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Alexander Kiss - One of the best experts on this subject based on the ideXlab platform.
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Clozapine impact on FosB/ΔFosB expression in stress preconditioned rats: response to a novel stressor.
Endocrine Regulations, 2019Co-Authors: Jana Osacka, Lubica Horvathova, Alena Cernackova, Alexander KissAbstract:OBJECTIVE Prolonged treatment with neuroleptics has been shown to induce FosB/ΔFosB expression in several brain regions including the medial prefrontal cortex, dorsomedial and dorsolateral striatum, ventrolateral and dorsolateral Septum, Nucleus accumbens shell and core, and the hypothalamic paraventricular Nucleus (PVN). Some of these regions are known to be also stress responsive. This study was designed to determine whether repeated clozapine (CLZ) administration for 7 consecutive days to Wistar rats may modify FosB/ΔFosB expression in the above-mentioned brain areas induced by acute stress or novel stressor that followed 13-day chronic mild stress preconditioning. METHODS Following experimental groups were used: unstressed animals treated with vehicle/ CLZ for 7 days; 7-day vehicle/CLZ-treated animals on the last day exposed to acute stress - forced swimming (FSW); and animals preconditioned with stress for 13 days treated from the 8th day with vehicle/CLZ and on the 14th day exposed to novel stress - FSW. RESULTS In the unstressed animals CLZ markedly increased FosB/ΔFosB immunoreactivity in the ventrolateral Septum and PVN. FSW elevated FosB/ΔFosB expression in the medial prefrontal cortex, striatum, and Septum. CLZ markedly potentiated the effect of the FSW on FosB/ΔFosB expression in the PVN, but suppressed it in the dorsomedial striatum. Novel stress with stress preconditioning increased FosB/ΔFosB immunoreactivity in the prefrontal cortex, striatum, ventrolateral Septum, and the PVN. In the Nucleus accumbens the effect of the novel stressor was potentiated by CLZ. CONCLUSION Our data indicate that CLZ may modulate the acute as well as novel stress effects on FosB/ΔFosB expression but its effect differs within the individual brain regions.
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Impact of repeated asenapine treatment on FosB/ΔFosB expression in the forebrain structures under normal conditions and mild stress preconditioning in the rat
Brain Research Bulletin, 2016Co-Authors: Zuzana Majercikova, Jana Osacka, Lubica Horvathova, Jan Pecenak, Alexander KissAbstract:Long-term effect of asenapine (ASE), an atypical antipsychotic drug, on FosB/ΔFosB quantitative variations in the striatum, Septum, Nucleus accumbens, and prefrontal cortex, was light microscopically evaluated in normal rats and rats preconditioned with chronic unpredictable mild stress (CMS). CMS included restraint, social isolation, crowding, swimming, and cold. The rats were exposed to CMS for 21 days. From the 7th day of CMS, the rats were injected subcutaneously with saline (300μl/rat) or ASE (0.3mg/kg b.w.), twice a day for 14 days. On the 22nd day, i.e. 16-18h after the last treatment, the animals were perfused with fixative and the brains cut into 30μm thick coronal sections. FosB/ΔFosB protein was immunohistochemically visualized by avidin-biotin peroxidase complex (ABC). Four groups of animals were investigated: control+vehicle, control+ASE, CMS+vehicle, and CMS+ASE. Repeated ASE treatment significantly increased the amount of FosB/ΔFosB immunostained cell nuclei in the dorsolateral and dorsomedial striatum and the shell of the Nucleus accumbens, followed by strVM and coACC, as assessed by numerical analysis in both total (different size for each structure) and unified (equal size for each structure) brain sectors. The effect of ASE was significantly lowered by CMS preconditioning only in the dorsolateral striatum, dorsomedial striatum, and the shell of the Nucleus accumbens, indicated by both total and unified calculations. Although, highest FosB/ΔFosB expression was seen in the prefrontal cortex and lowest in the dorsolateral and ventrolateral Septum, no differences between the groups occurred. CMS itself did not affect FosB/ΔFosB expression level. These findings demonstrate for the first time that repeated administration of ASE may result in eliciting of long-lasting FosB/ΔFosB-like transcription factors that could mediate some of the persistent and region-specific changes in brain function, interconnected with chronic drug exposure. However, it cannot be excluded that the impact of repeated ASE exposure might be influenced by an ambient stressogen leverage.
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Effect of acute asenapine treatment on Fos expression in the forebrain structures under normal conditions and mild stress preconditioning in the rat
Brain Research Bulletin, 2014Co-Authors: Zuzana Majercikova, Jana Osacka, Lubica Horvathova, Alena Cernackova, Jan Pecenak, Alexander KissAbstract:Abstract Asenapine (ASE) is a novel atypical antipsychotic drug approved for the treatment of schizophrenia and bipolar disorder. Stress is an inseparable part of the human life, which may interfere with the therapeutic effect of different drugs. The aim of the present study was: (1) to delineate the quantitative and qualitative profiles of the ASE effect on Fos expression in the striatum, Septum, Nucleus accumbens, and the prefrontal cortex and (2) to find out whether a chronic unpredictable variable mild stress (CMS) preconditioning may modify the effect of acute ASE treatment. Stress paradigms included restrain, social isolation, crowding, swimming, and cold. The animals were exposed to CMS for 21 days and on the 22nd day received an injection of vehicle (saline 300 μl/rat s.c.) or ASE (0.3 mg/kg s.c.). They were sacrificed 90 min after the treatments. Fos protein was visualized by avidin biotin peroxidase (ABC). Four groups of animals were investigated: controls + vehicle, controls + ASE, CMS + vehicle, and CMS + ASE. The number of Fos labeled neurons was calculated per total investigated area, which was selective for each structure, and also recalculated per unified sector. ASE treatment induced significant and very similar increase of the Fos expression in both ASE control and ASE CMS animals in comparison with saline control and CMS ones. Moreover, ASE induced regional differences in the number of Fos-positive neurons. In both ASE groups most pronounced response in the number of Fos profiles occurred in the dorsolateral striatum, ventrolateral Septum, shell of the Nucleus accumbens, and the medial prefrontal cortex. Mild Fos response was seen in the dorsomedial and ventromedial striatum and core of the Nucleus accumbens. No response was seen in the dorsolateral Septum. The present paper demonstrates for the first time the character of the Fos distribution in the forebrain structures induced by acute ASE treatment as well as ASE response to 21 days CMS preconditioning. The study provides an important comparative background that may help in the further understanding of the effect of ASE on the brain activation as well as its responsiveness to CMS challenges.
Horst W. Korf - One of the best experts on this subject based on the ideXlab platform.
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Vasoactive intestinal peptide-immunoreactive cerebrospinal fluid-contacting neurons in the reptilian lateral Septum Nucleus accumbens
Cell and Tissue Research, 1993Co-Authors: Kanjun Hirunagi, Elke Rommel, Andreas Oksche, Horst W. KorfAbstract:By means of immunocytochemical demonstration of vasoactive intestinal peptide (VIP) an accumulation of cerebrospinal fluid (CSF)-contacting neurons was found in a circumscribed region of the Nucleus accumbens/lateral Septum of eleven reptilian (chelonian, lacertilian, ophidian, crocodilian) species. Basal processes of these cells contribute to a subependymal plexus whose density displays considerable interspecific variation. VIP-immunoreactive nerve fibers occur also in the lateral Septum and the Nucleus accumbens where they encompass immunonegative cells in a basket-like pattern. The CSF-contacting neurons are surrounded by columnar ependymocytes frequently arranged in a pseudostratified manner. These specialized arrays of ependymal cells, however, occupy a more extended area than the VIP-immunoreactive CSF-contacting neurons and can be traced from the rostro-ventral pole of the lateral ventricle to the interventricular foramen. These observations suggest the existence of a telencephalic site of CSF-contacting neurons which may be more widespread than hitherto thought and which may participate in a circumventricular system of the lateral ventricle. Previous studies mainly performed with birds indicate that the VIP-immunoreactive CSF-contacting neurons of the Nucleus accumbens might form a part of the “encephalic” (extraretinal and extrapineal) photoreceptor. However, further experiments are required to test this supposition since the VIP-immunoreactive neurons of the Nucleus accumbens remained unlabeled by antibodies against bovine rodopsin and chicken cone-opsin in all eleven species analysed in this investigation.
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Vasoactive intestinal peptide-immunoreactive cerebrospinal fluid-contacting neurons in the reptilian lateral Septum/Nucleus accumbens
Cell & Tissue Research, 1993Co-Authors: Kanjun Hirunagi, Elke Rommel, Andreas Oksche, Horst W. KorfAbstract:By means of immunocytochemical demonstration of vasoactive intestinal peptide (VIP) an accumulation of cerebrospinal fluid (CSF)-contacting neurons was found in a circumscribed region of the Nucleus accumbens/lateral Septum of eleven reptilian (chelonian, lacertilian, ophidian, crocodilian) species. Basal processes of these cells contribute to a subependymal plexus whose density displays considerable interspecific variation. VIP-immunoreactive nerve fibers occur also in the lateral Septum and the Nucleus accumbens where they encompass immunonegative cells in a basket-like pattern. The CSF-contacting neurons are surrounded by columnar ependymocytes frequently arranged in a pseudostratified manner. These specialized arrays of ependymal cells, however, occupy a more extended area than the VIP-immunoreactive CSF-contacting neurons and can be traced from the rostro-ventral pole of the lateral ventricle to the interventricular foramen. These observations suggest the existence of a telencephalic site of CSF-contacting neurons which may be more widespread than hitherto thought and which may participate in a circumventricular system of the lateral ventricle. Previous studies mainly performed with birds indicate that the VIP-immunoreactive CSF-contacting neurons of the Nucleus accumbens might form a part of the “encephalic” (extraretinal and extrapineal) photoreceptor. However, further experiments are required to test this supposition since the VIP-immunoreactive neurons of the Nucleus accumbens remained unlabeled by antibodies against bovine rodopsin and chicken cone-opsin in all eleven species analysed in this investigation.
Kanjun Hirunagi - One of the best experts on this subject based on the ideXlab platform.
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Vasoactive intestinal peptide-immunoreactive cerebrospinal fluid-contacting neurons in the reptilian lateral Septum Nucleus accumbens
Cell and Tissue Research, 1993Co-Authors: Kanjun Hirunagi, Elke Rommel, Andreas Oksche, Horst W. KorfAbstract:By means of immunocytochemical demonstration of vasoactive intestinal peptide (VIP) an accumulation of cerebrospinal fluid (CSF)-contacting neurons was found in a circumscribed region of the Nucleus accumbens/lateral Septum of eleven reptilian (chelonian, lacertilian, ophidian, crocodilian) species. Basal processes of these cells contribute to a subependymal plexus whose density displays considerable interspecific variation. VIP-immunoreactive nerve fibers occur also in the lateral Septum and the Nucleus accumbens where they encompass immunonegative cells in a basket-like pattern. The CSF-contacting neurons are surrounded by columnar ependymocytes frequently arranged in a pseudostratified manner. These specialized arrays of ependymal cells, however, occupy a more extended area than the VIP-immunoreactive CSF-contacting neurons and can be traced from the rostro-ventral pole of the lateral ventricle to the interventricular foramen. These observations suggest the existence of a telencephalic site of CSF-contacting neurons which may be more widespread than hitherto thought and which may participate in a circumventricular system of the lateral ventricle. Previous studies mainly performed with birds indicate that the VIP-immunoreactive CSF-contacting neurons of the Nucleus accumbens might form a part of the “encephalic” (extraretinal and extrapineal) photoreceptor. However, further experiments are required to test this supposition since the VIP-immunoreactive neurons of the Nucleus accumbens remained unlabeled by antibodies against bovine rodopsin and chicken cone-opsin in all eleven species analysed in this investigation.
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Vasoactive intestinal peptide-immunoreactive cerebrospinal fluid-contacting neurons in the reptilian lateral Septum/Nucleus accumbens
Cell & Tissue Research, 1993Co-Authors: Kanjun Hirunagi, Elke Rommel, Andreas Oksche, Horst W. KorfAbstract:By means of immunocytochemical demonstration of vasoactive intestinal peptide (VIP) an accumulation of cerebrospinal fluid (CSF)-contacting neurons was found in a circumscribed region of the Nucleus accumbens/lateral Septum of eleven reptilian (chelonian, lacertilian, ophidian, crocodilian) species. Basal processes of these cells contribute to a subependymal plexus whose density displays considerable interspecific variation. VIP-immunoreactive nerve fibers occur also in the lateral Septum and the Nucleus accumbens where they encompass immunonegative cells in a basket-like pattern. The CSF-contacting neurons are surrounded by columnar ependymocytes frequently arranged in a pseudostratified manner. These specialized arrays of ependymal cells, however, occupy a more extended area than the VIP-immunoreactive CSF-contacting neurons and can be traced from the rostro-ventral pole of the lateral ventricle to the interventricular foramen. These observations suggest the existence of a telencephalic site of CSF-contacting neurons which may be more widespread than hitherto thought and which may participate in a circumventricular system of the lateral ventricle. Previous studies mainly performed with birds indicate that the VIP-immunoreactive CSF-contacting neurons of the Nucleus accumbens might form a part of the “encephalic” (extraretinal and extrapineal) photoreceptor. However, further experiments are required to test this supposition since the VIP-immunoreactive neurons of the Nucleus accumbens remained unlabeled by antibodies against bovine rodopsin and chicken cone-opsin in all eleven species analysed in this investigation.
Jana Osacka - One of the best experts on this subject based on the ideXlab platform.
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Clozapine impact on FosB/ΔFosB expression in stress preconditioned rats: response to a novel stressor.
Endocrine Regulations, 2019Co-Authors: Jana Osacka, Lubica Horvathova, Alena Cernackova, Alexander KissAbstract:OBJECTIVE Prolonged treatment with neuroleptics has been shown to induce FosB/ΔFosB expression in several brain regions including the medial prefrontal cortex, dorsomedial and dorsolateral striatum, ventrolateral and dorsolateral Septum, Nucleus accumbens shell and core, and the hypothalamic paraventricular Nucleus (PVN). Some of these regions are known to be also stress responsive. This study was designed to determine whether repeated clozapine (CLZ) administration for 7 consecutive days to Wistar rats may modify FosB/ΔFosB expression in the above-mentioned brain areas induced by acute stress or novel stressor that followed 13-day chronic mild stress preconditioning. METHODS Following experimental groups were used: unstressed animals treated with vehicle/ CLZ for 7 days; 7-day vehicle/CLZ-treated animals on the last day exposed to acute stress - forced swimming (FSW); and animals preconditioned with stress for 13 days treated from the 8th day with vehicle/CLZ and on the 14th day exposed to novel stress - FSW. RESULTS In the unstressed animals CLZ markedly increased FosB/ΔFosB immunoreactivity in the ventrolateral Septum and PVN. FSW elevated FosB/ΔFosB expression in the medial prefrontal cortex, striatum, and Septum. CLZ markedly potentiated the effect of the FSW on FosB/ΔFosB expression in the PVN, but suppressed it in the dorsomedial striatum. Novel stress with stress preconditioning increased FosB/ΔFosB immunoreactivity in the prefrontal cortex, striatum, ventrolateral Septum, and the PVN. In the Nucleus accumbens the effect of the novel stressor was potentiated by CLZ. CONCLUSION Our data indicate that CLZ may modulate the acute as well as novel stress effects on FosB/ΔFosB expression but its effect differs within the individual brain regions.
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Impact of repeated asenapine treatment on FosB/ΔFosB expression in the forebrain structures under normal conditions and mild stress preconditioning in the rat
Brain Research Bulletin, 2016Co-Authors: Zuzana Majercikova, Jana Osacka, Lubica Horvathova, Jan Pecenak, Alexander KissAbstract:Long-term effect of asenapine (ASE), an atypical antipsychotic drug, on FosB/ΔFosB quantitative variations in the striatum, Septum, Nucleus accumbens, and prefrontal cortex, was light microscopically evaluated in normal rats and rats preconditioned with chronic unpredictable mild stress (CMS). CMS included restraint, social isolation, crowding, swimming, and cold. The rats were exposed to CMS for 21 days. From the 7th day of CMS, the rats were injected subcutaneously with saline (300μl/rat) or ASE (0.3mg/kg b.w.), twice a day for 14 days. On the 22nd day, i.e. 16-18h after the last treatment, the animals were perfused with fixative and the brains cut into 30μm thick coronal sections. FosB/ΔFosB protein was immunohistochemically visualized by avidin-biotin peroxidase complex (ABC). Four groups of animals were investigated: control+vehicle, control+ASE, CMS+vehicle, and CMS+ASE. Repeated ASE treatment significantly increased the amount of FosB/ΔFosB immunostained cell nuclei in the dorsolateral and dorsomedial striatum and the shell of the Nucleus accumbens, followed by strVM and coACC, as assessed by numerical analysis in both total (different size for each structure) and unified (equal size for each structure) brain sectors. The effect of ASE was significantly lowered by CMS preconditioning only in the dorsolateral striatum, dorsomedial striatum, and the shell of the Nucleus accumbens, indicated by both total and unified calculations. Although, highest FosB/ΔFosB expression was seen in the prefrontal cortex and lowest in the dorsolateral and ventrolateral Septum, no differences between the groups occurred. CMS itself did not affect FosB/ΔFosB expression level. These findings demonstrate for the first time that repeated administration of ASE may result in eliciting of long-lasting FosB/ΔFosB-like transcription factors that could mediate some of the persistent and region-specific changes in brain function, interconnected with chronic drug exposure. However, it cannot be excluded that the impact of repeated ASE exposure might be influenced by an ambient stressogen leverage.
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Effect of acute asenapine treatment on Fos expression in the forebrain structures under normal conditions and mild stress preconditioning in the rat
Brain Research Bulletin, 2014Co-Authors: Zuzana Majercikova, Jana Osacka, Lubica Horvathova, Alena Cernackova, Jan Pecenak, Alexander KissAbstract:Abstract Asenapine (ASE) is a novel atypical antipsychotic drug approved for the treatment of schizophrenia and bipolar disorder. Stress is an inseparable part of the human life, which may interfere with the therapeutic effect of different drugs. The aim of the present study was: (1) to delineate the quantitative and qualitative profiles of the ASE effect on Fos expression in the striatum, Septum, Nucleus accumbens, and the prefrontal cortex and (2) to find out whether a chronic unpredictable variable mild stress (CMS) preconditioning may modify the effect of acute ASE treatment. Stress paradigms included restrain, social isolation, crowding, swimming, and cold. The animals were exposed to CMS for 21 days and on the 22nd day received an injection of vehicle (saline 300 μl/rat s.c.) or ASE (0.3 mg/kg s.c.). They were sacrificed 90 min after the treatments. Fos protein was visualized by avidin biotin peroxidase (ABC). Four groups of animals were investigated: controls + vehicle, controls + ASE, CMS + vehicle, and CMS + ASE. The number of Fos labeled neurons was calculated per total investigated area, which was selective for each structure, and also recalculated per unified sector. ASE treatment induced significant and very similar increase of the Fos expression in both ASE control and ASE CMS animals in comparison with saline control and CMS ones. Moreover, ASE induced regional differences in the number of Fos-positive neurons. In both ASE groups most pronounced response in the number of Fos profiles occurred in the dorsolateral striatum, ventrolateral Septum, shell of the Nucleus accumbens, and the medial prefrontal cortex. Mild Fos response was seen in the dorsomedial and ventromedial striatum and core of the Nucleus accumbens. No response was seen in the dorsolateral Septum. The present paper demonstrates for the first time the character of the Fos distribution in the forebrain structures induced by acute ASE treatment as well as ASE response to 21 days CMS preconditioning. The study provides an important comparative background that may help in the further understanding of the effect of ASE on the brain activation as well as its responsiveness to CMS challenges.
Lubica Horvathova - One of the best experts on this subject based on the ideXlab platform.
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Clozapine impact on FosB/ΔFosB expression in stress preconditioned rats: response to a novel stressor.
Endocrine Regulations, 2019Co-Authors: Jana Osacka, Lubica Horvathova, Alena Cernackova, Alexander KissAbstract:OBJECTIVE Prolonged treatment with neuroleptics has been shown to induce FosB/ΔFosB expression in several brain regions including the medial prefrontal cortex, dorsomedial and dorsolateral striatum, ventrolateral and dorsolateral Septum, Nucleus accumbens shell and core, and the hypothalamic paraventricular Nucleus (PVN). Some of these regions are known to be also stress responsive. This study was designed to determine whether repeated clozapine (CLZ) administration for 7 consecutive days to Wistar rats may modify FosB/ΔFosB expression in the above-mentioned brain areas induced by acute stress or novel stressor that followed 13-day chronic mild stress preconditioning. METHODS Following experimental groups were used: unstressed animals treated with vehicle/ CLZ for 7 days; 7-day vehicle/CLZ-treated animals on the last day exposed to acute stress - forced swimming (FSW); and animals preconditioned with stress for 13 days treated from the 8th day with vehicle/CLZ and on the 14th day exposed to novel stress - FSW. RESULTS In the unstressed animals CLZ markedly increased FosB/ΔFosB immunoreactivity in the ventrolateral Septum and PVN. FSW elevated FosB/ΔFosB expression in the medial prefrontal cortex, striatum, and Septum. CLZ markedly potentiated the effect of the FSW on FosB/ΔFosB expression in the PVN, but suppressed it in the dorsomedial striatum. Novel stress with stress preconditioning increased FosB/ΔFosB immunoreactivity in the prefrontal cortex, striatum, ventrolateral Septum, and the PVN. In the Nucleus accumbens the effect of the novel stressor was potentiated by CLZ. CONCLUSION Our data indicate that CLZ may modulate the acute as well as novel stress effects on FosB/ΔFosB expression but its effect differs within the individual brain regions.
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Impact of repeated asenapine treatment on FosB/ΔFosB expression in the forebrain structures under normal conditions and mild stress preconditioning in the rat
Brain Research Bulletin, 2016Co-Authors: Zuzana Majercikova, Jana Osacka, Lubica Horvathova, Jan Pecenak, Alexander KissAbstract:Long-term effect of asenapine (ASE), an atypical antipsychotic drug, on FosB/ΔFosB quantitative variations in the striatum, Septum, Nucleus accumbens, and prefrontal cortex, was light microscopically evaluated in normal rats and rats preconditioned with chronic unpredictable mild stress (CMS). CMS included restraint, social isolation, crowding, swimming, and cold. The rats were exposed to CMS for 21 days. From the 7th day of CMS, the rats were injected subcutaneously with saline (300μl/rat) or ASE (0.3mg/kg b.w.), twice a day for 14 days. On the 22nd day, i.e. 16-18h after the last treatment, the animals were perfused with fixative and the brains cut into 30μm thick coronal sections. FosB/ΔFosB protein was immunohistochemically visualized by avidin-biotin peroxidase complex (ABC). Four groups of animals were investigated: control+vehicle, control+ASE, CMS+vehicle, and CMS+ASE. Repeated ASE treatment significantly increased the amount of FosB/ΔFosB immunostained cell nuclei in the dorsolateral and dorsomedial striatum and the shell of the Nucleus accumbens, followed by strVM and coACC, as assessed by numerical analysis in both total (different size for each structure) and unified (equal size for each structure) brain sectors. The effect of ASE was significantly lowered by CMS preconditioning only in the dorsolateral striatum, dorsomedial striatum, and the shell of the Nucleus accumbens, indicated by both total and unified calculations. Although, highest FosB/ΔFosB expression was seen in the prefrontal cortex and lowest in the dorsolateral and ventrolateral Septum, no differences between the groups occurred. CMS itself did not affect FosB/ΔFosB expression level. These findings demonstrate for the first time that repeated administration of ASE may result in eliciting of long-lasting FosB/ΔFosB-like transcription factors that could mediate some of the persistent and region-specific changes in brain function, interconnected with chronic drug exposure. However, it cannot be excluded that the impact of repeated ASE exposure might be influenced by an ambient stressogen leverage.
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Effect of acute asenapine treatment on Fos expression in the forebrain structures under normal conditions and mild stress preconditioning in the rat
Brain Research Bulletin, 2014Co-Authors: Zuzana Majercikova, Jana Osacka, Lubica Horvathova, Alena Cernackova, Jan Pecenak, Alexander KissAbstract:Abstract Asenapine (ASE) is a novel atypical antipsychotic drug approved for the treatment of schizophrenia and bipolar disorder. Stress is an inseparable part of the human life, which may interfere with the therapeutic effect of different drugs. The aim of the present study was: (1) to delineate the quantitative and qualitative profiles of the ASE effect on Fos expression in the striatum, Septum, Nucleus accumbens, and the prefrontal cortex and (2) to find out whether a chronic unpredictable variable mild stress (CMS) preconditioning may modify the effect of acute ASE treatment. Stress paradigms included restrain, social isolation, crowding, swimming, and cold. The animals were exposed to CMS for 21 days and on the 22nd day received an injection of vehicle (saline 300 μl/rat s.c.) or ASE (0.3 mg/kg s.c.). They were sacrificed 90 min after the treatments. Fos protein was visualized by avidin biotin peroxidase (ABC). Four groups of animals were investigated: controls + vehicle, controls + ASE, CMS + vehicle, and CMS + ASE. The number of Fos labeled neurons was calculated per total investigated area, which was selective for each structure, and also recalculated per unified sector. ASE treatment induced significant and very similar increase of the Fos expression in both ASE control and ASE CMS animals in comparison with saline control and CMS ones. Moreover, ASE induced regional differences in the number of Fos-positive neurons. In both ASE groups most pronounced response in the number of Fos profiles occurred in the dorsolateral striatum, ventrolateral Septum, shell of the Nucleus accumbens, and the medial prefrontal cortex. Mild Fos response was seen in the dorsomedial and ventromedial striatum and core of the Nucleus accumbens. No response was seen in the dorsolateral Septum. The present paper demonstrates for the first time the character of the Fos distribution in the forebrain structures induced by acute ASE treatment as well as ASE response to 21 days CMS preconditioning. The study provides an important comparative background that may help in the further understanding of the effect of ASE on the brain activation as well as its responsiveness to CMS challenges.
