scholarly journals Effect of mother alcoholization on the activity of ghrelin system in prenatal and early postnatal periods of rat offspring

2015 ◽  
Vol 13 (2) ◽  
pp. 10-13 ◽  
Author(s):  
Marat Igorevich Airapetov ◽  
Platon Platonovich Khokhlov ◽  
Eugeny Rudolfovich Bychkov ◽  
Edgar Arturovich Sekste ◽  
Natalia Dmitrievna Yakushina ◽  
...  
Keyword(s):  
Blood Serum ◽  
Mrna Expression ◽  
Brain Structures ◽  
Postnatal Period ◽  
Receptor Expression ◽  
Dopaminergic Receptors ◽  
Adult Rats ◽  
Ghrelin Receptor ◽  
Chronic Alcoholization ◽  
The Brain

The purpose of the paper was to study both the desacylghrelin (unacylated ghrelin) level in the blood serum and expression of mRNA ghrelin receptor in the brain structures in ontogeny after chronic alcoholization in rats. The results proved that the prenatal effect of ethanol negatively affected the maturation of dopaminergic and ghrelin systems of the brain as well as involvement of ghrelin system in mechanisms of alcohol dependence formation. The decrease of COMT mRNA expression simultaneoully with the increase of expression of D2 long and short isoforms of dopaminergic receptors and misbalance of ghrelin system were observed. Alcoholization of mothers reduced desacylghrelin level in the blood serum in early postnatal period in offsprings although mRNA expression of ghrelin receptor in the brain was elevated. Chronic alcoholization of adult rats also affected the ghrelin system. In the alcoholiztion process, the reduced contents of desacylghrelin in the blood serum with compensatory increase of ghrelin receptor expression in the brain were registered. After withdrawal of ethanol, the recovery of desacylghrelin level (tendency to normalization) was observed.

scholarly journals Temporal Profile of Transporter mRNA Expression in the Brain after Traumatic Brain Injury in Developing Rats

2019 ◽  
Author(s):  
Solomon M. Adams ◽  
Fanuel T. Hagos ◽  
Jeffrey P. Cheng ◽  
Robert S. B. Clark ◽  
Patrick M. Kochanek ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mrna Expression ◽  
Neurovascular Unit ◽  
Post Injury ◽  
Adult Rats ◽  
Order Of Magnitude ◽  
Liver And Kidney ◽  
The Central Nervous System ◽  
The Brain

ABSTRACTTraumatic brain injury (TBI) is a leading cause of death in children and young adults; however, new pharmacologic approaches have failed to improve outcomes in clinical trials. Transporter proteins are central to the maintenance of homeostasis within the neurovascular unit, and regulate drug penetration into the brain. Our objective was to measure transporter temporal changes in expression in the hippocampus and cortex after experimental TBI in developing rats. We also evaluated the expression of transporters in brain, liver, and kidney across the age spectrum in both pediatric and adult rats. Eighty post-natal day (PND)-17 rats and four adult rats were randomized to receive controlled cortical impact (CCI), sham surgery, or no surgery. mRNA transcript counts for 27 ATP-binding cassette and solute carrier transporters were measured in the hippocampus, cortex, choroid plexus, liver, and kidney at 3h, 12h, 24h, 72h, 7d, and 14d post injury. After TBI, the expression of many transporters (Abcc2, Slc15a2, Slco1a2) decreased significantly in the first 24 hours, with a return to baseline over 7-14 days. Some transporters (Abcc4, Abab1a/b, Slc22a4) showed a delayed increase in expression. Baseline expression of transporters was of a similar order of magnitude in brain tissues relative to liver and kidney. Findings suggest that transporter-regulated processes may be impaired in the brain early after TBI and are potentially involved in the recovery of the neurovascular unit. Our data also suggest that transport-dependent processes in the brain are of similar importance as those seen in organs involved in drug metabolism and excretion.Significance StatementBaseline transporter mRNA expression in the central nervous system is of similar magnitude as liver and kidney, and experimental traumatic brain injury is associated with acute decrease in expression of several transporters, while others show delayed increase or decrease in expression. Pharmacotherapy following traumatic brain injury should consider potential pharmacokinetic changes associated with transporter expression.

scholarly journals Alteration of the Leptin Network in Late Morbid Obesity Induced in Mice by Brain Infection with Canine Distemper Virus

1999 ◽  
Vol 73 (9) ◽  
pp. 7317-7327 ◽  
Author(s):  
Arlette Bernard ◽  
Richard Cohen ◽  
Seng-Thuon Khuth ◽  
Bruno Vedrine ◽  
Olivier Verlaeten ◽  
...  
Keyword(s):  
Canine Distemper Virus ◽  
Leptin Receptor ◽  
Motor Impairment ◽  
Brain Structures ◽  
Receptor Expression ◽  
Leptin Resistance ◽  
Obese Mice ◽  
Canine Distemper ◽  
New Paradigm ◽  
The Brain

ABSTRACT Viruses can induce progressive neurologic disorders associated with diverse pathological manifestations, and therefore, viral infection of the brain can impair differentiated neural functions, depending on the initial viral tropism. We have previously reported that canine distemper virus (CDV) targets certain mouse brain structures, including the hypothalamus, early and selectively. Infected mice exhibit acute encephalitis, with late disease, characterized by motor impairment or obesity syndrome, appearing in some of the surviving mice several months after the initial viral replication. In the present study, we show viral persistence in the hypothalami of obese mice, as demonstrated by low, but still significant, levels of CDV nucleoprotein transcripts, associated with a dramatic decrease in F gene mRNAs. Given the pivotal role of the hypothalamus in obesity (eating behavior, energy consumption, and neuroendocrine function) and that of leptin, the adipose tissue-derived satiety factor acting through hypothalamic receptors, we analyzed the leptin networks in both obese and nonobese mice. The discrepancy found between the chronic and dramatic increase in blood leptin levels and the occurrence of obesity may be due to leptin resistance in the brain. In fact, expression of the long leptin receptor isoform, representing the functional leptin receptor, was specifically downregulated in the hypothalami of obese mice, explaining their inability to generate an adequate response to leptin in the brain. Intriguingly, during the acute phase of infection, its expression was increased in CDV-targeted structures in all infected mice and remained high in obese mice in all CDV-targeted structures, except for the hypothalamus. The biphasic change in hypothalamic leptin receptor expression seen during the progression of CDV-induced obesity provides a new paradigm for understanding mechanisms of neuroendocrinological, virus-induced abnormalities.

scholarly journals Effect of afobazole and levodopa on the activity of proline-specific proteinases and adenosine deaminase in blood serum and brain structures of rats with experimental Parkinson's syndrome induced by systemic administration of rotenone

2017 ◽  
Vol 63 (6) ◽  
pp. 565-569
Author(s):  
E.A. Ivanova ◽  
N.N. Zolotov ◽  
I.G. Kapitsa ◽  
V.F. Pozdnev ◽  
E.A. Valdman ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Blood Serum ◽  
Adenosine Deaminase ◽  
Intraperitoneal Administration ◽  
Brain Structures ◽  
The Other ◽  
Parkinson's Syndrome ◽  
Parkinson’S Syndrome ◽  
Increased Activity ◽  
The Brain

Rats with experimental Parkinson’s syndrome induced by seven-day intraperitoneal administration of rotenone at a dose of 2.75 mg/kg have an increased activity of prolylendopeptidase (EC 3.4.21.26, PREP) in blood serum and a decreased activity of adenosine deaminase (EC 3.5.4.4, ADA) in serum and in the prefrontal cortex. PREP and ADA activity in other brain structures (in the striatum, hypothalamus and hippocampus) did not change; dipeptidyl peptidase IV activity (EC 3.4.14.5, DPP-4, CD26) also remained constant in serum and in all the brain structures investigated. Afobazole and levodopa, which exhibit antiparkinsonian activity in this model of Parkinson’s syndrome, decrease elevated PREP activity in serum and increase reduced ADA activity in the prefrontal cortex of rats with the experimental pathology. Meanwhile, treatment with the study drugs was associated with a decrease of ADA activity in the other brain structures.

scholarly journals Dynamic Changes in Oxytocin Receptor Expression and Activation at Parturition in the Rat Brain

Endocrinology ◽  
2007 ◽  
Vol 148 (10) ◽  
pp. 5095-5104 ◽  
Author(s):  
Simone L. Meddle ◽  
Valerie R. Bishop ◽  
Effimia Gkoumassi ◽  
Fred W. van Leeuwen ◽  
Alison J. Douglas
Keyword(s):  
Mrna Expression ◽  
Paraventricular Nucleus ◽  
Maternal Behavior ◽  
Brain Regions ◽  
Oxytocin Receptor ◽  
Lateral Septum ◽  
Receptor Expression ◽  
Olfactory Bulbs ◽  
Bed Nucleus ◽  
The Brain

Oxytocin plays a pivotal role in rat parturition, acting within the brain to facilitate its own release in the supraoptic nucleus (SON) and paraventricular nucleus, and to stimulate maternal behavior. We investigated oxytocin receptor (OTR) expression and activation perinatally. Using a 35S-labeled riboprobe complementary to OTR mRNA, OTR expression was quantified in proestrus virgin, 21- and 22-day pregnant, parturient (90 min. from pup 1 birth), and postpartum (4–12 h from parturition) rats. Peak OTR mRNA expression was observed at parturition in the SON, brainstem regions, medial preoptic area (mPOA), bed nucleus of the stria terminalis (BnST), and olfactory bulbs, but there was no change in the paraventricular nucleus and lateral septum. OTR mRNA expression was increased on the day of expected parturition in the SON and brainstem, suggesting that oxytocin controls the pathway mediating input from uterine signals. Likewise, OTR mRNA expression was increased in the mPOA and BnST during labor/birth. In the olfactory bulbs and medial amygdala, parturition induced increased OTR mRNA expression compared with pre-parturition, reflecting their immediate response to new stimuli at birth. Postpartum OTR expression in all brain regions returned to levels observed in virgin rats. Parturition significantly increased the number of double-immunolabeled cells for Fos and OTR within the SON, brainstem, BnST, and mPOA regions compared with virgin rats. Thus, there are dynamic region-dependent changes in OTR-expressing cells at parturition. This altered OTR distribution pattern in the brain perinatally reflects the crucial role oxytocin plays in orchestrating both birth and maternal behavior.

scholarly journals Distribution of Glut1 Glucose Transporters in Different Brain Structures Compared to Glucose Utilization and Capillary Density of Adult Rat Brains

1997 ◽  
Vol 17 (2) ◽  
pp. 204-209 ◽  
Author(s):  
Karin Zeller ◽  
Sylvia Rahner-Welsch ◽  
Wolfgang Kuschinsky
Keyword(s):  
Glucose Utilization ◽  
Brain Structures ◽  
Capillary Density ◽  
Brain Regions ◽  
Capillary Endothelium ◽  
Tight Coupling ◽  
Adult Rats ◽  
Heterogeneous Distribution ◽  
Adult Rat ◽  
The Brain

Glut1 is a specific transporter system that mediates glucose transfer across the blood–brain barrier (BBB). Although the main location of Glut1 is in the capillary endothelium of the brain, its local distribution in different brain regions is not as well defined. In the present investigation, the local pattern of Glut1 distribution was determined in 13 brain structures using an immunoautoradiographic method developed for this purpose. A polyclonal antibody directed against the C-terminal amino acid sequence of Glut1 was applied to cryosections of rat brains. A secondary antibody was added that had been coupled to [35S]. Results show a heterogeneous distribution of Glut1 in the brain with activities of [35S] ranging from 65% below to 15% above the mean. White matter activity was lower than gray matter activity. For comparison, capillary sections were counted in corresponding cryosections by indirect immunofluorescence using fibronectin antibodies. In addition, local cerebral glucose utilization (LCGU) was analyzed in identical brain structures of conscious rats by the quantitative autoradiographic 2-deoxyglucose method. Significant correlations were found between Glut1 density and either LCGU or capillary density. Results indicate a tight coupling of Glut1 transporter density and capillary density to the LCGU of different BBB structures in adult rats.

scholarly journals Effect of hemic hypoxia on dynamics of GFAP concentrations in the structures of the brain and blood serum of rats

2016 ◽  
Vol 24 (1) ◽  
pp. 143-150 ◽  
Author(s):  
T. I. Duka ◽  
V. I. Chоrna
Keyword(s):  
Blood Flow ◽  
Quantitative Analysis ◽  
Intermediate Filaments ◽  
Regional Differences ◽  
Brain Structures ◽  
Astroglial Cells ◽  
Adult Rats ◽  
Cellular Population ◽  
The Brain ◽  
Neurospecific Protein

This article clarifies the questions on study of hypoxic influence on distribution of filament and soluble forms of GFAP in various structures of the brain (neocortex, cerebellum, hippocampus, striatum, middle brain, pons) and blood of the rats. Quantitative analysis of the contents of GFAP in the brain structures of hypoxic rats has established that hemic hypoxia results in changes in intracellular levels of GFAP forms and also in updating their ratio, which allows one to assume not only a change in astroglial cells, but also testifies to reorganization in the system of intermediate filaments of astrocytes. The level of GFAP substantially changed in all cerebral formations, which was already investigated in the early terms of hypoxic period. Observations showed that hemic hypoxia exerted a varied influence on expression of neurospecific protein in the different structures of cerebrum of rats. Differences in expression of GFAP can be caused by the regional differences in astroglial cellular population, and also their internal features that define the possible answers to hypoxic damage in different functional and morphological structures of the brain. An increase in expression of the investigated form of protein can explain strengthening of astroglial reactivity, a feature of the brain that appears in various types of pathologies of the CNS. Reactive asters in such exhibit hypertrophy and are characterized by an increased level of GFAP, which is an early and reliable indicator of astroglial pathology. An increase in expression of the investigated form of protein may be explained by strengthening of astroglial reactivity, a feature of the brain that appears in various types of pathologies of the CNS. The contents of GFAP in the blood of adult rats, as a result of the hypoxic influence received from it, can indicate a release of GFAP from damaged astrocytes in the blood flow. 

scholarly journals Regulation of GH secretagogue receptor gene expression in the rat nodose ganglion

2007 ◽  
Vol 194 (1) ◽  
pp. 41-46 ◽  
Author(s):  
Miho Sato ◽  
Keiko Nakahara ◽  
Mikiya Miyazato ◽  
Kenji Kangawa ◽  
Noboru Murakami
Keyword(s):  
Mrna Expression ◽  
Receptor Gene ◽  
Nodose Ganglion ◽  
Mrna Levels ◽  
Dynamic Changes ◽  
Ghrelin Receptor ◽  
Axon Terminals ◽  
Gastrointestinal Peptides ◽  
The Brain ◽  
Receptor Gene Expression

It has been shown that the ghrelin receptor, GH secretagogue receptor (GHS-R), is synthesized in neurons of the nodose ganglion and then transmitted to axon terminals, where it binds to ghrelin. The orexigenic signal of ghrelin secreted from the stomach is transmitted to the brain via the vagal afferent nerve. To explore the regulation of GHS-R synthesis in the nodose ganglion, we examined whether or not GHS-R type a mRNA expression shows circadian rhythm, and is affected by starvation, vagotomy, or i.v. administration of gastrointestinal peptides. Nodose ganglion GHS-R mRNA levels showed a diurnal rhythm, being high during periods of light and low during darkness. Although starvation tended to increase the level of GHS-R mRNA, a more significant increase was observed upon re-feeding. Vagotomy decreased the level of GHS-R mRNA significantly in comparison with animals that underwent a sham procedure. Cholecystokinin and gastrin increased the level of GHS-R mRNA after 2 h, but after 4 h, the level decreased. These results suggest that GHS-R synthesis in the nodose ganglion is regulated centrally and peripherally by neuronal and humoral information, and that these dynamic changes of GHS-R mRNA expression may be involved in the regulation of feeding by ghrelin.

scholarly journals Ghrelin and Growth Hormone Secretagogue Receptor Expression in Mice during Aging

Endocrinology ◽  
2007 ◽  
Vol 148 (3) ◽  
pp. 1323-1329 ◽  
Author(s):  
Yuxiang Sun ◽  
Jose Manuel Garcia ◽  
Roy G. Smith
Keyword(s):  
Pituitary Gland ◽  
Receptor Expression ◽  
Elderly Subjects ◽  
Mrna Levels ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Ghrelin Receptor ◽  
Igf I ◽  
The Impact ◽  
The Brain

In well-nourished humans, GH and IGF-I decline during aging, and the responsiveness of the GH axis to exogenous ghrelin is attenuated with age. Intriguingly, the GH/IGF-I axis is rejuvenated by chronic treatment with the ghrelin mimetic MK-0677, resulting in improvements in body composition, suggesting that frail elderly subjects might benefit from treatment with ghrelin and ghrelin mimetics. Mouse models are widely used to study the effects of ghrelin, but the impact of age on the ghrelin pathway is unclear. In this study, total and active ghrelin peptides were measured in plasma, and ghrelin mRNA was quantitated in brain tissue from different aged C57BL/6J mice. Surprisingly, plasma levels of ghrelin peptide slightly increased with age; ghrelin mRNA levels were similar in brains from mice aged 2, 6, 12, and 28 months but higher in mice aged 18 and 24 months. The tissue distribution of Ghsr1a mRNA (ghrelin receptor) was also characterized, and pituitary and brain exhibited the highest levels of expression. In the pituitary gland, the highest concentration of Ghsr1a mRNA was observed at age 1–2 months, it was lower at 6 months, and remained unchanged for up to 30 months of age. This result is consistent with the finding that GH release in response to exogenous ghrelin was not significantly different in mice aged 7–30 months. In the brain, Ghsr1a mRNA levels remained stable during aging. Hence, in C57BL/6J male mice, aging is not associated with changes in circulating ghrelin levels or changes in ghrelin receptor expression in the pituitary gland and brain.

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