surgery, or other forms of brief global cerebral ischemia.
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Perani, Daniela, Cristina Colombo, Sergio Bressi, Annamaria Bonfanti, Franco Grassi, Silvio Scarone, Laura Bellodi, Enrico Smeraldi, and Ferruccio Fazio. "[18F]FDG PET Study in Obsessive–Compulsive Disorder." British Journal of Psychiatry 166, no. 2 (February 1995): 244–50. http://dx.doi.org/10.1192/bjp.166.2.244.
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BackgroundWe used [18F]FDG and PET in patients with obsessive–compulsive disorder (OCD) to evaluate cerebral metabolic involvement before and after treatment with serotonin-specific reuptake inhibitors.MethodIn 11 untreated, drug-free adults, regional cerebral metabolic rate for glucose (rCMRglu) was compared with that of 15 age-matched normal controls.ResultsrCMRglu values were significantly increased in the cingulate cortex, thalamus and pallidum/putamen complex. After treatment a significant improvement in obsessive–compulsive symptoms on the Y-BOC scale (t = 3.59, P < 0.01) was associated with a significant bilateral decrease of metabolism in the whole cingulate cortex (P < 0.001). Clinical and metabolic data were significantly intercorrelated (Kendall's τ = 0.65; P < 0.01).ConclusionsThese findings indicate that OCD is associated with functional hyperactivity of a selected neuronal network and that treatment to reduce symptoms may have a selective neuromodulatory effect on cingulate cortex.
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Limsoontarakul, Sunsern, Meghan C. Campbell, and Kevin J. Black. "A Perfusion MRI Study of Emotional Valence and Arousal in Parkinson’s Disease." Parkinson's Disease 2011 (2011): 1–10. http://dx.doi.org/10.4061/2011/742907.
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Background. Brain regions subserving emotion have mostly been studied using functional magnetic resonance imaging (fMRI) during emotion provocation procedures in healthy participants.Objective. To identify neuroanatomical regions associated with spontaneous changes in emotional state over time.Methods. Self-rated emotional valence and arousal scores, and regional cerebral blood flow (rCBF) measured by perfusion MRI, were measured 4 or 8 times spanning at least 2 weeks in each of 21 subjects with Parkinson’s disease (PD). A random-effects SPM analysis, corrected for multiple comparisons, identified significant clusters of contiguous voxels in which rCBF varied with valence or arousal.Results. Emotional valence correlated positively with rCBF in several brain regions, including medial globus pallidus, orbital prefrontal cortex (PFC), and white matter near putamen, thalamus, insula, and medial PFC. Valence correlated negatively with rCBF in striatum, subgenual cingulate cortex, ventrolateral PFC, and precuneus—posterior cingulate cortex (PCC). Arousal correlated positively with rCBF in clusters including claustrum-thalamus-ventral striatum and inferior parietal lobule and correlated negatively in clusters including posterior insula—mediodorsal thalamus and midbrain.Conclusion. This study demonstrates that the temporal stability of perfusion MRI allows within-subject investigations of spontaneous fluctuations in mental state, such as mood, over relatively long-time intervals.
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Guirado, Salvador. "The dorsal thalamic connection in the origin of the isocortex." Behavioral and Brain Sciences 26, no. 5 (October 2003): 557–58. http://dx.doi.org/10.1017/s0140525x03270126.
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The origin of the isocortex may be seen as a series of gradual changes (each one with an adaptive value) from a reptilian-like cerebral cortex, as proposed by Aboitiz et al., or as a new dorsal pallium derivative in mammals which undergoes a surface expansion concomitant with the expansion of the dorsal tier of the dorsal thalamus.
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Jones, Edward G. "Synchrony in the Interconnected Circuitry of the Thalamus and Cerebral Cortex." Annals of the New York Academy of Sciences 1157, no. 1 (March 2009): 10–23. http://dx.doi.org/10.1111/j.1749-6632.2009.04534.x.
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Bonhomme, V., P. Fiset, P. Meuret, S. Backman, G. Plourde, T. Paus, M. C. Bushnell, and A. C. Evans. "Propofol Anesthesia and Cerebral Blood Flow Changes Elicited by Vibrotactile Stimulation: A Positron Emission Tomography Study." Journal of Neurophysiology 85, no. 3 (March 1, 2001): 1299–308. http://dx.doi.org/10.1152/jn.2001.85.3.1299.
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We investigated the effects of the general anesthetic agent propofol on cerebral structures involved in the processing of vibrotactile information. Using positron emission tomography (PET) and the H2 15O bolus technique, we measured regional distribution of cerebral blood flow (CBF) in eight healthy human volunteers. They were scanned under five different levels of propofol anesthesia. Using a computer-controlled infusion, the following plasma levels of propofol were targeted: Level W (Waking, 0 μg/ml), Level 1 (0.5 μg/ml), Level 2 (1.5 μg/ml), Level 3 (3.5 μg/ml), and Level R (Recovery). At each level of anesthesia, two 3-min scans were acquired with vibrotactile stimulation of the right forearm either on or off. The level of consciousness was evaluated before each scan by the response of the subject to a verbal command. At Level W, all volunteers were fully awake. They reported being slightly drowsy at Level 1, they had a slurred speech and slow response at Level 2, and they were not responding at all at Level 3. The following variations in regional CBF (rCBF) were observed. During the waking state (Level W), vibrotactile stimulation induced a significant rCBF increase in the left thalamus and in several cortical regions, including the left primary somatosensory cortex and the left and right secondary somatosensory cortex. During anesthesia, propofol reduced in a dose-dependent manner rCBF in the thalamus as well as in a number of visual, parietal, and prefrontal cortical regions. At Level 1 through 3, propofol also suppressed vibration-induced increases in rCBF in the primary and secondary somatosensory cortex, whereas the thalamic rCBF response was abolished only at Level 3, when volunteers lost consciousness. We conclude that propofol interferes with the processing of vibrotactile information first at the level of the cortex before attenuating its transfer through the thalamus.
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Takano, Harumasa, Nobutaka Motohashi, Takeshi Uema, Kenichi Ogawa, Takashi Ohnishi, Masami Nishikawa, Haruo Kashima, and Hiroshi Matsuda. "Changes in regional cerebral blood flow during acute electroconvulsive therapy in patients with depression." British Journal of Psychiatry 190, no. 1 (January 2007): 63–68. http://dx.doi.org/10.1192/bjp.bp.106.023036.
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BackgroundAlthough electroconvulsive therapy (ECT) is widely used to treat psychiatric disorders such as depression, its precise neural mechanisms remain unknown.AimsTo investigate the time course of changes in cerebral blood flow during acute ECT.MethodCerebral blood flow was quantified serially prior to, during and after acute ECT in six patients with depression under anaesthesia using [15O]H2O positron emission tomography (PET).ResultsCerebral blood flow during ECT increased particularly in the basal ganglia, brain-stem, diencephalon, amygdala, vermis and the frontal, temporal and parietal cortices compared with that before ECT. The flow increased in the thalamus and decreased in the anterior cingulate and medial frontal cortex soon after ECT compared with that before ECT.ConclusionsThese results suggest a relationship between the centrencephalic system and seizure generalisation. Further, they suggest that some neural mechanisms of action of ECT are mediated via brain regions including the anterior cingulate and medial frontal cortex and thalamus.
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Kita, Hideyuki, Katsuji Shima, Miwako Tatsumi, and Hiroo Chigasaki. "Cerebral Blood Flow and Glucose Metabolism of the Ischemic Rim in Spontaneously Hypertensive Stroke-Prone Rats with Occlusion of the Middle Cerebral Artery." Journal of Cerebral Blood Flow & Metabolism 15, no. 2 (March 1995): 235–41. http://dx.doi.org/10.1038/jcbfm.1995.29.
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To determine acute postischemic metabolic changes of the ischemic rim under conditions of poor collateral circulation, we examined cerebral blood flow and glucose metabolism in the area of the brain around the ischemic tissue in 36 male spontaneously hypertensive stroke-prone rats (SHRSP) in the acute stage of focal ischemia. The right middle cerebral artery (MCA) was occluded dorsal to the rhinal fissure. Four hours after occlusion, local cerebral blood flow (LCBF), glucose content (LCGC), and glucose utilization (LCGU) were measured by quantitative autoradiographic techniques. The lumped constant was determined from the corresponding LCGC. LCBF showed a widespread and marked decrease in the cortex surrounding the ischemic core, in the thalamus, and in the medial portion of the striatum in the MCA-occluded hemisphere, while the lateral segment of the striatum showed an increase of 36%, compared with findings on the contralateral side. LCGC showed little regional variation, but there was an increase of 38% in the zone bordering the ischemic area. LCGU at the cortex surrounding the ischemic core and in the external capsule showed an increase of 55%. The cortex surrounding the ischemic core, the thalamus, and the lateral segment of the striatum in the MCA-occluded hemisphere showed significant decreases in LCGU. It has been speculated that a high accumulation of glucose reflects a demand for glucose for anaerobic glycolysis in the border areas and that such a demand is probably greater in cases of impaired oxygen delivery due to the presence of microcirculatory disturbances in the MCA-occluded SHRSP. The enhancement of glucose consumption may reflect anaerobic glycolysis. Because the hypermetabolic band was present in the cortex and the white matter, hypermetabolism of the white matter may be related to the glial cell.
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Paschen, Wulf, Joachim Hallmayer, Günter Mies, and Gabriele Röhn. "Ornithine Decarboxylase Activity and Putrescine Levels in Reversible Cerebral Ischemia of Mongolian Gerbils: Effect of Barbiturate." Journal of Cerebral Blood Flow & Metabolism 10, no. 2 (March 1990): 236–42. http://dx.doi.org/10.1038/jcbfm.1990.40.
Full textAbstract:
Reversible cerebral ischemia was produced in anesthetized Mongolian gerbils by occluding both common carotid arteries. After 5 min of ischemia, brains were recirculated for 8 or 24 h. Treated animals received a single intraperitoneal injection of pentobarbitol (50 mg/kg) immediately after the anuerysm clips were removed. At the end of the experiments, animals were reanesthetized and their brains frozen in situ. Tissue samples were taken from the cerebral cortex, lateral striatum, CA1 subfield of the hippocampus, thalamus, and cerebellum for measuring ornithine decarboxylase (ODC) activity and putrescine levels. In addition, 20-μm-thick coronal tissue sections were taken from the level of the striatum and stained with hematoxylin/eosin for evaluating the extent of ischemic neuronal necrosis in the lateral striatum. In control animals ODC activity and putrescine levels amounted, respectively, to 0.32 ± 0.03 nmol/g/h and 10.2 ±0.5 nmol/g in the cerebral cortex; 0.34 ± 0.02 nmol/g/h and 12.8 ± 0.5 nmol/g in the lateral striatum; 0.58 ± 0.05 nmol/g/h and 10.5 ± 0.7 nmol/g in the hippocampal CA1 subfield; 0.35 ± 0.01 nmol/g/h and 9.8 ± 0.4 nmol/g in the thalamus; and 0.25 ± 0.01 nmol/g/h and 8.3 ± 0.6 nmol/g in the cerebellum. After 5 min cerebral ischemia and 8 h recirculation, a significant 7- to 16-fold increase in ODC activity was observed in all forebrain structures studied. Following 24 h recirculation, ODC activity normalized in the cortex, striatum, and thalamus but was still significantly above control values in the hippocampal CA1 subfield. In the cerebellum ODC activity did not change significantly. Putrescine levels were significantly increased in all forebrain structures after 8 h (two- to threefold) and even more after 24 h recirculation (up to fivefold). In barbiturate-treated animals, ODC activity was not significantly changed in relation to untreated ones. There was, however, a trend to higher activity in the cerebral cortex, lateral striatum, and hippocampal CA1 subfield. Barbiturate did not produce a significant effect on postischemic putrescine levels except in the CA1 subfield. Here the putrescine content of treated animals was significantly below that found in untreated ones. In the lateral striatum, severe cell damage (>90% of neurons were necrotic) was observed in 5 of 12 untreated animals but in none of the barbiturate-treated ones (<10% of neurons necrotic). In animals with severe cell necrosis in the lateral striatum, putrescine levels amounted to 70.9 ± 3.4 nmol/g but to only 32.0 ± 2.9 nmol/g in animals in which <10% of neurons were affected (p ⩽ 0.001).
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Hyodo, Fuminori, Kai-Hsiang Chuang, Artem G. Goloshevsky, Agnieszka Sulima, Gary L. Griffiths, James B. Mitchell, Alan P. Koretsky, and Murali C. Krishna. "Brain Redox Imaging Using Blood—Brain Barrier-Permeable Nitroxide MRI Contrast Agent." Journal of Cerebral Blood Flow & Metabolism 28, no. 6 (February 13, 2008): 1165–74. http://dx.doi.org/10.1038/jcbfm.2008.5.
Full textAbstract:
Reactive oxygen species (ROS) and compromised antioxidant defense may contribute to brain disorders such as stroke, amyotrophic lateral sclerosis, etc. Nitroxides are redox-sensitive paramagnetic contrast agents and antioxidants. The ability of a blood—brain barrier (BBB)-permeable nitroxide, methoxycarbonyl-2,2,5,5-tetramethylpyrrolidine-1-oxyl (MC-P), as a magnetic resonance-imaging (MRI) contrast agent for brain tissue redox imaging was tested. MC-P relaxation in rodent brain was quantified by MRI using a fast Look-Locker T1-mapping sequence. In the cerebral cortex and thalamus, the MRI signal intensity increased up to 50% after MC-P injection, but increased only by 2.7% when a BBB-impermeable nitroxide, 3CxP (3-carboxy-2,2,5,5,5-tetramethylpyrrolidine-1-oxyl) was used. The maximum concentrations in the thalamus and cerebral cortex after MC-P injection were calculated to be 1.9±0.35 and 3.0±0.50 mmol/L, respectively. These values were consistent with the ex vivo data of brain tissue and blood concentration obtained by electron paramagnetic resonance (EPR) spectroscopy. Also, reduction rates of MC-P were significantly decreased after reperfusion following transient MCAO (middle cerebral artery occlusion), a condition associated with changes in redox status resulting from oxidative damage. These results show the use of BBB-permeable nitroxides as MRI contrast agents and antioxidants to evaluate the role of ROS in neurologic diseases.
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Lockwood, Alan H., Eddy W. H. Yap, Howard M. Rhoades, and Wai-Hoi Wong. "Altered Cerebral Blood Flow and Glucose Metabolism in Patients with Liver Disease and Minimal Encephalopathy." Journal of Cerebral Blood Flow & Metabolism 11, no. 2 (March 1991): 331–36. http://dx.doi.org/10.1038/jcbfm.1991.66.
Full textAbstract:
We measured CBF and the CMRglc in normal controls and in patients with severe liver disease and evidence for minimal hepatic encephalopathy using positron emission tomography. Regions were defined in frontal, temporal, parietal, and visual cortex; the thalamus; the caudate; the cerebellum; and the white matter along with a whole-slice value obtained at the level of the thalamus. There was no difference in whole-slice CBF and CMRglc values. Individual regional values were normalized to the whole-slice value and subjected to a two-way repeated measures analysis of variance. When normalized CBF and CMRglc values for regions were compared between groups, significant differences were demonstrated ( F = 5.650, p = 0.00014 and F = 4.58, p = 0.0073, respectively). These pattern differences were due to higher CBF and CMRglc in the cerebellum, thalamus, and caudate in patients and lower values in the cortex. Standardized coefficients extracted from a discriminant function analysis permitted correct group assignment for 95.5% of the CBF studies and for 92.9% of the CMRglc studies. The similarity of the altered pattern of cerebral metabolism and flow in our patients to that seen in rats subjected to portacaval shunts or ammonia infusions suggests that this toxin may alter flow and metabolism and that this, in turn, causes the clinical expression of encephalopathy.
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Honkaniemi, Jari, Bradley A. States, Philip R. Weinstein, Jose Espinoza, and Frank R. Sharp. "Expression of Zinc Finger Immediate Early Genes in Rat Brain After Permanent Middle Cerebral Artery Occlusion." Journal of Cerebral Blood Flow & Metabolism 17, no. 6 (June 1997): 636–46. http://dx.doi.org/10.1097/00004647-199706000-00005.
Full textAbstract:
The prolonged expression of the leucine zipper fos/jun immediate early genes (IEG) has been correlated with neuronal death after cerebral ischemia. In this study, the expression of six zinc finger IEG was examined using in situ hybridization in adult rats after middle cerebral artery occlusion (MCAO) with the suture model. NGFI-A, NGFI-B, NGFI-C, egr-2, egr-3, and Nurr1 mRNA were all induced throughout the ipsilateral cortex at 1 hour to 12 hours after MCAO. The cortical induction for most of the genes was greatest in the anterior cingulate and the anterior cerebral artery (ACA) and middle cerebral artery (MCA) transition zone. All of the zinc finger IEG were induced at 1 hour in all regions of hippocampus. NGFI-A and NGFI-B were induced in ipsilateral thalamus. Within areas of infarction, the basal IEG mRNA expression, and expression of the housekeeping gene cyclophilin A mRNA, decreased below control levels by 12 hours after the ischemia. Immediate early gene expression outside areas of infarction returned to control levels in most brain regions by 24 hours except for egr-3, which continued to be induced in the MCA/ACA transition zone for 24 hours, and NGFI-A, which continued to be expressed in specific regions of the thalamus for 72 hours. The induction of these IEG in the cortex is likely caused by ischemia-induced cortical spreading depression, with the hippocampal and thalamic IEG induction being caused by activation of efferent cortical pathways to these regions. The prominent induction of NGFI-B, NGFI-C, egr-2, and egr-3 in the anterior cingulate cortex, the ACA/MCA transition zone, and medial striatum could reflect the ischemic regions around MCA infarcts. The prolonged NGFI-A expression observed in thalamus in this study, and in CA1 of hippocampus after global ischemia in the gerbil in a previous study, suggests that the prolonged NGFI-A expression could be the result of or the cause of the delayed cell death. Prolonged NGFI-A expression, like c-fos and c-jun, seems to provide a marker for slowly dying neurons.
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Lowe, Mark J., Joseph T. Lurito, Vincent P. Mathews, Micheal D. Phillips, and Gary D. Hutchins. "Quantitative Comparison of Functional Contrast from BOLD-Weighted Spin-Echo and Gradient-Echo Echoplanar Imaging at 1.5 Tesla and H215O PET in the Whole Brain." Journal of Cerebral Blood Flow & Metabolism 20, no. 9 (September 2000): 1331–40. http://dx.doi.org/10.1097/00004647-200009000-00008.
Full textAbstract:
Spin-echo and gradient-echo echoplanar functional magnetic resonance imaging (fMRI) studies at 1.5 Tesla (T) were used to obtain blood oxygenation level-dependent (BOLD) contrast images of the whole brain in seven strongly right-handed women during execution of a complex motor task. Five subjects underwent subsequent H215O positron emission tomography (PET) studies while performing the same task. Group-averaged results for changes in the MRI relaxation rates R2* and R2 at 1.5T in response to neuronal activation in nine cortical, subcortical, and cerebellar motor regions are reported. Results for each method are grouped according to tissue type—cerebral cortex (precentral gyrus and supplementary motor area), subcortical regions (thalamus and putamen), and cerebellar cortex (superior lobule). The observed changes in R2* from activation-induced oxygenation changes were more variable across brain regions with different tissue characteristics than observed changes in R2. The ratio of ΔR2* to ΔR2 was 3.3 ± 0.9 for cerebral cortex and 2.0 ± 0.6 for subcortical tissue. ΔR2*, ΔR2, and relative blood flow changes were ΔR2* = −0.201 ± 0.040 s−1, ΔR2 = −0.064 ± 0.011 s−1, and Δf/f = 16.7 ± 0.8% in the cerebral cortex; ΔR2* = −0.100 ± 0.026 s−1, ΔR2 = −0.049 ± 0.009 s−1, and Δf/f = 9.4 ± 0.7% in the subcortical regions; and ΔR2* = −0.215 ± 0.093 s−1, ΔR2 = −0.069 ± 0.012 s−1, and Δf/f = 16.2 ± 1.2% in the cerebellar cortex.
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Sheldrick, A., S. Camara, M. Ilieva, P. Riederer, and T. M. Michel. "Brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3) levels in post-mortem brain tissue from patients with depression compared to healthy individuals – a proof of concept study." European Psychiatry 46 (October 2017): 65–71. http://dx.doi.org/10.1016/j.eurpsy.2017.06.009.
Full textAbstract:
AbstractThe neurotrophic factors (NTF) hypothesis of depression was postulated nearly a decade ago and is nowadays widely acknowledged. Previous reports suggest that cerebral concentrations of NTF may be reduced in suicide victims who received minimal or no antidepressant pharmacotherapy. Recent evidence suggests that antidepressant treatment may improve or normalise cerebral concentrations of neurotrophic factors. Therefore, we examined the concentration of brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3) in different brain regions (cortex, cingulate gyrus, thalamus, hippocampus, putamen and nucleus caudatus) of 21 individuals – 7 patients of which 4 patients with major depressive disorder (MDD) and overall age 86.8 ± 5 years who received antidepressant pharmacotherapy (selective serotonin re-uptake inhibitors [SSRI]; tricyclic antidepressants [TCA]), 3 patients with MDD without antidepressant treatment and overall age 84.3 ± 5 years versus 14 unaffected subjects at age 70.3 ± 13.8. We detected significant elevation of BDNF (parietal cortex) and NT3 (parietal, temporal and occipital cortex, cingulate gyrus, thalamus, putamen and nucleus caudatus regions) in MDD patients who received antidepressant medication compared to MDD untreated patients and controls. Moreover, we detected a significant decrease of NT3 levels in the parietal cortex of patients suffering from MDD non-treated patients without treatment compared to healthy individuals. Although the limited statistical power due to the small sample size in this proof of concept study corroborates data from previous studies, which show that treatment with antidepressants mediates alterations in neuroplasticity via the action of NTF. However, more research using post-mortem brain tissue with larger samples needs to be carried out as well as longitudinal studies to further verify these results.
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Murphy, K., D. R. Corfield, A. Guz, G. R. Fink, R. J. S. Wise, J. Harrison, and L. Adams. "Cerebral areas associated with motor control of speech in humans." Journal of Applied Physiology 83, no. 5 (November 1, 1997): 1438–47. http://dx.doi.org/10.1152/jappl.1997.83.5.1438.
Full textAbstract:
Murphy, K., D. R. Corfield, A. Guz, G. R. Fink, R. J. S. Wise, J. Harrison, and L. Adams. Cerebral areas associated with motor control of speech in humans. J. Appl. Physiol. 83(5): 1438–1447, 1997.—We have defined areas in the brain activated during speaking, utilizing positron emission tomography. Six normal subjects continuously repeated the phrase “Buy Bobby a poppy” (requiring minimal language processing) in four ways: A) spoken aloud, B) mouthed silently, C) without articulation, and D) thought silently. Statistical comparison of images from conditions Awith C and B with D highlighted areas associated with articulation alone, because control of breathing for speech was controlled for; we found bilateral activations in sensorimotor cortex and cerebellum with right-sided activation in the thalamus/caudate nucleus. Contrasting images from conditions A with B and C with D highlighted areas associated with the control of breathing for speech, vocalization, and hearing, because articulation was controlled for; we found bilateral activations in sensorimotor and motor cortex, close to but distinct from the activations in the preceding contrast, together with activations in thalamus, cerebellum, and supplementary motor area. In neither subtraction was there activation in Broca’s area. These results emphasize the bilaterality of the cerebral control of “speaking” without language processing.
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Zarrinpar, Amir, and Edward M. Callaway. "Local Connections to Specific Types of Layer 6 Neurons in the Rat Visual Cortex." Journal of Neurophysiology 95, no. 3 (March 2006): 1751–61. http://dx.doi.org/10.1152/jn.00974.2005.
Full textAbstract:
Because layer 6 of the cerebral cortex receives direct thalamic input and provides projections back to the thalamus, it is in a unique position to influence thalamocortical interactions. Different types of layer 6 pyramidal neurons provide output to different thalamic nuclei, and it is therefore of interest to understand the sources of functional input to these neurons. We studied the morphologies and local excitatory input to individual layer 6 neurons in rat visual cortex by combining intracellular labeling and recording with laser-scanning photostimulation. As in previous photostimulation studies, we found significant differences in the sources of local excitatory input to different cell types. Most notably, there were differences in local input to neurons that, based on analogy to barrel cortex, are likely to project only to the lateral geniculate nucleus of the thalamus versus those that are likely to also project to the lateral posterior nucleus. The more striking finding, however, was the paucity of superficial layer input to layer 6 neurons in the rat visual cortex, contrasting sharply with layer 6 neurons in the primate visual cortex. These observations provide insight into differences in function between cortical projections to first-order versus higher-order thalamic nuclei and also show that these circuits can be organized differently in different species.