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1
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
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Wróg, wybawca, trener personalny czy guru? Zrozumieć stres i wypracować równowagę

100%
Chocyk A., Majcher-Maslanka I.
Wszechświat
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2023
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tom 124
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nr 01-03
2
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Dopamine D1-like receptors agonist SKF 38393 increases cFos expression in the paraventricular nucleus of the hypothalamus - impact of acute and chronic cocaine

81%
Chocyk A., Czyrak A., Wedzony K.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 3
425-440
The present study indicates that activation of dopamine D1-like receptors by administration of SKF 38393 leads to dose-dependent (doses: 5, 10 and 20 mg/kg) increases in the expression of cFos proteins in the rat paraventricular nucleus of the hypothalamus (PVN). This effect was abolished by administration of SCH 23390, a dopamine D1-like receptor antagonist (0.5 and 1 mg/kg, given 30 min before SKF 38393 - 10 mg/kg), suggesting that the apparent effect is specific for activation of dopamine D1-like receptors. Expression of cFos after SKF 38393 (10 mg/kg) was observed in some, but not all, CRF-immunoreactive neurons, as well as in small portion of oxytocin- but not vasopressin-immunoreactive neurons (double-immunofluorescence experiments). There were also certain populations of nuclei that showed expression of cFos but did not co-localize with the above markers. We also found that both acute and repeated (once daily for 5 consecutive days) exposure to cocaine (25 mg/kg) attenuated the induction of cFos expression triggered by SKF 38393 when administered 24 hours after single or the last dose of cocaine (25 mg/kg). Attenuation was observed at the same level after single and chronic exposure to cocaine, indicating a rapid functional down-regulation of dopamine D1-like receptors that are resistant to subsequent doses of cocaine. These data provide evidence for the functional role of dopamine D1-like receptors in the PVN and indicate a functional adaptation of dopamine D1-like receptors following a single dose of cocaine without further progression of adaptation or resistance of D1-like receptor-mediated genomic function in the course of repeated cocaine intake.
3

Blockade on NMDA receptors in postnatal period decreased density of tyrosine hydroxylase immunoreactive axonal arbors in the medial prefrontal cortex of adult rats

80%
Wedzony K., Fijal K., Chocyk A.
Journal of Physiology and Pharmacology
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2005
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tom 56
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nr 2
Malfunction of glutamatergic neurotransmission in postnatal period is considered to be a risk factor for development of schizophrenia. Thus, the present study investigates the impact of NMDA receptor blockade in the postnatal period on the density of tyrosine hydroxylase immunoreactive axonal arbors in the rat medial prefrontal cortex. Behavioral experiments revealed that adult rats (60 days old) treated in the postnatal period with a competitive antagonist of NMDA receptors, CGP 40116 (1.25 mg/kg on days 1, 3, 6, 9; 2.5 mg/kg on days 12, 15, 18; and finally 5 mg/kg on day 21, all injections s.c.), showed enhancement of the locomotor activity stimulated by quinpirole (0.3 mg/kg s.c.) and amphetamine (0.5 mg/kg s.c.), which suggests development of functional supersensitivity of dopaminergic systems. It has been found that CGP 40116, given in postnatal period decreased the density of tyrosine hydroxylase immunoreactive axonal arbors in the medial prefrontal cortex of adult animals. The decrease was observed in superficial (II/III) and deep (V/VI) layers of the medial prefrontal cortex, while the average length of tyrosine hydroxylase immunoreactive axonal arbors was increased in both superficial and deep cortical layers. Changes in the density of tyrosine hydroxylase immunoreactive axonal arbors have not been followed by a significant decrease in the content of tyrosine hydroxylase protein measured by Western blot. Thus, NMDA receptor blockade in the early period of life evokes changes in architecture of tyrosine hydroxylase immunoreactive axonal arbors and that malfunction of glutamatergic neurotransmission, in early period of life may produce anatomical changes which resemble those observed in the brains of schizophrenics.
4
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A search for colocalization of serotonin 5-HT2A and 5-HT1A receptors in the rat medial prefrontal and entorhinal cortices-immunohistochemical studies

80%
Wedzony K., Chocyk A., Mackowiak M.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 2
Recently developed antipsychotic drugs ameliorating the negative symptoms of schizophrenia act not only on dopamine D2 receptors but also on serotonin 2A (5-HT2A) and 1A (5-HT1A) receptors in specific regions of the cerebral cortex. Since it is not yet known whether serotonin 5-HT1A and 5-HT2A receptors coexist in the same population of neurons in the cortex, the present study investigated their colocalization in the rat medial prefrontal (MPC) and entorhinal (EC) cortices. Using antibodies that recognize epitopes specific to the serotonin 5-HT2A or 5-HT1A receptors, studies employing confocal microscopy have shown that in the MPC 5-HT2A receptors are preferentially, if not exclusively, present on the pyramidal neurons and that 5-HT1A-immunopositive material is present in the axonal hillocks and, to lower extend, in cytoplasm of presumably pyramidal cell bodies. With the regard of labeling of active receptors (i.e. present in shafts and axonal hillocks) we found that about 38% of neurons positive for the presence of serotonin 5-HT2A receptors, are also positive for serotonin 5-HT1A receptors in the MPC. In the EC, only 22% of serotonin 5-HT2A-positive neurons were positive for serotonin 5-HT1A receptor-immunoreactivity. In the respect of cytoplasmatic serotonin 5-HT1A receptor-immunoreactivity (possibly inactive receptors), 65% and 73% of serotonin 5-HT2A receptor-positive neurons were colocalized with serotonin 5-HT1A receptors in the MPC and EC, respectively. Data obtained on serotonin 5-HT2A and 5-HT1A receptor localization provide anatomical grounds for at least three distinct populations of pyramidal neurons, one governed only by 5-HT2A, one only by 5-HT1A and one by both types of serotonin receptors.
5
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Glutamatergic neurons of rat medial prefrontal cortex innervating the ventral tegmental area are positive for serotonin 5-HT1A receptor protein

80%
Wedzony K., Chocyk A., Kolasiewicz W., Mackowiak M.
Journal of Physiology and Pharmacology
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2007
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tom 58
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nr 4
The present study was designed to investigate whether serotonin 5-HT1A receptor protein (5-HT1A receptor-immunoreactivity), is present on cortical pyramidal neurons of the rat medial prefrontal cortex (MPC) innervating the ventral tegmental area (VTA). Recent data stress the role of serotonin 5-HT1A receptors in the pathology of schizophrenia, and in the mechanism of action of novel antipsychotic drugs. It was found that approximately 52% of cells in layers II/III of the MPC whose axons initial segments were immunoreactive for serotonin 5HT1A receptor were also labeled with Fluoro-Gold (FG), a retrograde tracer injected into the VTA, indicating that certain portion of neurons forming glutamatergic innervations of the VTA may be controlled by serotonin 5-HT1A receptors. In deep cortical layers (V/VI) retrogradely labeled neurons never colocalized with serotonin 5-HT1A receptor-mmunoreactivity. These anatomical data indicate that serotonin 5-HT1A receptors might potentially control the excitability and propagation of information transmitted by the pyramidal cells to the VTA. Moreover, our results indicate that the drugs operating via serotonin 5-HT1A receptors in the MPC, might control from this level the release of glutamate in the VTA and restore function of glutamate neurotransmission, whose dysfunction is observed for example in schizophrenia.
6

Electrophysiological effects of CX3CL1 on rat amygdala neurons

71%
Sowa J. E., Solarz A., Chocyk A., Hess G., Tokarski K.
Acta Neurobiologiae Experimentalis
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2019
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tom 79
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nr Suppl.1
INTRODUCTION: Chemokines, together with neurotransmitters and hormones, are signaling molecules that play a key role in the maintenance of the neuro‑immune‑endocrine system homeostasis. Accumulating evidence shows that they can modulate the activity of neurons through different mechanisms. One of their members, CX3CL1, and its cognate receptor, CX3CR1, play a crucial role in neuronal‑microglia signaling. AIM(S): As the amygdala is a relevant structure for integrating stress signaling as well as inflammatory responses from the periphery, this study aimed to elucidate the role of the CX3CL1/CX3CR1 axis on circuits within the amygdala. METHOD(S): We used whole-cell patch-clamp and immunohistochemistry and focused on two nuclei of the amygdala: the basolateral (BLA, main input structure), and central (CeA, output structure) nuclei. Electrophysiological recordings were performed using acute brain slices (300 μm) containing the BLA and CeA. Recordings of both spontaneous inhibitory and excitatory currents (sIPSC/sEPSC), as well as, basal membrane properties of recorded cells were collected during baseline and after CX3CL1 (2nM) application. The specificity of observed effects was investigated using the same experimental protocol with additional incubation in a CX3CR1 antibody. Additionally, to specify the cell types that express CX3CR1 and CX3CL1, appropriate immunostainings were performed. RESULTS: Our results revealed that CX3CL1 was mostly expressed within the BLA and it significantly hyperpolarized resting membrane potential of most of the recorded principal cells (70%) and decreased their excitability; however, CX3CL1 did not alter their membrane resistance. CONCLUSIONS: Our data show that CX3CL1 has a profound effect on synaptic activity in the rat amygdala, indicating that this protein can be an active modulator of neuronal activity in the fear-related response circuitry, which may have significant scientific and therapeutic implications. FINANCIAL SUPPORT: Supported by National Science Centre, grant 2016/21/N/NZ4/03621.
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Maternal separation affects tyrosine hydroxylase and NCAM expression in dopaminergic structures of juvenile adolescent and adult rat brain

71%
Chocyk A., Mackowiak M., Dudys D., Przyborowska A., Wedzony K.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
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nr 3
Stressful experiences in early life can infl uence brain development and increase the risk for mental disorders. However the specifi c impact of early life stress on maturation of dopaminergic (DA) system is still unknown. We applied maternal separation (MS) paradigm in rats, on postnatal (P) days 1–14, to investigate its impact on expression of tyrosine hydroxylase (TH) and NCAM proteins in DA structures of juvenile (P15), adolescent (P35) and adult (P70) rat brain. On P15 MS decreased the number of TH+ neurons in the substantia nigra (SN) pars compacta of females as well as in the SN pars reticulata (SNr) and the ventral tegmental area (VTA) of both females and males. The effect persisted until P35 only in the VTA of MS females. Oppositely on P70, an increase in the number of TH+ neurons was observed in the VTA of females. Additionally on P35 a transient rise in TH+ cells was detected in the SNr of MS females. MS did not change the expression of TH in the striatum, nucleus accumbens and medial prefrontal cortex (mPFC). On P15 a decrease in the level of 140 kDa NCAM was observed in the SN and striatum of MS females and a decrease in 180 kDa NCAM in the VTA of MS males. On P35 MS diminished the expression of 180 kDa NCAM in the SN and mPFC of females. Finally, on P70 a decrease in 180 kDa NCAM was observed in the mPFC of MS males. The results of the present study strongly indicate that early life stress can affect maturation and plasticity of DA system at different life stages.
8

Early life stress sex-dependently affects tyrosine hydroxylase immunoreactivity in the prelimbic cortex and striatum during different stages of ontogenesis

71%
Przyborowska A., Dudys D., Majcher I., Chocyk A., Wedzony K.
Acta Neurobiologiae Experimentalis
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2011
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tom 71
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nr S
Clinical studies indicate that early life adversity increases the risk for psychiatric disorders, like e.g., depression, schizophrenia and addiction. Moreover, behavioral data imply that early life stress has enduring impact on dopaminergic neurotransmission. The mechanisms engaged in the above effects are poorly understood. Our recent study has revealed that maternal separation (MS) in rats, a model of early life stress, affects the number of midbrain neurons expressing tyrosine hydroxylase (TH), a rate-limiting enzyme in dopamine synthesis. In the present work, we investigated the impact of MS on TH expression in brain regions containing dopaminergic axonal terminals, i.e., in the prelimbic cortex (PLC), dorsal striatum (caudate-putamen, CPu) and nucleus accumbens (NAc) of juvenile, adolescent and adult rats of both sexes. Specifically, we applied immunohistochemical method and quantified the length density of TH-immunoreactive (IR) terminals in the PLC (by stereological estimation) and TH expression in the CPu and NAc, using optical densitometry. It was found that MS affected the length density of TH-IR terminals in the PLC in males only. MS increased the length density of TH-IR terminals (in layers I and II-VI) in adolescent male rats, however the opposite effect (a decrease) was observed in a layer I of the PLC in adults. Optical densitometry revealed that, in juvenile male rats, MS reduced TH expression in the CPu, NAc shell and core. Interestingly, in juvenile females an increase in TH level was observed as an effect of MS. In adolescence, MS did not affect optical density of TH immunoractivity in the CPu and NAc. Though, in adulthood, MS selectively increased TH expression in the NAc core in males only. Our results indicate that early life stress, sex- and age-dependently, disturbs density of dopaminergic innervation of the PLC, CPu and NAc. Moreover, they imply how early adversity affects synaptic plasticity and evokes dysfunction of dopaminergic systems.
9
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Cortical localization of dopamine D4 receptors in the rat brain - immunocytochemical study

71%
Wedzony K., Chocyk A., Mackowiak M., Fijal K., Czyrak A.
Journal of Physiology and Pharmacology
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2000
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tom 51
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nr 2
10

Prolonged corticosterone treatment alters biochemical and functional parameters of serotonergic neurotransmission associated with a 5-HT1A receptors

61%
Czyrak A., Mackowiak A., Fijal K., Chocyk A., Tokarski K., Bijak M., Wedzony K.
Acta Neurobiologiae Experimentalis
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1997
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tom 57
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nr 5
11

Distribution of calbindin-D28k and parvalbumin immunoreactive neurones in the cerebral cortex of rats neonatally treated with competitive NMDA receptor antagonist.

61%
Fijal K., Chocyk A., Czyrak A., Mackowiak M., Zajaczkowski W., Wedzony K.
Acta Neurobiologiae Experimentalis
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1999
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tom 59
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nr 3
12

A comparison of psychotomimetic effects of MK-801 and CGP 40116 in behavioural paradigms

61%
Zajaczkowski W., Chocyk A., Fijal K., Mackowiak M., Czyrak A., Wedzony K.
Acta Neurobiologiae Experimentalis
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1999
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tom 59
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nr 3
13
Content available remote

DOI, an agonist of 5-HT2A-2C serotonin receptor, alters the expression of cyclooxygenase-2 in the rat parietal cortex

61%
Mackowiak M., Chocyk A., Sanak M., Czyrak A., Fijal K., Wedzony K.
Journal of Physiology and Pharmacology
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2002
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tom 53
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nr 3
The hallucinogenic effect of DOI, serotonin 5-HT2A/2C receptor agonist, is known to be associated with the activation of cortical 5-HT2 receptors. However, the effect of DOI on excitability of cortical neurons and their subsequent function is still not quite understood. Previous immunohistochemical studies using Fos proteins expression as a marker of neuronal activity showed the involvement of arachidonic acid cascade, particularly cyclooxygenase metabolic pathway, in DOI-induced Fos proteins expression in the rat parietal cortex. DOI increases arachidonic acid release which is transformed itself via acceleration of cyclooxygenase metabolic pathway to biologically active metabolites, such as prostaglandins and tromboxanes. Since cyclooxygenase-2 (COX-2) expression correlates with neuronal activity, it was of interest to investigate whether DOI is capable of influencing the level of COX-2 protein and mRNA expression in the rat parietal cortex. It was observed that neurons which were positive for 5-HT2A receptors showed constitutive COX-2 immunoreactivity. It was found further, that COX-2 protein level was increased at 1h, and returned to the control level at 3 and 6 h after DOI (5 mg/kg) administration. In contrast, DOI decreased the COX-2 mRNA expression at all tested time points (1h, 3h and 6h after DOI treatment). The obtained results further support the suggestion that COX-2 activation and possibly arachidonic acid metabolites generated by COX-2 may be considered as important mediators of functional responses generated by activation of cortical 5-HT2A/2C receptors.
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