Partial saturation and regional variation in the blood-to-brain transport of leptin in normal weight mice

2000 ◽  
Vol 278 (6) ◽  
pp. E1158-E1165 ◽  
Author(s):  
William A. Banks ◽  
Cecilia M. Clever ◽  
Catherine L. Farrell
Keyword(s):  
Arcuate Nucleus ◽  
Maximum Velocity ◽  
Brain Perfusion ◽  
Serum Levels ◽  
Brain Regions ◽  
Normal Weight ◽  
Normal Serum ◽  
Optimal Function ◽  
The Central Nervous System ◽  
The Brain

Impaired blood-brain barrier transport of leptin into the arcuate nucleus has been suggested to underlie obesity in humans and outbred aging mice. Here, we used a brain perfusion method in mice to measure transport rates and kinetic parameters for leptin at vascular concentrations between 0.15 and 130 ng/ml. Transport into whole brain was partially saturated at all concentrations, not only those seen in obesity. Leptin entered all regions of the brain, not only the hypothalamus, with entry and saturation rates differing among the brain regions. The value of the Michaelis-Menten constant of the transporter approximates normal serum levels and the maximum velocity value varies significantly among brain regions. These results suggest an important role for low serum levels signaling starvation status to the brain and show that the levels of leptin seen in obesity greatly saturate the transporter. Differences in regional uptake and saturation provide a mechanism by which leptin can control events mediated at the arcuate nucleus and other regions of the central nervous system with different regional thresholds for optimal function.

Mechanism of the induction of brain c-Fos-positive neurons by lipid absorption

2007 ◽  
Vol 292 (1) ◽  
pp. R268-R273 ◽  
Author(s):  
Chun-Min Lo ◽  
Liyun Ma ◽  
Dian Ming Zhang ◽  
Rachel Lee ◽  
Abby Qin ◽  
...  
Keyword(s):  
Arcuate Nucleus ◽  
Ventromedial Hypothalamus ◽  
Brain Regions ◽  
Lipid Absorption ◽  
Neuronal Activation ◽  
Positive Neuron ◽  
The Central Nervous System ◽  
Chylomicron Formation ◽  
The Brain

Many gastrointestinal meal-related signals are transmitted to the central nervous system via the vagus nerve and thereby control changes in meal size. The c-Fos-positive neuron has been used as a marker of neuronal activation after lipid meals to examine the contribution of a selective macronutrient on brain neurocircuit activity. In rats fed Intralipid, the c-Fos-positive neurons were highly stimulated in the nucleus of the solitary tract (NTS) and in the hypothalamus, including the paraventricular nucleus (PVN), arcuate nucleus of the hypothalamus (ARC), and ventromedial hypothalamus at 4 h lipid feeding. However, c-Fos-like immunoreactivity was markedly attenuated in these brain regions when chylomicron formation/secretion was blocked by Pluronic L-81. After lymph was diverted from the lymph cannulated animals, the rats had a lower number of c-Fos-positive cells in the NTS and ARC. In contrast, the rats had higher c-Fos-positive neurons in PVN. The present study also revealed that c-Fos-positive neurons induced by feeding of Intalipid were abolished by CCK type 1 receptor antagonist, Lorglumide. We conclude that the formation and/or secretion of chylomicron are critical steps for initiating neuronal activation in the brain.

Dexamethasone rapidly increases hypothalamic neuropeptide Y secretion in adrenalectomized ob/ob mice

1996 ◽  
Vol 271 (1) ◽  
pp. E151-E158 ◽  
Author(s):  
H. L. Chen ◽  
D. R. Romsos
Keyword(s):  
Neuropeptide Y ◽  
Arcuate Nucleus ◽  
Rapid Onset ◽  
Brown Adipose ◽  
Specific Enhancement ◽  
Brown Adipose Tissue Thermogenesis ◽  
The Central Nervous System ◽  
Rapid Transport ◽  
The Brain

A single intracerebroventricular injection of dexamethasone (DEX) rapidly (within 30 min) suppresses brown adipose tissue thermogenesis and increases plasma insulin concentrations in adrenal-ectomized (ADX) ob/ob mice but not in ADX lean mice. Intracerebroventricular neuropeptide Y (NPY) administered intracerebroventricularly causes these same metabolic changes within 30 min in both ob/ob and lean ADX mice. We therefore hypothesized that DEX exerts these rapid-onset metabolic actions in ob/ob mice via a phenotype-specific enhancement of NPY secretion within the central nervous system. In support of this hypothesis, DEX (a type II glucocorticoid receptor agonist) administered intracerebroventricularly selectively lowered NPY concentrations in the whole hypothalamus of ADX ob/ob mice by 35% and in the arcuate nucleus region by approximately 70% within 30 min but not in the brain stem or hippocampus or in any of these regions of lean mice. DEX also functioned in vitro to enhance depolarization-dependent release of NPY from hypothalamic blocks of ADX ob/ob mice but not of ADX lean mice. Thus DEX acts in the hypothalamus of ob/ob mice in a phenotype-specific manner to evoke rapid transport of NPY from cell bodies within the arcuate nucleus to terminal regions including the dorsomedial and ventromedial hypothalamic regions for release.

scholarly journals Immunohistochemical study of the blood-brain barrier. Production of an artifact.

1980 ◽  
Vol 28 (6) ◽  
pp. 570-572 ◽  
Author(s):  
J R Sparrow
Keyword(s):  
Central Nervous System ◽  
Blood Vessels ◽  
Serum Proteins ◽  
Immunohistochemical Study ◽  
Normal Serum ◽  
Frozen Sections ◽  
Immunohistochemical Technique ◽  
The Central Nervous System ◽  
Cryostat Sections ◽  
The Brain

The permeability to normal serum proteins of blood vessels in the central nervous system (CNS) was studied by means of the peroxidase-antiperoxidase immunohistochemical technique. Frozen sections were cut in a cryostat and then fixed briefly in 95% ethanol. The localization of serum proteins outside blood vessels in the brain was shown to be an artifact produced during the preparation of cryostat sections. It was concluded that such cryostat sections are unsuitable for studies of vascular permeability in the CNS.

scholarly journals Effects of tiletamine-xylazine-tramadol combination and its specific antagonist on AMPK in the brain of rats

2019 ◽  
Vol 63 (2) ◽  
pp. 285-292
Author(s):  
Ning Ma ◽  
Xin Li ◽  
Hong-bin Wang ◽  
Li Gao ◽  
Jian-hua Xiao
Keyword(s):  
Mrna Expression ◽  
Opposite Effect ◽  
Brain Regions ◽  
Control Group ◽  
Sprague Dawley ◽  
Sd Rats ◽  
The Central Nervous System ◽  
Specific Antagonist ◽  
Sedation And Analgesia ◽  
The Brain

AbstractIntroduction:Tiletamine-xylazine-tramadol (XFM) has few side effects and can provide good sedation and analgesia. Adenosine 5’-monophosphate-activated protein kinase (AMPK) can attenuate trigeminal neuralgia. The study aimed to investigate the effects of XFM and its specific antagonist on AMPK in different regions of the brain.Material and Methods:A model of XFM in the rat was established. A total of 72 Sprague Dawley (SD) rats were randomly divided into three equally sized groups: XFM anaesthesia (M group), antagonist (W group), and XFM with antagonist interactive groups (MW group). Eighteen SD rats were in the control group and were injected intraperitoneally with saline (C group). The rats were sacrificed and the cerebral cortex, cerebellum, hippocampus, thalamus, and brain stem were immediately separated, in order to detect AMPKα mRNA expression by quantitative PCR.Results:XFM was able to increase the mRNA expression of AMPKα1 and AMPKα2 in all brain regions, and the antagonist caused the opposite effect, although the effects of XFM could not be completely reversed in some areas.Conclusion:XFM can influence the expression of AMPK in the central nervous system of the rat, which can provide a reference for the future development of anaesthetics for animals.

scholarly journals Astrocytes, Noradrenaline, α1-Adrenoreceptors, and Neuromodulation: Evidence and Unanswered Questions

2021 ◽  
Vol 15 ◽  
Author(s):  
Jérôme Wahis ◽  
Matthew G. Holt
Keyword(s):  
Critical Appraisal ◽  
Brain Regions ◽  
Synaptic Activity ◽  
Physiological Effects ◽  
Astrocyte Heterogeneity ◽  
Main Effect ◽  
The Central Nervous System ◽  
Noradrenergic Modulation ◽  
The Brain ◽  
Experimental Strategies

Noradrenaline is a major neuromodulator in the central nervous system (CNS). It is released from varicosities on neuronal efferents, which originate principally from the main noradrenergic nuclei of the brain – the locus coeruleus – and spread throughout the parenchyma. Noradrenaline is released in response to various stimuli and has complex physiological effects, in large part due to the wide diversity of noradrenergic receptors expressed in the brain, which trigger diverse signaling pathways. In general, however, its main effect on CNS function appears to be to increase arousal state. Although the effects of noradrenaline have been researched extensively, the majority of studies have assumed that noradrenaline exerts its effects by acting directly on neurons. However, neurons are not the only cells in the CNS expressing noradrenaline receptors. Astrocytes are responsive to a range of neuromodulators – including noradrenaline. In fact, noradrenaline evokes robust calcium transients in astrocytes across brain regions, through activation of α1-adrenoreceptors. Crucially, astrocytes ensheath neurons at synapses and are known to modulate synaptic activity. Hence, astrocytes are in a key position to relay, or amplify, the effects of noradrenaline on neurons, most notably by modulating inhibitory transmission. Based on a critical appraisal of the current literature, we use this review to argue that a better understanding of astrocyte-mediated noradrenaline signaling is therefore essential, if we are ever to fully understand CNS function. We discuss the emerging concept of astrocyte heterogeneity and speculate on how this might impact the noradrenergic modulation of neuronal circuits. Finally, we outline possible experimental strategies to clearly delineate the role(s) of astrocytes in noradrenergic signaling, and neuromodulation in general, highlighting the urgent need for more specific and flexible experimental tools.

The somatic error hypothesis of anxiety

2018 ◽  
Author(s):  
Sahib S. Khalsa ◽  
Justin S. Feinstein
Keyword(s):  
Central Nervous System ◽  
Physiological State ◽  
Brain Regions ◽  
Novel Therapies ◽  
Body State ◽  
Long Term Changes ◽  
The Central Nervous System ◽  
And Behavior ◽  
The Brain

A regulatory battle for control ensues in the central nervous system following a mismatch between the current physiological state of an organism as mapped in viscerosensory brain regions and the predicted body state as computed in visceromotor control regions. The discrepancy between the predicted and current body state (i.e. the “somatic error”) signals a need for corrective action, motivating changes in both cognition and behavior. This chapter argues that anxiety disorders are fundamentally driven by somatic errors that fail to be adaptively regulated, leaving the organism in a state of dissonance where the predicted body state is perpetually out of line with the current body state. Repeated failures to quell somatic error can result in long-term changes to interoceptive circuitry within the brain. This chapter explores the neuropsychiatric sequelae that can emerge following chronic allostatic dysregulation of somatic errors and discusses novel therapies that might help to correct this dysregulation.

Increased µ-opioid receptors in sheep brain after transport

1995 ◽  
Vol 1995 ◽  
pp. 204-204
Author(s):  
E.A. Azaga ◽  
R.G. Rodway
Keyword(s):  
Opioid Receptors ◽  
Opioid Peptide ◽  
Brain Regions ◽  
Long Distance ◽  
Long Distance Transport ◽  
The Central Nervous System ◽  
Sheep Brain ◽  
Transport Stress ◽  
Distance Transport ◽  
The Brain

The long distance transport of sheep before slaughter is at present a very important topic in animal welfare. However, Modulation of opioid receptors can be influenced by chronic treatment with opioid agonists and antagonists (Blanchard, and Chang, 1988). Similarly, opioid receptors can be up or down-regulated by stressful stimuli such as restraint, electric footshock or social isolation and housing (Zeman et al., 1988 and Zanella et al., 1991). The present study was carried out to assess the effects of transport stress on the properties of one class of opioid peptide receptor in the brain of sheep after transport stress. Opioid peptides such as β-endorphin are released by the central nervous system during application of stresses such as transport. They are believed to exert analgesic properties and their effectiveness depends partly on the concentration (Bmax) and affinity (Kd) of their receptors. µ-Opioid receptors are found in various brain regions and are selective for endorphins and similar peptides.

Prevention of reflex natriuresis after acute unilateral nephrectomy by neonatal administration of MSG

1987 ◽  
Vol 252 (2) ◽  
pp. F276-F282 ◽  
Author(s):  
S. Y. Lin ◽  
E. Wiedemann ◽  
C. F. Deschepper ◽  
R. H. Alper ◽  
M. H. Humphreys
Keyword(s):  
Arcuate Nucleus ◽  
Monosodium Glutamate ◽  
Brain Regions ◽  
Anterior Lobe ◽  
Unilateral Nephrectomy ◽  
Reflex Pathways ◽  
Before And After ◽  
Hypothalamic Arcuate Nucleus ◽  
The Central Nervous System ◽  
Neonatal Administration

Acute unilateral nephrectomy (AUN) results in natriuresis from the remaining kidney through reflex pathways involving the central nervous system and requiring an intact pituitary gland. The natriuresis is accompanied by an increase in the plasma concentration of a peptide or peptides derived from the N-terminal fragment (NTF) of proopiomelanocortin. We measured plasma immunoreactive NTF-like material (IR-NTF) before and after AUN in control rats and rats treated neonatally with monosodium glutamate (MSG), a procedure that produces neuroendocrine dysfunction by destroying cell bodies in the hypothalamic arcuate nucleus, median eminence, and other brain regions. In control rats, IR-NTF increased from 85.8 +/- 54.9 (SD) to 207 +/- 98.1 fmol/ml after AUN (P less than 0.02) as sodium excretion (UNaV) doubled. In MSG-treated rats, AUN produced no change in plasma IR-NTF concentration (58.8 +/- 21.3 vs. 68.3 +/- 18.5 fmol/ml (P = NS), nor did UNaV increase. Tissue content of IR-NTF was reduced in the arcuate nucleus and anterior lobe of pituitaries from MSG-treated rats compared with controls, but was no different in the neurointermediate lobe. These results indicate that the hypothalamic lesion produced by neonatal administration of MSG prevents both the increase in plasma IR-NTF concentration and the natriuresis after AUN, and therefore lend further support to the concept of a causal relationship between these two consequences of AUN.

Increased serum levels of the brain damage marker S100B after apnea in trained breath-hold divers: a study including respiratory and cardiovascular observations

2009 ◽  
Vol 107 (3) ◽  
pp. 809-815 ◽  
Author(s):  
Johan P. A. Andersson ◽  
Mats H. Linér ◽  
Henrik Jönsson
Keyword(s):  
Brain Damage ◽  
Serum Levels ◽  
Breath Hold ◽  
Long Term Effects ◽  
Arterial Blood ◽  
The Central Nervous System ◽  
Serious Injury ◽  
Protein S100b ◽  
The Brain ◽  
Damage Marker

The concentration of the protein S100B in serum is used as a brain damage marker in various conditions. We wanted to investigate whether a voluntary, prolonged apnea in trained breath-hold divers resulted in an increase of S100B in serum. Nine trained breath-hold divers performed a protocol mimicking the procedures they use during breath-hold training and competition, including extensive preapneic hyperventilation and glossopharyngeal insufflation, in order to perform a maximum-duration apnea, i.e., “static apnea” (average: 335 s, range: 281–403 s). Arterial blood samples were collected and cardiovascular variables recorded. Arterial partial pressures of O2 and CO2 (PaO2 and PaCO2) were 128 Torr and 20 Torr, respectively, at the start of apnea. The degree of asphyxia at the end of apnea was considerable, with PaO2 and PaCO2 reaching 28 Torr and 45 Torr, respectively. The concentration of S100B in serum transiently increased from 0.066 μg/l at the start of apnea to 0.083 μg/l after the apnea ( P < 0.05). The increase in S100B is attributed to the asphyxia or to other physiological responses to apnea, for example, increased blood pressure, and probably indicates a temporary opening of the blood-brain barrier. It is not possible to conclude that the observed increase in S100B levels in serum after a maximal-duration apnea reflects a serious injury to the brain, although the results raise concerns considering negative long-term effects. At the least, the results indicate that prolonged, voluntary apnea affects the integrity of the central nervous system and do not preclude cumulative effects.

Exposure to 835 MHz radiofrequency electromagnetic field induces autophagy in hippocampus but not in brain stem of mice

2017 ◽  
Vol 34 (1) ◽  
pp. 23-35 ◽  
Author(s):  
Ju Hwan Kim ◽  
Da-Hyeon Yu ◽  
Hyo-Jeong Kim ◽  
Yang Hoon Huh ◽  
Seong-Wan Cho ◽  
...  
Keyword(s):  
Brain Stem ◽  
Mobile Phones ◽  
Hippocampal Neurons ◽  
Brain Regions ◽  
Pcr Analysis ◽  
Limited Information ◽  
The Central Nervous System ◽  
Neuronal Functions ◽  
Adaptation Processes ◽  
The Brain

The exploding popularity of mobile phones and their close proximity to the brain when in use has raised public concern regarding possible adverse effects from exposure to radiofrequency electromagnetic fields (RF-EMF) on the central nervous system. Numerous studies have suggested that RF-EMF emitted by mobile phones can influence neuronal functions in the brain. Currently, there is still very limited information on what biological mechanisms influence neuronal cells of the brain. In the present study, we explored whether autophagy is triggered in the hippocampus or brain stem after RF-EMF exposure. C57BL/6 mice were exposed to 835 MHz RF-EMF with specific absorption rates (SAR) of 4.0 W/kg for 12 weeks; afterward, the hippocampus and brain stem of mice were dissected and analyzed. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis demonstrated that several autophagic genes, which play key roles in autophagy regulation, were significantly upregulated only in the hippocampus and not in the brain stem. Expression levels of LC3B-II protein and p62, crucial autophagic regulatory proteins, were significantly changed only in the hippocampus. In parallel, transmission electron microscopy (TEM) revealed an increase in the number of autophagosomes and autolysosomes in the hippocampal neurons of RF-EMF-exposed mice. The present study revealed that autophagy was induced in the hippocampus, not in the brain stem, in 835 MHz RF-EMF with an SAR of 4.0 W/kg for 12 weeks. These results could suggest that among the various adaptation processes to the RF-EMF exposure environment, autophagic degradation is one possible mechanism in specific brain regions.

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