scholarly journals Eff ect of a single asenapine treatment on Fos expression in the brain catecholamine-synthesizing neurons: impact of a chronic mild stress preconditioning

2017 ◽  
Vol 51 (2) ◽  
pp. 73-83
Author(s):  
J. Osacka ◽  
L. Horvathova ◽  
Z. Majercikova ◽  
Alexander Kiss

AbstractObjective. Fos protein expression in catecholamine-synthesizing neurons of the substantia nigra (SN) pars compacta (SNC, A8), pars reticulata (SNR, A9), and pars lateralis (SNL), the ventral tegmental area (VTA, A10), the locus coeruleus (LC, A6) and subcoeruleus (sLC), the ventrolateral pons (PON-A5), the nucleus of the solitary tract (NTS-A2), the area postrema (AP), and the ventrolateral medulla (VLM-A1) was quantitatively evaluated aft er a single administration of asenapine (ASE) (designated for schizophrenia treatment) in male Wistar rats preconditioned with a chronic unpredictable variable mild stress (CMS) for 21 days. Th e aim of the present study was to reveal whether a single ASE treatment may 1) activate Fos expression in the brain areas selected; 2) activate tyrosine hydroxylase (TH)-synthesizing cells displaying Fos presence; and 3) be modulated by CMS preconditioning.Methods. Control (CON), ASE, CMS, and CMS+ASE groups were used. CMS included restraint, social isolation, crowding, swimming, and cold. Th e ASE and CMS+ASE groups received a single dose of ASE (0.3 mg/kg, s.c.) and CON and CMS saline (300 μl/rat, s.c.). The animals were sacrificed 90 min aft er the treatments. Fos protein and TH-labeled immunoreactive perikarya were analyzed on double labeled histological sections and enumerated on captured pictures using combined light and fluorescence microscope illumination.Results. Saline or CMS alone did not promote Fos expression in any of the structures investigated. ASE alone or in combination with CMS elicited Fos expression in two parts of the SN (SNC, SNR) and the VTA. Aside from some cells in the central gray tegmental nuclei adjacent to LC, where a small number of Fos profiles occurred, none or negligible Fos occurrence was detected in the other structures investigated including the LC and sLC, PON-A5, NTS-A2, AP, and VLM-A1. CMS preconditioning did not infl uence the level of Fos induction in the SN and VTA elicited by ASE administration. Similarly, the ratio between the amount of free Fos and Fos colocalized with TH was not aff ected by stress preconditioning in the SNC, SNR, and the VTA.Conclusions. Th e present study provides an anatomical/functional knowledge about the nature of the acute ASE treatment on the catecholamine-synthesizing neurons activity in certain brain structures and their missing interplay with the CMS preconditioning.

1999 ◽  
Vol 277 (2) ◽  
pp. R532-R540 ◽  
Author(s):  
Kathleen S. Curtis ◽  
J. Thomas Cunningham ◽  
Cheryl M. Heesch

Fos and dopamine β-hydroxylase immunoreactivity were evaluated in the brain stems of 21-day pregnant and virgin female rats injected with either hydralazine (HDZ; 10 mg/kg iv) or vehicle. HDZ produced significant hypotension in both groups, although baseline blood pressure was lower in pregnant rats (96 ± 2.5 mmHg) than in virgin female rats (121 ± 2.8 mmHg). There were no differences in Fos immunoreactivity in the brain stems of pregnant and virgin female rats after vehicle treatment. HDZ-induced hypotension significantly increased Fos expression in both groups; however, the magnitude of the increases differed in the caudal ventrolateral medulla (CVL), the area postrema (AP), and the rostral ventrolateral medulla (RVL). Fos expression after HDZ in pregnant rats was augmented in noncatecholaminergic neurons of the CVL but was attenuated in the AP and in noncatecholaminergic neurons in the RVL. These results are consistent with differences in the sympathetic response to hypotension between pregnant and virgin female rats and indicate that the central response to hypotension may be different in pregnant rats.


1997 ◽  
Vol 273 (6) ◽  
pp. R2059-R2071 ◽  
Author(s):  
Hubert Mönnikes ◽  
Gerd Lauer ◽  
Christoph Bauer ◽  
Johannes Tebbe ◽  
Tillmann T. Zittel ◽  
...  

Exogenous cholecystokinin (CCK) injected peripherally mimics effects of lipid entering the intestine on food intake and gastric motility via vagal afferents and induces c- fos expression in the locus ceruleus complex (LCC), nucleus of the solitary tract (NTS), area postrema (AP), and paraventricular nucleus (PVN). However, the role of peripheral endogenous CCK in induction of c- fos expression in the brain at ingestion of nutrients is controversial. In awake rats, intraduodenal lipid infusion markedly increased Fos protein-like immunoreactivity (FLI) in these brain nuclei. Perivagal capsaicin pretreatment reduced the increase of FLI in the LCC, NTS, and PVN by 66–86% and in the AP by 46%. The CCK-A receptor antagonist MK-329 (0.1 mg/kg ip) diminished the FLI increase in LC, NTS, AP, and PVN by 39–100%; the CCK-B receptor antagonist L-365,260 reduced the increased FLI in the AP by 54%. After capsaicin pretreatment, both CCK antagonists had additional inhibitory effects only on FLI in the AP. These findings suggest that entry of lipid into the intestine activates c- fos in the LCC, NTS, and PVN predominantly via CCK-A receptors on vagal afferents and in the AP via vagal and nonvagal pathways, as well as CCK-B and CCK-A receptors.


2004 ◽  
Vol 18 (3) ◽  
pp. 200-203 ◽  
Author(s):  
Weiyun Zhang ◽  
Jianmei Li ◽  
Jixiao Zhu ◽  
Zhenqiu Shi ◽  
Yong Wang ◽  
...  

Author(s):  
Mohammad Amin Safari ◽  
Maryam Koushkie Jahromi ◽  
Rasoul Rezaei ◽  
Hadi Aligholi ◽  
Serge Brand

This study assessed the effect of swimming training on anxiety-like behaviors and corticosterone. Thirty adult male Wistar rats were randomly assigned to five study conditions: swimming training (ST); exposure to chronic mild stress (CS); exposure to chronic mild stress followed by swimming training (CS + ST); exposure to chronic mild stress followed by a recovery period (CS + recovery); control. The exercise training consisted of 60 min of swimming exercise per day, for five days a week, and four consecutive weeks. A chronic mild stress program (CMS) was applied for a period of four weeks. Anxiety-like behaviors were measured by open field test (OFT). The number of excrements and blood corticosterone were used as physiological parameters of anxiety. To assess corticosterone, blood samples were taken 48 h after the last session of experiments. Compared to other study conditions, the lowest anxiety-like behaviors and corticosterone concentrations were observed in the ST condition in unstressed rats. In stressed rats, as in the ST + CS group, swimming training probably reduced some anxiety behaviors, but the results showed increased corticosterone compared to control and CS + Recovery. Anxiety parameters and corticosterone concentrations were greatest in the CS condition. In the ST group, anxiety parameters were less than for the ST + CS group. In the CS + Recovery group, anxiety parameters were less than for the CS group. In summary, self-paced swimming training could attenuate some anxiety parameters in both stressed and non-stressed rats. The effect of swimming training in unstressed rats was more prominent than in stressed rats. In stressed rats, a period of recovery was more effective than swimming training in reducing corticosterone. Mechanisms of anxiety reduction other than cortisol should be investigated in future research.


1997 ◽  
Vol 272 (1) ◽  
pp. R126-R133 ◽  
Author(s):  
S. L. Hochstenbach ◽  
J. Ciriello

Two series of experiments were done in male Wistar rats to investigate the medullary pathways that mediate the depressor responses from sodium-sensitive sites in the nucleus of the solitary tract (NTS). In the first series, the anterograde tract tracer Phaseolus vulgaris leucoagglutinin (PHA-L) was iontophoresed unilaterally at sites in the NTS at which microinjections (20 nl) of a 154-175 mM NaCl solution elicited depressor responses. PHA-L injection sites were found to be localized within the medial subnucleus of the NTS (Sm). In the medulla, PHA-L-labeled fibers and presumptive terminal boutons were observed bilaterally, but with an ipsilateral predominance, throughout the rostrocaudal extent of the NTS the dorsal motor nucleus of the vagus, area postrema, the ventrolateral medulla (VLM), and nucleus ambiguus. The pontine region, containing the A5 catecholaminergic cell group and the parabrachial nucleus, also received projections from Sm. In the second series of experiments, the effect of blocking synaptic transmission in VLM with cobalt chloride (CoCl2; 5 mM, 100 nl) on the cardiovascular response elicited by microinjection (20 nl) of hypertonic saline (154-175 mM) into the ipsilateral Sm was investigated in the alpha-chloralose-anesthetized, paralyzed, and artificially ventilated rat. Microinjection of CoCl2 into VLM, at sites shown in the previous study to receive efferent projections from Sm, significantly attenuated the depressor (60%) and bradycardic (80%) responses to stimulation of Sm. These data indicate that the sodium-sensitive region of the caudal Sm innervates VLM neurons and suggest that these VLM neurons are involved in mediating the depressor and bradycardic responses elicited by changes in the extracellular concentration of sodium.


2014 ◽  
Vol 30 (2) ◽  
pp. 545-553 ◽  
Author(s):  
Gislaine Z. Réus ◽  
Helena M. Abelaira ◽  
Amanda L. Maciel ◽  
Maria Augusta B. dos Santos ◽  
Anelise S. Carlessi ◽  
...  

2016 ◽  
Vol 33 (S1) ◽  
pp. S527-S527
Author(s):  
D. Martín Hernández ◽  
Á.G. Bris ◽  
K.S. MacDowell ◽  
A. Sayd ◽  
D. Azpiazu ◽  
...  

IntroductionPatients with major depression who are otherwise medically healthy have activated inflammatory pathways. It has been described that depression is not only escorted by inflammation but also by induction of multiple oxidative/nitrosative stress pathways. Nevertheless, there are finely regulated mechanisms involved in preserving cells from damage, such as the nuclear factor Nrf2.AimsTo explore in a depression-like model the Nrf2 pathway in the prefrontal cortex (PFC) and the hippocampus of rats and to analyze which classic antidepressants affect the antioxidant activity of the Nrf2 pathway.MethodsMale Wistar rats were exposed to chronic mild stress (CMS) and some of them were treated with desipramine, escitalopram or duloxetine. We studied the expression in the PFC and hippocampus of upstream and downstream elements of the Nrf2 pathway and the oxidative damage induced by the CMS.ResultsAfter exposure to a CMS protocol, in the PFC, there is an inhibition of upstream and downstream elements of the Nrf2 pathway. Moreover, antidepressant treatments, particularly desipramine and duloxetine, are able to recover some of these elements and to reduce the oxidative damage induced by the depression model. In the hippocampus however, Nrf2 pathways are not that affected and antidepressants do not have many actions.ConclusionsNrf2 pathway is differentially regulated by antidepressants in the PFC and hippocampus. The Nrf2 pathway is involved in the oxidative/nitrosative damage detected in the PFC after CMS exposure. However, it seems that Nrf2 is not very involved in the effects caused by the CMS in the hippocampus.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2007 ◽  
Vol 292 (1) ◽  
pp. R373-R381 ◽  
Author(s):  
Marc F. Doobay ◽  
Lauren S. Talman ◽  
Teresa D. Obr ◽  
Xin Tian ◽  
Robin L. Davisson ◽  
...  

Angiotensin-converting enzyme 2 (ACE2) is a newly discovered carboxy-peptidase responsible for the formation of vasodilatory peptides such as angiotensin-(1–7). We hypothesized that ACE2 is part of the brain renin-angiotensin system, and its expression is regulated by the other elements of this system. ACE2 immunostaining was performed in transgenic mouse brain sections from neuron-specific enolase-AT1A (overexpressing AT1A receptors), R+A+ (overexpressing angiotensinogen and renin), and control (nontransgenic littermates) mice. Results show that ACE2 staining is widely distributed throughout the brain. Using cell-type-specific antibodies, we observed that ACE2 staining is present in the cytoplasm of neuronal cell bodies but not in glial cells. In the subfornical organ, an area lacking the blood-brain barrier and sensitive to blood-borne angiotensin II, ACE2 was significantly increased in transgenic mice. Interestingly, ACE2 mRNA and protein expression were inversely correlated in the nucleus of tractus solitarius/dorsal motor nucleus of the vagus and the ventrolateral medulla, when comparing transgenic to nontransgenic mice. These results suggest that ACE2 is localized to the cytoplasm of neuronal cells in the brain and that ACE2 levels appear highly regulated by other components of the renin-angiotensin system, confirming its involvement in this system. Moreover, ACE2 expression in brain structures involved in the control of cardiovascular function suggests that the carboxypeptidase may have a role in the central regulation of blood pressure and diseases involving the autonomic nervous system, such as hypertension.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Ru-Peng Liu ◽  
Ji-Liang Fang ◽  
Pei-Jing Rong ◽  
Yufeng Zhao ◽  
Hong Meng ◽  
...  

To explore new noninvasive treatment options for depression, this study investigated the effects of electroacupuncture (EA) at the auricular concha region (ACR) of depression rat models. Depression in rats was induced by unpredictable chronic mild stress (UCMS) combined with isolation for 21 days. Eighty male Wistar rats were randomly assigned into four groups: normal, UCMS alone, UCMS with EA-ACR treatment, and UCMS with EA-ear-tip treatment. Rats under inhaled anesthesia were treated once daily for 14 days. The results showed that blood pressure and heart rate were significantly reduced in the EA-ACR group than in the UCMS alone group or the EA-ear-tip group. The open-field test scores significantly decreased in the UCMS alone and EA-ear-tip groups but not in the EA-ACR group. Both EA treatments downregulated levels of plasma cortisol and ACTH in UCMS rats back to normal levels. The present study suggested that EA-ACR can elicit similar cardioinhibitory effects as vagus nerve stimulation (VNS), and EA-ACR significantly antagonized UCMS-induced depressive status in UCMS rats. The antidepressant effect of EA-ACR is possibly mediated via the normalization of the hypothalamic-pituitary-adrenal (HPA) axis hyperactivity.


2013 ◽  
Vol 25 (6) ◽  
pp. 328-333 ◽  
Author(s):  
Helena Mendes Abelaira ◽  
Gislaine Zilli Réus ◽  
Giselli Scaini ◽  
Emilio Luiz Streck ◽  
José Alexandre Crippa ◽  
...  

ObjectivesThe present study was aimed at evaluating the effects of the administration of β-carboline harmine on behaviour and citrate synthase activity in the brain of rats exposed to chronic mild stress (CMS) procedure.MethodsTo this aim, after 40 days of exposure to CMS procedure, rats were treated with harmine (15 mg/kg/day) for 7 days, then memory, anhedonia and citrate synthase activity were assessed.ResultOur findings demonstrated that stressed rats treated with saline increased the sucrose intake, and the stressed rats treated with harmine reversed this effect. Neither stress nor harmine treatment altered memory performance in rats. In addition, chronic stressful situations induced increase in citrate synthase activity in the prefrontal cortex, but not in the hippocampus and striatum. Treatment with harmine reversed the increase in citrate synthase activity in the prefrontal cortex.ConclusionThese findings support the hypothesis that harmine could be involved in controlling the energy metabolism.


Sign in / Sign up

Export Citation Format

Share Document