scholarly journals Angiotensin II AT1Receptors Are Involved in Neuronal Activation Induced by Amphetamine in a Two-Injection Protocol

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Maria Constanza Paz ◽  
Natalia Andrea Marchese ◽  
Liliana M. Cancela ◽  
Claudia Bregonzio
Keyword(s):  
Prefrontal Cortex ◽  
Early Gene ◽  
Receptor Blocker ◽  
Prelimbic Cortex ◽  
Ang Ii ◽  
Neuronal Activation ◽  
Single Exposure ◽  
Injection Protocol ◽  
Fos Expression ◽  
Amphetamine Sensitization

It was already found that Ang II AT1receptors are involved in the neuroadaptative changes induced by a single exposure to amphetamine, and such changes are related to the development of behavioral and neurochemical sensitization. The induction of the immediately early gene c-fos has been used to define brain activated areas by amphetamine. Our aim was to evaluate the participation of AT1receptors in the neuronal activation induced by amphetamine sensitization. The study examined the c-fos expression in mesocorticolimbic areas induced by amphetamine challenge (0.5 mg/kg i.p) in animals pretreated with candesartan, a selective AT1receptor blocker (3 mg/kg p.o × 5 days), and amphetamine (5 mg/kg i.p) 3 weeks before the challenge. Increased c-fos immunoreactivity was found in response to the amphetamine challenge in the dorsomedial caudate-putamen and nucleus accumbens, and both responses were blunted by the AT1receptor blocker pretreatment. In the infralimbic prefrontal cortex, increased c-fos immunoreactivity was found in response to amphetamine and saline challenge, and both were prevented by the AT1receptor blocker. No differences were found neither in ventral tegmental area nor prelimbic cortex between groups. Our results indicate an important role for brain Ang II in the behavioral and neuronal sensitization induced by amphetamine.

Sensitized Fos expression in subterritories of the rat medial prefrontal cortex and nucleus accumbens following amphetamine sensitization as revealed by stereology

2002 ◽  
Vol 950 (1-2) ◽  
pp. 165-179 ◽  
Author(s):  
Gaël Hédou ◽  
Ana Lúcia Jongen-Rêlo ◽  
Carol A Murphy ◽  
Christian A Heidbreder ◽  
Joram Feldon
Keyword(s):  
Prefrontal Cortex ◽  
Nucleus Accumbens ◽  
Medial Prefrontal Cortex ◽  
Fos Expression ◽  
Amphetamine Sensitization

Decreased c-fos expression in experimental neonatal hydrocephalus: evidence for reduced neuronal activation

1999 ◽  
Vol 7 (4) ◽  
pp. E14 ◽  
Author(s):  
James P. McAllister ◽  
Arcangela S. Wood ◽  
Martha J. Johnson ◽  
Robert W. Connelly ◽  
David J. Skarupa ◽  
...  
Keyword(s):  
Immunohistochemical Analysis ◽  
Cellular Level ◽  
Early Gene ◽  
Neuronal Activation ◽  
Cellular Mechanisms ◽  
Tissue Samples ◽  
Functional Changes ◽  
Fos Expression ◽  
Regulate Protein ◽  
Cortical Regions

Although neonatal hydrocephalus often results in residual neurological impairments, little is known about the cellular mechanisms responsible for these deficits. The immediate early gene, fos (c-fos), functions as a “third messenger” to regulate protein synthesis and is a good marker for neuronal activation. To identify functional changes in neurons at the cellular level, the authors quantified fos RNA expression and localized fos protein in the H-Tx rat model of congenital hydrocephalus. Tissue samples from sensorimotor and auditory regions were obtained from hydrocephalic rats and age-matched, normal litter mates at 1, 6, 12, and 21 days of age (four-six animals in each group) and processed for immunohistochemical analysis of fos and Northern blot analysis of RNA. At 12 days of age, hydrocephalic animals exhibited significant decreases in the ratio of fos immunoreactive cells to Nissl-stained neurons from both cortical regions, but no statistical differences were noted in fos expression. At 21 days of age, both the ratio of fos immunoreactive cells to Nissl-stained neurons and fos expression decreased significantly. The number of fos-positive neurons decreased in all cortical layers but was most prominent in layers V through VI. This decrease did not appear to be caused by neuronal death because examination of Nissl-stained sections revealed many viable neurons within the areas where fos immunoreactivity was absent. These results suggest that progressive neonatal hydrocephalus reduces the capacity for neuronal activation in the cerebral cortex, primarily in those neurons that provide corticofugal projections, and that this impairment may begin during relatively early stages of ventriculomegaly.

scholarly journals Sex-dependent effects of traumatic stress on social behavior and neuronal activation in the prefrontal cortex and amygdala

2021 ◽  
Author(s):  
Mariia Dorofeikova ◽  
Chandrashekhar D Borkar ◽  
Katherine Weissmuller ◽  
Lydia Smith-Osborne ◽  
Samhita Basavanhalli ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Social Interaction ◽  
Social Behavior ◽  
Acute Stress ◽  
Negative Impact ◽  
Early Gene ◽  
Central Nucleus ◽  
Dependent Manner ◽  
Neuronal Activation ◽  
Footshock Stress

Social behavior is complex and fundamental, and deficits in social behavior are common pathological features for a variety of psychiatric disorders including anxiety, depression, and posttraumatic stress disorder. Acute stress has a negative impact on social behavior, and these effects may vary based on sex. The aim of this study was to explore the effect of footshock stress on the sociability of male and female C57Bl/6J mice. Animals were divided into two main groups of footshock exposure or context exposure control. Each group had mice that were treated with either the benzodiazepine alprazolam, or vehicle. Neuronal activation during social interaction was assessed using immunohistochemistry against the immediate early gene product cFos. Footshock stress induced a significantly increased latency to approach a social interaction counterpart in both sexes. Stress-induced increases in defensive tail-rattling behavior elicited during the sociability test were sex-dependent and alleviated by alprazolam. Alprazolam also lowered social exploration and neuronal activation in the infralimbic medial prefrontal cortex. Social interaction induced sex-dependent differences in cFos activation in the lateral subdivision of the central nucleus of the amygdala and ventromedial intercalated cell clusters. Overall, our results suggest that acute footshock stress induces alterations in sociability and patterns of cFos activation in a sex-dependent manner.

Central neuronal activation and pressor responses induced by circulating ANG II: role of the brain aldosterone-“ouabain” pathway

2010 ◽  
Vol 299 (2) ◽  
pp. H422-H430 ◽  
Author(s):  
Bing S. Huang ◽  
Sara Ahmadi ◽  
Monir Ahmad ◽  
Roselyn A. White ◽  
Frans H. H. Leenen
Keyword(s):  
Mineralocorticoid Receptor ◽  
Pressor Response ◽  
Plasma Aldosterone ◽  
Receptor Blocker ◽  
Ang Ii ◽  
Neuronal Activation ◽  
Intracerebroventricular Infusion ◽  
Pressor Responses ◽  
Hypothalamic Nuclei

An increase in plasma ANG II causes neuronal activation in hypothalamic nuclei and a slow pressor response, presumably by increasing sympathetic drive. We evaluated whether the activation of a neuromodulatory pathway, involving aldosterone and “ouabain,” is involved in these responses. In Wistar rats, the subcutaneous infusion of ANG II at 150 and 500 ng·kg−1·min−1 gradually increased blood pressure up to 60 mmHg at the highest dose. ANG II at 500 ng·kg−1·min−1 increased plasma ANG II by 4-fold, plasma aldosterone by 25-fold, and hypothalamic aldosterone by 3-fold. The intracerebroventricular infusion of an aldosterone synthase (AS) inhibitor prevented the ANG II-induced increase in hypothalamic aldosterone without affecting the increase in plasma aldosterone. Neuronal activity, as assessed by Fra-like immunoreactivity, increased transiently in the subfornical organ (SFO) but progressively in the paraventricular nucleus (PVN) and supraoptic nucleus (SON). The central infusion of the AS inhibitor or a mineralocorticoid receptor blocker markedly attenuated the ANG II-induced neuronal activation in the PVN but not in the SON. Pressor responses to ANG II at 150 ng·kg−1·min−1 were abolished by an intracerebroventricular infusion of the AS inhibitor. Pressor responses to ANG II at 500 ng·kg−1·min−1 were attenuated by the central infusion of the AS inhibitor or the mineralocorticoid receptor blocker by 70–80% and by Digibind (to bind “ouabain”) by 50%. These results suggest a novel central nervous system mechanism for the ANG II-induced slow pressor response, i.e., circulating ANG II activates the SFO, leading to the direct activation of the PVN and SON, and, in addition, via aldosterone-dependent amplifying mechanisms, causes sustained activation of the PVN and thereby hypertension.

scholarly journals Adjustment of Whey:Casein Ratio from 20:80 to 60:40 in Milk Formulation Affects Food Intake and Brainstem and Hypothalamic Neuronal Activation and Gene Expression in Laboratory Mice

Foods ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 658
Author(s):  
Erin L. Wood ◽  
David G. Christian ◽  
Mohammed Arafat ◽  
Laura K. McColl ◽  
Colin G. Prosser ◽  
...  
Keyword(s):  
Food Intake ◽  
Area Postrema ◽  
Energy Levels ◽  
Early Gene ◽  
Hypothalamic Nucleus ◽  
Laboratory Mice ◽  
Neuronal Activation ◽  
Short Term ◽  
Animal Milk ◽  
The Impact

Adjustment of protein content in milk formulations modifies protein and energy levels, ensures amino acid intake and affects satiety. The shift from the natural whey:casein ratio of ~20:80 in animal milk is oftentimes done to reflect the 60:40 ratio of human milk. Studies show that 20:80 versus 60:40 whey:casein milks differently affect glucose metabolism and hormone release; these data parallel animal model findings. It is unknown whether the adjustment from the 20:80 to 60:40 ratio affects appetite and brain processes related to food intake. In this set of studies, we focused on the impact of the 20:80 vs. 60:40 whey:casein content in milk on food intake and feeding-related brain processes in the adult organism. By utilising laboratory mice, we found that the 20:80 whey:casein milk formulation was consumed less avidly and was less preferred than the 60:40 formulation in short-term choice and no-choice feeding paradigms. The relative PCR analyses in the hypothalamus and brain stem revealed that the 20:80 whey:casein milk intake upregulated genes involved in early termination of feeding and in an interplay between reward and satiety, such as melanocortin 3 receptor (MC3R), oxytocin (OXT), proopiomelanocortin (POMC) and glucagon-like peptide-1 receptor (GLP1R). The 20:80 versus 60:40 whey:casein formulation intake differently affected brain neuronal activation (assessed through c-Fos, an immediate-early gene product) in the nucleus of the solitary tract, area postrema, ventromedial hypothalamic nucleus and supraoptic nucleus. We conclude that the shift from the 20:80 to 60:40 whey:casein ratio in milk affects short-term feeding and relevant brain processes.

Amphetamine sensitization is accompanied by an increase in prelimbic cortex activity

Neuroscience ◽  
2015 ◽  
Vol 288 ◽  
pp. 1-9 ◽  
Author(s):  
M.I. Aguilar-Rivera ◽  
J.P. Casanova ◽  
R.I. Gatica ◽  
G.J. Quirk ◽  
J.A. Fuentealba
Keyword(s):  
Prelimbic Cortex ◽  
Amphetamine Sensitization

Central angiotensin induction of fetal brain c-fos expression and swallowing activity

2001 ◽  
Vol 280 (6) ◽  
pp. R1837-R1843 ◽  
Author(s):  
Zhice Xu ◽  
Calvario Glenda ◽  
Linda Day ◽  
Jiaming Yao ◽  
Michael G. Ross
Keyword(s):  
Body Fluid ◽  
Drinking Behavior ◽  
Fetal Brain ◽  
Cellular Responses ◽  
Ang Ii ◽  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Fluid Regulation ◽  
Fos Expression ◽  
Near Term

The present study examined physiological and cellular responses to central application of ANG II in ovine fetuses and determined the fetal central ANG-mediated dipsogenic sites in utero. Chronically prepared near-term ovine fetuses (130 ± 2 days) received injection of ANG II (1.5 μg/kg icv). Fetuses were monitored for 3.5 h for swallowing activity, after which animals were killed and fetal brains were perfused for subsequent Fos staining. Intracerebroventricular ANG II significantly increased fetal swallowing in near-term ovine fetuses (1.1 ± 0.2 to 4.5 ± 1.0 swallows/min). The initiation of stimulated fetal swallowing activity was similar to the latency of thirst responses (drinking behavior) elicited by central ANG II in adult animals. ANG II evoked increased Fos staining in putative dipsogenic centers, including the subfornical organ, organum vasculosum of the lamina terminalis, and median preoptic nucleus. Intracerebroventricular injection of ANG II also caused c- fos expression in the fetal hindbrain. These results indicate that an ANG II-mediated central dipsogenic mechanism is intact before birth, acting at sites consistent with the dipsogenic neural network. Central ANG II mechanisms likely contribute to fetal body fluid and amniotic fluid regulation.

Neuronal Activation Visualized by Fos-Expression after Intracerebral Microdialysis of Drugs

1997 ◽  
pp. 1161-1166
Author(s):  
M. Feenstra ◽  
M. Bubser ◽  
E. Erdtsieck-Ernste ◽  
A. van der Wal ◽  
M. Botterblom ◽  
...  
Keyword(s):  
Intracerebral Microdialysis ◽  
Neuronal Activation ◽  
Fos Expression
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