“…The data indicating the existence of antipsychotics-induced variabilities in Fos distribution in the PVN, SON, and ACS may be helpful in understanding the extent of their extra-forebrain actions with possible presumption of their functional impact and side effect consequences (Kiss et al 2010). These results are in line with study showing that hypothalamic NPY mRNA level did not change after longterm neuroleptic administration in rats (Rojczyk et al 2015).…”
Section: Resultssupporting
confidence: 92%
“…A decrease in the hypothalamic NUCB2 and nesfatin-1 expression after chronic haloperidol administration has been recently reported (Rojczyk et al 2015). It is also worth mentioning that there is a substantial diversity in the stimulatory effects of antipsychotics on Fos, Fos/OXY, and Fos/AVP immunostainings with the preferential action of the atypical clozapine over olanzapine and with little effects of risperidone and haloperidol.…”
Neuropeptide S (NPS) has a multidirectional regulatory activity, especially when considered as a potent endogenous anxiolytic factor. Accumulating data suggests that neuroleptics affect peptidergic signaling in various brain structures. However, there is no information regarding the influence of treatment with antipsychotics on brain NPS expression. In the current study, we assessed the NPS and NPS receptor (NPSR) mRNA levels in the brains of rats shortly and chronically treated with chlorpromazine and olanzapine using quantitative real-time PCR. Both single-dose and long-term (4 months) olanzapine treatment led to the upregulation of NPS expression in the rat hypothalamus. It supports the hypothesis that NPS is involved in the dopamine-dependent anxiolytic actions of selected neuroleptics and possibly also in the pathophysiology of mental disorders. On the other hand, NPSR expression decreased after single-dose and chronic chlorpromazine administration in the hypothalamus, as well as after chronic olanzapine and chlorpromazine administration in the striatum and hippocampus. These results cast a new light on the pharmacology of antipsychotics and contribute to a better understanding of the mechanisms responsible for their action. Furthermore, our findings underline the complex nature of potential interactions between dopamine receptors and brain peptidergic pathways, which has potential clinical applications.
“…The data indicating the existence of antipsychotics-induced variabilities in Fos distribution in the PVN, SON, and ACS may be helpful in understanding the extent of their extra-forebrain actions with possible presumption of their functional impact and side effect consequences (Kiss et al 2010). These results are in line with study showing that hypothalamic NPY mRNA level did not change after longterm neuroleptic administration in rats (Rojczyk et al 2015).…”
Section: Resultssupporting
confidence: 92%
“…A decrease in the hypothalamic NUCB2 and nesfatin-1 expression after chronic haloperidol administration has been recently reported (Rojczyk et al 2015). It is also worth mentioning that there is a substantial diversity in the stimulatory effects of antipsychotics on Fos, Fos/OXY, and Fos/AVP immunostainings with the preferential action of the atypical clozapine over olanzapine and with little effects of risperidone and haloperidol.…”
Neuropeptide S (NPS) has a multidirectional regulatory activity, especially when considered as a potent endogenous anxiolytic factor. Accumulating data suggests that neuroleptics affect peptidergic signaling in various brain structures. However, there is no information regarding the influence of treatment with antipsychotics on brain NPS expression. In the current study, we assessed the NPS and NPS receptor (NPSR) mRNA levels in the brains of rats shortly and chronically treated with chlorpromazine and olanzapine using quantitative real-time PCR. Both single-dose and long-term (4 months) olanzapine treatment led to the upregulation of NPS expression in the rat hypothalamus. It supports the hypothesis that NPS is involved in the dopamine-dependent anxiolytic actions of selected neuroleptics and possibly also in the pathophysiology of mental disorders. On the other hand, NPSR expression decreased after single-dose and chronic chlorpromazine administration in the hypothalamus, as well as after chronic olanzapine and chlorpromazine administration in the striatum and hippocampus. These results cast a new light on the pharmacology of antipsychotics and contribute to a better understanding of the mechanisms responsible for their action. Furthermore, our findings underline the complex nature of potential interactions between dopamine receptors and brain peptidergic pathways, which has potential clinical applications.
“…Chlorpromazine as well as haloperidol gives rise to increased POMC expression, with seven-times higher modulation by haloperidol than chlorpromazine. The similar trend was reported in other experiments, where the effects of long-term treatment (28 days) with both first and second-generation neuroleptics on POMC gene expression were evaluated (Rojczyk et al 2015). Despite a relatively limited increase of atypical olanzapine expression, significant statistical changes were observed as well as typical haloperidol expression compared to control.…”
Section: Resultssupporting
confidence: 83%
“…Furthermore, haloperidol increases, but risperidone decreases neurotensin levels in the rat striatum, hippocampus and frontal cortex (Gruber et al 2002). Decreased NUCB2/nesfatin-1 expression is reported in the rat hypothalamus after long-term haloperidol administration (Rojczyk et al 2015). It has also been reported that olanzapine increases calcitonin gene-related peptide (CGRP) in the rat brain (Angelucci et al 2008).…”
Neuroleptics modulate the expression level of some regulatory neuropeptides in the brain. However, if these therapeutics influence the peptidergic circuits in the amygdala remains unclear. This study specifies the impact profile of the classical antipsychotic drugs on mRNA expression of the spexin/NPQ, kisspeptin-1 and POMC in the rat amygdala. Animals were treated with haloperidol and chlorpromazine for 28 days prior to transcript quantification via qPCR. Haloperidol and chlorpromazine induced a change in the expression of all neuropeptides analyzed. Both drugs led to the decrease of Kiss-1 expression, whereas in POMC and spexin/NPQ their up-regulation in the amygdala was detected. These modulating effects on may represent alternative, so far unknown mechanisms, of classical antipsychotic drugs triggering pharmacological responses.
“…Reactive oxygen species have been shown to be part of both intracellular signalling and intracellular communication, the processes involved in maintaining homeostasis, but when excessively produced in vivo, they are deleterious to integral components of the cell and cause their dysfunctions (Rojczyk et al 2015). Some experimental data indicate that ROS-mediated LPO, protein oxidation and oxidative alterations to nucleic acids are crucial events of unfavourable actions of ROS (Juranek and Bezek 2005).…”
This study was aimed to study the potentially beneficial effects of agmatine on oxidative/ nitrosative stress development in the brain of Wistar rats during subacute chlorpromazine treatment. The animals were divided into control (0.9% saline), chlorpromazine (38.7 mg/kg b.w.), chlorpromazine+agmatine (agmatine 75 mg/kg b.w. immediately after chlorpromazine, 38.7 mg/ kg b.w. i.p.) and agmatine (75 mg/kg b.w.) groups. All the tested substances were administered intraperitoneally for 15 consecutive days and the rats were sacrificed by decapitation on day 15. Subacute administration of chlorpromazine resulted in increased lipid peroxidation, nitric oxide concentration and superoxide anion production, while completely damaging the antioxidant defence system in the cerebral cortex, striatum, and hippocampus. However, the combined treatment with chlorpromazine and agmatine significantly attenuated the oxidative/nitrosative stress indices and restored the antioxidant capacity to the control values in all of the examined brain regions. Western blot analysis supported biochemical findings in all groups, but the most notable changes were found in the hippocampus. Our results suggest potentially beneficial effects of agmatine, which may be useful in the modified antioxidant approach in chlorpromazinetherapy.
Antioxidant defence, brain, oxidative stress
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