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 ◽  
...  
Nutrients ◽  
2018 ◽  
Vol 10 (9) ◽  
pp. 1246 ◽  
Author(s):  
Yvan Peterschmitt ◽  
Souleymane Abdoul-Azize ◽  
Babar Murtaza ◽  
Marie Barbier ◽  
Amira Khan ◽  
...  

The origin of spontaneous preference for dietary lipids in humans and rodents is debated, though recent compelling evidence has shown the existence of fat taste that might be considered a sixth taste quality. We investigated the implication of gustatory and reward brain circuits, triggered by linoleic acid (LA), a long-chain fatty acid. The LA was applied onto the circumvallate papillae for 30 min in conscious C57BL/6J mice, and neuronal activation was assessed using c-Fos immunohistochemistry. By using real-time reverse transcription polymerase chain reaction (RT-qPCR), we also studied the expression of mRNA encoding brain-derived neurotrophic factor (BDNF), Zif-268, and Glut-1 in some brain areas of these animals. LA induced a significant increase in c-Fos expression in the nucleus of solitary tract (NST), parabrachial nucleus (PBN), and ventroposterior medialis parvocellularis (VPMPC) of the thalamus, which are the regions known to be activated by gustatory signals. LA also triggered c-Fos expression in the central amygdala and ventral tegmental area (VTA), involved in food reward, in conjunction with emotional traits. Interestingly, we noticed a high expression of BDNF, Zif-268, and Glut-1 mRNA in the arcuate nucleus (Arc) and hippocampus (Hipp), where neuronal activation leads to memory formation. Our study demonstrates that oral lipid taste perception might trigger the activation of canonical gustatory and reward pathways.


2001 ◽  
Vol 281 (6) ◽  
pp. H2626-H2635 ◽  
Author(s):  
A. Caston-Balderrama ◽  
M. J. M. Nijland ◽  
T. J. McDonald ◽  
M. G. Ross

We previously demonstrated a functional systemic dipsogenic response in the near-term fetal sheep (128–130 days; 145 days = full-term) with swallowing activity stimulated in response to central and systemic hypertonic saline. Preterm fetal sheep (110–115 days) do not consistently demonstrate swallowing in response to hypertonic stimuli, and it is unclear whether this is due to immaturity of osmoreceptor mechanisms or neuronal pathways activating swallowing motor neurons. To determine whether osmoreceptive regions in the preterm fetus are activated by changes in plasma tonicity, we examined Fos expression with immunostaining in these neurons in response to an osmotic challenge. Nine preterm fetal sheep [five hypertonic saline-treated fetuses (Hyp) and four isotonic saline-treated fetuses (Iso)] were prepared with vascular and intraperitoneal catheters. Seventy-five minutes before tissue collection, hypertonic (1.5 M) or isotonic saline was infused (12 ml/kg) via an intraperitoneal catheter to fetuses. Brains were examined for patterns of neuronal activation (demonstrated by Fos protein expression). Hyp demonstrated increases in plasma osmolality (∼10 mosmol/kg H2O) and Na concentrations (5 meq/l). Increased Fos expression was detected in Hyp in the organum vasculosum of the lamina terminalis (OVLT), subfornical organ (SFO), median preoptic nucleus (MnPO), supraoptic (SON), and paraventricular nuclei (PVN) compared with Iso animals. Neuronal activation within the OVLT, SFO, and MnPO indicates intact osmoregulatory mechanisms, whereas activation of the SON and PVN suggests intact fetal neural pathways to arginine vasopressin neurons. These results suggest that preterm fetal swallowing insensitivity to osmotic stimuli may be due to immaturity of integrated motor neuron pathways.


2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Maria Constanza Paz ◽  
Natalia Andrea Marchese ◽  
Liliana M. Cancela ◽  
Claudia Bregonzio

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.


Science ◽  
2007 ◽  
Vol 318 (5850) ◽  
pp. 655-658 ◽  
Author(s):  
Marco Contreras ◽  
Francisco Ceric ◽  
Fernando Torrealba

Addiction profoundly alters motivational circuits so that drugs become powerful reinforcers of behavior. The interoceptive system continuously updates homeostatic and emotional information that are important elements in motivational decisions. We tested the idea that interoceptive information is essential in drug craving and in the behavioral signs of malaise. We inactivated the primary interoceptive cortex in amphetamine-experienced rats, which prevented the urge to seek amphetamine in a place preference task. Interoceptive insula inactivation also blunted the signs of malaise induced by acute lithium administration. Drug-seeking and malaise both induced Fos expression, a marker of neuronal activation, in the insula. We conclude that the insular cortex is a key structure in the perception of bodily needs that provides direction to motivated behaviors.


1999 ◽  
Vol 7 (4) ◽  
pp. E14 ◽  
Author(s):  
James P. McAllister ◽  
Arcangela S. Wood ◽  
Martha J. Johnson ◽  
Robert W. Connelly ◽  
David J. Skarupa ◽  
...  

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.


2004 ◽  
Vol 83 (1) ◽  
pp. 50-54 ◽  
Author(s):  
C.M. Magdalena ◽  
V.P. Navarro ◽  
D.M. Park ◽  
M.B.S. Stuani ◽  
M.J.A. Rocha

In the rat experimental model, molar tooth movement induced by Waldo’s method is known to cause a temporally and spatially defined pattern of brain neuronal activation. Since orthodontic correction usually involves the entire dental arch, we used a spring-activated appliance to extend the investigation to incisors, and we included brain regions related to antinociception. Adjustment of the non-activated appliance on incisors resulted in c-fos expression in the dorsal raphe, peri-aqueductal gray matter, and the locus coeruleus, in addition to trigeminal sensory subnuclei and the parabrachial nucleus, where neuronal activation has already been detected in previous studies on molar tooth movement. Appliance activation with a 70- g force resulted in a further increase in Fos-immunoreactive neurons in the trigeminal sensory subnucleus caudalis and in the dorsal raphe. This result suggests that there is a recruitment of neurons related to nociception and to antinociception when tooth movement is increased.


MethodsX ◽  
2021 ◽  
pp. 101348
Author(s):  
Cristina Cosi ◽  
Michael Millar ◽  
Mariana Beltran ◽  
Lorcan Sherry ◽  
Silvia Gatti-McArthur

2014 ◽  
Vol 281 (1783) ◽  
pp. 20140025 ◽  
Author(s):  
P. E. Jorge ◽  
J. B. Phillips ◽  
A. Gonçalves ◽  
P. A. M. Marques ◽  
P. Nĕmec

The dorsolateral area of the hippocampal formation of birds is commonly assumed to play a central role in processing information needed for geographical positioning and homing. Previous work has interpreted odour-induced activity in this region as evidence for an ‘olfactory map’. Here, we show, using c-Fos expression as a marker, that neuronal activation in the dorsolateral area of the hippocampal formation of pigeons is primarily a response to odour novelty, not to the spatial distribution of odour sources that would be necessary for an olfactory map. Pigeons exposed to odours had significantly more neurons activated in this area of the brain than pigeons exposed to filtered air with odours removed. This increased activity was observed only in response to unfamiliar odours. No change in activity was observed when pigeons were exposed to home odours. These findings are consistent with non-home odours activating non-olfactory components of the pigeon's navigation system. The pattern of neuronal activation in the triangular and dorsomedial areas of the hippocampal formation was, by contrast, consistent with the possibility that odours play a role in providing spatial information.


Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Amit H Shah ◽  
Bradley D Hammond ◽  
Gregory D Fink ◽  
David L Kreulen

Sympathetic activity is chronically elevated in hypertensive human patients and in many animal models of hypertension, including the deoxycorticosterone (DOCA)-salt rat model. Sympathetic ganglia receive signals from the central nervous system and relay them to blood vessels and peripheral organs. How sympathetic ganglia respond to activation signals differently in hypertension is not fully understood. We examined how direct and indirect activators of sympathetic ganglia would influence neuronal activation. 2-deoxy-D-glucose (2-DG) is a glucose analog that causes hypoglycemia leading to centrally-mediated, indirect activation of celiac ganglia, a prevertebral sympathetic ganglion. Nicotine directly activates sympathetic ganglia by acting on cholinergic receptors found on most sympathetic neurons. Acute neuronal activation was examined by measuring c-fos immunoreactivity (ir). We hypothesized that since there is higher chronic sympathetic activity in DOCA-salt hypertensive than normotensive rats, both direct and indirect acute activators will induce higher c-fos expression in sympathetic ganglia of normotensive than hypertensive rats. Maximal c-fos expression for 2-DG (800mg/kg i.p.) and nicotine (2mg/kg s.c.) treatments was observed 2hrs post-treatment and for all following experiments, celiac ganglia were dissected and fixed 2hrs post-treatment. Following nicotine treatment, c-fos expression was significantly higher in celiac ganglia of normotensive (25.5 ± 9.7 c-fos ir neurons/m^2) than hypertensive (12.0 ± 4.8 c-fos ir neurons/m^2) rats. However, following 2-DG treatment, c-fos expression was similar in celiac ganglia of normotensive (49.1 ± 17.6 c-fos ir neurons/m^2) and hypertensive (49.4 ± 16.0 c-fos ir neurons/m^2). In contrast with our hypothesis, only the direct but not the indirect activation of sympathetic ganglia induced higher sympathetic neuronal activation in normotensive than hypertensive rats. Thus, a centrally-mediated metabolic stimulus does not activate pathways to sympathetic ganglia differentially in normotension versus hypertension. However, direct ganglionic stimulation leads to greater neuronal activation in normotensive than hypertensive ganglia.


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