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Thalamic arousal network disturbances in temporal lobe epilepsy and improvement after surgery.
González HFJ, Chakravorti S, Goodale SE, Gupta K, Claassen DO, Dawant B, Morgan VL, Englot DJ
(2019) J Neurol Neurosurg Psychiatry 90: 1109-1116
MeSH Terms: Adult, Arousal, Brain Stem, Case-Control Studies, Epilepsy, Temporal Lobe, Female, Functional Neuroimaging, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Neocortex, Neural Pathways, Neurosurgical Procedures, Thalamic Nuclei, Thalamus
Show Abstract · Added June 22, 2019
OBJECTIVE - The effects of temporal lobe epilepsy (TLE) on subcortical arousal structures remain incompletely understood. Here, we evaluate thalamic arousal network functional connectivity in TLE and examine changes after epilepsy surgery.
METHODS - We examined 26 adult patients with TLE and 26 matched control participants and used resting-state functional MRI (fMRI) to measure functional connectivity between the thalamus (entire thalamus and 19 bilateral thalamic nuclei) and both neocortex and brainstem ascending reticular activating system (ARAS) nuclei. Postoperative imaging was completed for 19 patients >1 year after surgery and compared with preoperative baseline.
RESULTS - Before surgery, patients with TLE demonstrated abnormal thalamo-occipital functional connectivity, losing the normal negative fMRI correlation between the intralaminar central lateral (CL) nucleus and medial occipital lobe seen in controls (p < 0.001, paired t-test). Patients also had abnormal connectivity between ARAS and CL, lower ipsilateral intrathalamic connectivity, and smaller ipsilateral thalamic volume compared with controls (p < 0.05 for each, paired t-tests). Abnormal brainstem-thalamic connectivity was associated with impaired visuospatial attention (ρ = -0.50, p = 0.02, Spearman's rho) while lower intrathalamic connectivity and volume were related to higher frequency of consciousness-sparing seizures (p < 0.02, Spearman's rho). After epilepsy surgery, patients with improved seizures showed partial recovery of thalamo-occipital and brainstem-thalamic connectivity, with values more closely resembling controls (p < 0.01 for each, analysis of variance).
CONCLUSIONS - Overall, patients with TLE demonstrate impaired connectivity in thalamic arousal networks that may be involved in visuospatial attention, but these disturbances may partially recover after successful epilepsy surgery. Thalamic arousal network dysfunction may contribute to morbidity in TLE.
© Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.
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16 MeSH Terms
Low-rank plus sparse compressed sensing for accelerated proton resonance frequency shift MR temperature imaging.
Cao Z, Gore JC, Grissom WA
(2019) Magn Reson Med 81: 3555-3566
MeSH Terms: Ablation Techniques, Animals, Brain, Humans, Image Processing, Computer-Assisted, Magnetic Resonance Imaging, Magnetic Resonance Imaging, Interventional, Models, Biological, Phantoms, Imaging, Thalamus, Thermography
Show Abstract · Added March 26, 2019
PURPOSE - To improve multichannel compressed sensing (CS) reconstruction for MR proton resonance frequency (PRF) shift thermography, with application to MRI-induced RF heating evaluation and MR guided high intensity focused ultrasound (MRgFUS) temperature monitoring.
METHODS - A new compressed sensing reconstruction is proposed that enforces joint low rank and sparsity of complex difference domain PRF data between post heating and baseline images. Validations were performed on 4 retrospectively undersampled dynamic data sets in PRF applications, by comparing the proposed method to a previously described L and total variation- (TV-) based CS approach that also operates on complex difference domain data, and to a conventional low rank plus sparse (L+S) separation-based CS reconstruction applied to the original domain data.
RESULTS - In all 4 retrospective validations, the proposed reconstruction method outperformed the conventional L+S and L +TV CS reconstruction methods with a 3.6× acceleration ratio in terms of temperature accuracy with respect to fully sampled data. For RF heating evaluation, the proposed method achieved RMS error of 12%, compared to 19% for the L+S method and 17% for the L +TV method. For in vivo MRgFUS thalamotomy, the peak temperature reconstruction errors were 19%, 31%, and 35%, respectively.
CONCLUSION - The complex difference-based low rank and sparse model enhances compressibility for dynamic PRF temperature imaging applications. The proposed multichannel CS reconstruction method enables high acceleration factors for PRF applications including RF heating evaluation and MRgFUS sonication.
© 2019 International Society for Magnetic Resonance in Medicine.
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11 MeSH Terms
Human Semaphorin 3 Variants Link Melanocortin Circuit Development and Energy Balance.
van der Klaauw AA, Croizier S, Mendes de Oliveira E, Stadler LKJ, Park S, Kong Y, Banton MC, Tandon P, Hendricks AE, Keogh JM, Riley SE, Papadia S, Henning E, Bounds R, Bochukova EG, Mistry V, O'Rahilly S, Simerly RB, INTERVAL, UK10K Consortium, Minchin JEN, Barroso I, Jones EY, Bouret SG, Farooqi IS
(2019) Cell 176: 729-742.e18
MeSH Terms: Adolescent, Adult, Animals, Body Weight, Cell Line, Child, Child, Preschool, Disease Models, Animal, Eating, Energy Metabolism, Female, Genetic Variation, Homeostasis, Humans, Hypothalamus, Leptin, Male, Melanocortins, Mice, Mice, Inbred C57BL, Middle Aged, Nerve Tissue Proteins, Neurons, Obesity, Receptors, Cell Surface, Semaphorins, Young Adult, Zebrafish
Show Abstract · Added April 11, 2019
Hypothalamic melanocortin neurons play a pivotal role in weight regulation. Here, we examined the contribution of Semaphorin 3 (SEMA3) signaling to the development of these circuits. In genetic studies, we found 40 rare variants in SEMA3A-G and their receptors (PLXNA1-4; NRP1-2) in 573 severely obese individuals; variants disrupted secretion and/or signaling through multiple molecular mechanisms. Rare variants in this set of genes were significantly enriched in 982 severely obese cases compared to 4,449 controls. In a zebrafish mutagenesis screen, deletion of 7 genes in this pathway led to increased somatic growth and/or adiposity demonstrating that disruption of Semaphorin 3 signaling perturbs energy homeostasis. In mice, deletion of the Neuropilin-2 receptor in Pro-opiomelanocortin neurons disrupted their projections from the arcuate to the paraventricular nucleus, reduced energy expenditure, and caused weight gain. Cumulatively, these studies demonstrate that SEMA3-mediated signaling drives the development of hypothalamic melanocortin circuits involved in energy homeostasis.
Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.
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28 MeSH Terms
Late onset obesity in mice with targeted deletion of potassium inward rectifier Kir7.1 from cells expressing the melanocortin-4 receptor.
Anderson EJP, Ghamari-Langroudi M, Cakir I, Litt MJ, Chen V, Reggiardo RE, Millhauser GL, Cone RD
(2019) J Neuroendocrinol 31: e12670
MeSH Terms: Animals, Feeding Behavior, Female, Hypothalamus, Male, Membrane Potentials, Mice, Inbred C57BL, Mice, Knockout, Neurons, Obesity, Potassium Channels, Inwardly Rectifying, Receptor, Melanocortin, Type 4
Show Abstract · Added January 8, 2019
Energy stores in fat tissue are determined in part by the activity of hypothalamic neurones expressing the melanocortin-4 receptor (MC4R). Even a partial reduction in MC4R expression levels in mice, rats or humans produces hyperphagia and morbid obesity. Thus, it is of great interest to understand the molecular basis of neuromodulation by the MC4R. The MC4R is a G protein-coupled receptor that signals efficiently through Gα , and this signalling pathway is essential for normal MC4R function in vivo. However, previous data from hypothalamic slice preparations indicated that activation of the MC4R depolarised neurones via G protein-independent regulation of the ion channel Kir7.1. In the present study, we show that deletion of Kcnj13 (ie, the gene encoding Kir7.1) specifically from MC4R neurones produced resistance to melanocortin peptide-induced depolarisation of MC4R paraventricular nucleus neurones in brain slices, resistance to the sustained anorexic effect of exogenously administered melanocortin peptides, late onset obesity, increased linear growth and glucose intolerance. Some MC4R-mediated phenotypes appeared intact, including Agouti-related peptide-induced stimulation of food intake and MC4R-mediated induction of peptide YY release from intestinal L cells. Thus, a subset of the consequences of MC4R signalling in vivo appears to be dependent on expression of the Kir7.1 channel in MC4R cells.
© 2018 British Society for Neuroendocrinology.
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12 MeSH Terms
Attenuation of diet-induced hypothalamic inflammation following bariatric surgery in female mice.
Herrick MK, Favela KM, Simerly RB, Abumrad NN, Bingham NC
(2018) Mol Med 24: 56
MeSH Terms: Animals, Bariatric Surgery, Diet, High-Fat, Female, Hypothalamus, Inflammation, Mice, Inbred C57BL, Obesity
Show Abstract · Added April 11, 2019
BACKGROUND - Exposure of rodents to chronic high-fat diet (HFD) results in upregulation of inflammatory markers and proliferation of microglia within the mediobasal hypothalamus. Such hypothalamic inflammation is associated with metabolic dysfunction, central leptin resistance, and maintenance of obesity. Bariatric surgeries result in long-term stable weight loss and improved metabolic function. However, the effects of such surgical procedures on HFD-induced hypothalamic inflammation are unknown. We sought to characterize the effects of two bariatric surgical procedures, Roux-en-Y gastric bypass (RYGB) and biliary diversion (BD-IL), in female mice with particular emphasis on HFD-induced hypothalamic inflammation and microgliosis.
METHODS - RYGB and BD-IL were performed on diet-induced obese (DIO) mice. Quantitative RT-PCR and fluorescent microscopy were used to evaluate hypothalamic inflammatory gene expression and microgliosis. Results were compared to lean (CD), DIO sham-surgerized mice (DIO-SHAM), and dietary weight loss (DIO-Rev) controls.
RESULTS - In female mice, RYGB and BD-IL result in normalization of hypothalamic inflammatory gene expression and microgliosis within 8 weeks of surgery, despite ongoing exposure to HFD. Paralleling these results, the hypothalamic expression levels of the orexigenic neuropeptide Agrp and the anorexic response of surgical mice to exogenous leptin were comparable to lean controls (CD). In contrast, results from DIO-Rev mice were comparable to DIO-SHAM mice, despite transition back to standard rodent show and normalization of weight.
CONCLUSION - Bariatric surgery attenuates HFD-induced hypothalamic inflammation and microgliosis and restores leptin sensitivity, despite ongoing exposure to HFD.
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MeSH Terms
Deep brain stimulation for the treatment of disorders of consciousness and cognition in traumatic brain injury patients: a review.
Kundu B, Brock AA, Englot DJ, Butson CR, Rolston JD
(2018) Neurosurg Focus 45: E14
MeSH Terms: Animals, Brain Injuries, Traumatic, Cognition, Consciousness, Deep Brain Stimulation, Epilepsy, Humans, Thalamus
Show Abstract · Added September 25, 2018
Traumatic brain injury (TBI) is a looming epidemic, growing most rapidly in the elderly population. Some of the most devastating sequelae of TBI are related to depressed levels of consciousness (e.g., coma, minimally conscious state) or deficits in executive function. To date, pharmacological and rehabilitative therapies to treat these sequelae are limited. Deep brain stimulation (DBS) has been used to treat a number of pathologies, including Parkinson disease, essential tremor, and epilepsy. Animal and clinical research shows that targets addressing depressed levels of consciousness include components of the ascending reticular activating system and areas of the thalamus. Targets for improving executive function are more varied and include areas that modulate attention and memory, such as the frontal and prefrontal cortex, fornix, nucleus accumbens, internal capsule, thalamus, and some brainstem nuclei. The authors review the literature addressing the use of DBS to treat higher-order cognitive dysfunction and disorders of consciousness in TBI patients, while also offering suggestions on directions for future research.
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8 MeSH Terms
Genetic loss of GluN2B in D1-expressing cell types enhances long-term cocaine reward and potentiation of thalamo-accumbens synapses.
Joffe ME, Turner BD, Delpire E, Grueter BA
(2018) Neuropsychopharmacology 43: 2383-2389
MeSH Terms: Animals, Cocaine, Gene Deletion, Locomotion, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Nucleus Accumbens, Receptors, Dopamine D1, Receptors, N-Methyl-D-Aspartate, Reward, Thalamus
Show Abstract · Added April 2, 2019
Transient upregulation of GluN2B-containing NMDA receptors (R) in the nucleus accumbens (NAc) is proposed as an intermediate to long-term AMPAR plasticity associated with persistent cocaine-related behaviors. However, cell type- and input-specific contributions of GluN2B underlying lasting actions of cocaine remain to be elucidated. We utilized GluN2B cell type-specific knockouts and optogenetics to deconstruct the role of GluN2B in cocaine-induced NAc synaptic and behavioral plasticity. While reward learning was unaffected, loss of GluN2B in D1 dopamine receptor-expressing cells (D1) led to prolonged retention of reward memory. In control mice, prefrontal cortex (PFC)-D1(+) NAc AMPAR function was unaffected by cocaine exposure, while midline thalamus (mThal)-D1(+) NAc AMPAR function was potentiated but diminished after withdrawal. In D1-GluN2B mice, the potentiation of mThal-D1(+) NAc AMPAR function persisted following withdrawal, corresponding with continued expression of cocaine reward behavior. These data suggest NAc GluN2B-containing NMDARs serve a feedback role and may weaken reward-related memories.
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MeSH Terms
Forebrain Ptf1a Is Required for Sexual Differentiation of the Brain.
Fujiyama T, Miyashita S, Tsuneoka Y, Kanemaru K, Kakizaki M, Kanno S, Ishikawa Y, Yamashita M, Owa T, Nagaoka M, Kawaguchi Y, Yanagawa Y, Magnuson MA, Muratani M, Shibuya A, Nabeshima YI, Yanagisawa M, Funato H, Hoshino M
(2018) Cell Rep 24: 79-94
MeSH Terms: Animals, Cell Lineage, Embryo, Mammalian, Female, Gene Expression Regulation, Developmental, Gonads, Hypothalamus, Male, Mice, Inbred C57BL, Mice, Knockout, Prosencephalon, Sex Differentiation, Sexual Behavior, Animal, Transcription Factors
Show Abstract · Added July 27, 2018
The mammalian brain undergoes sexual differentiation by gonadal hormones during the perinatal critical period. However, the machinery at earlier stages has not been well studied. We found that Ptf1a is expressed in certain neuroepithelial cells and immature neurons around the third ventricle that give rise to various neurons in several hypothalamic nuclei. We show that conditional Ptf1a-deficient mice (Ptf1a cKO) exhibit abnormalities in sex-biased behaviors and reproductive organs in both sexes. Gonadal hormone administration to gonadectomized animals revealed that the abnormal behavior is caused by disorganized sexual development of the knockout brain. Accordingly, expression of sex-biased genes was severely altered in the cKO hypothalamus. In particular, Kiss1, important for sexual differentiation of the brain, was drastically reduced in the cKO hypothalamus, which may contribute to the observed phenotypes in the Ptf1a cKO. These findings suggest that forebrain Ptf1a is one of the earliest regulators for sexual differentiation of the brain.
Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.
3 Communities
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14 MeSH Terms
Androgen excess in pancreatic β cells and neurons predisposes female mice to type 2 diabetes.
Navarro G, Allard C, Morford JJ, Xu W, Liu S, Molinas AJ, Butcher SM, Fine NH, Blandino-Rosano M, Sure VN, Yu S, Zhang R, Münzberg H, Jacobson DA, Katakam PV, Hodson DJ, Bernal-Mizrachi E, Zsombok A, Mauvais-Jarvis F
(2018) JCI Insight 3:
MeSH Terms: Androgens, Animals, Diabetes Mellitus, Type 2, Diet, Western, Dihydrotestosterone, Female, Glucose, Humans, Hyperinsulinism, Hypothalamus, Insulin Resistance, Insulin-Secreting Cells, Mice, Mice, Inbred C57BL, Mice, Knockout, Mitochondria, Neurons, Receptors, Androgen, Streptozocin
Show Abstract · Added June 28, 2018
Androgen excess predisposes women to type 2 diabetes (T2D), but the mechanism of this is poorly understood. We report that female mice fed a Western diet and exposed to chronic androgen excess using dihydrotestosterone (DHT) exhibit hyperinsulinemia and insulin resistance associated with secondary pancreatic β cell failure, leading to hyperglycemia. These abnormalities are not observed in mice lacking the androgen receptor (AR) in β cells and partially in neurons of the mediobasal hypothalamus (MBH) as well as in mice lacking AR selectively in neurons. Accordingly, i.c.v. infusion of DHT produces hyperinsulinemia and insulin resistance in female WT mice. We observe that acute DHT produces insulin hypersecretion in response to glucose in cultured female mouse and human pancreatic islets in an AR-dependent manner via a cAMP- and mTOR-dependent pathway. Acute DHT exposure increases mitochondrial respiration and oxygen consumption in female cultured islets. As a result, chronic DHT exposure in vivo promotes islet oxidative damage and susceptibility to additional stress induced by streptozotocin via AR in β cells. This study suggests that excess androgen predisposes female mice to T2D following AR activation in neurons, producing peripheral insulin resistance, and in pancreatic β cells, promoting insulin hypersecretion, oxidative injury, and secondary β cell failure.
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19 MeSH Terms
Modulation of thalamocortical oscillations by TRIP8b, an auxiliary subunit for HCN channels.
Zobeiri M, Chaudhary R, Datunashvili M, Heuermann RJ, Lüttjohann A, Narayanan V, Balfanz S, Meuth P, Chetkovich DM, Pape HC, Baumann A, van Luijtelaar G, Budde T
(2018) Brain Struct Funct 223: 1537-1564
MeSH Terms: Action Potentials, Adenine, Adenylyl Cyclase Inhibitors, Animals, Cardiovascular Agents, Cerebral Cortex, Cyclic AMP, Cyclic GMP, Female, Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels, Male, Membrane Proteins, Mice, Mice, Inbred C57BL, Mice, Transgenic, Models, Neurological, Neural Pathways, Peroxins, Pyrimidines, Sodium Channel Blockers, Tetrodotoxin, Thalamus, Thionucleotides
Show Abstract · Added April 2, 2019
Hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channels have important functions in controlling neuronal excitability and generating rhythmic oscillatory activity. The role of tetratricopeptide repeat-containing Rab8b-interacting protein (TRIP8b) in regulation of hyperpolarization-activated inward current, I , in the thalamocortical system and its functional relevance for the physiological thalamocortical oscillations were investigated. A significant decrease in I current density, in both thalamocortical relay (TC) and cortical pyramidal neurons was found in TRIP8b-deficient mice (TRIP8b). In addition basal cAMP levels in the brain were found to be decreased while the availability of the fast transient A-type K current, I , in TC neurons was increased. These changes were associated with alterations in intrinsic properties and firing patterns of TC neurons, as well as intrathalamic and thalamocortical network oscillations, revealing a significant increase in slow oscillations in the delta frequency range (0.5-4 Hz) during episodes of active-wakefulness. In addition, absence of TRIP8b suppresses the normal desynchronization response of the EEG during the switch from slow-wave sleep to wakefulness. It is concluded that TRIP8b is necessary for the modulation of physiological thalamocortical oscillations due to its direct effect on HCN channel expression in thalamus and cortex and that mechanisms related to reduced cAMP signaling may contribute to the present findings.
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