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1

Bialka G - rola niedocenianego kompleksu beta-gamma

100%
Zelek-Molik A.
Wszechświat
|
2002
|
tom 103
|
nr 07-09
205-207
2

Depletion noradrenaline counteracts the increase of alpfaIA-adrenoceptor mRNA expression induced by treatment with antidepressant

81%
Kreiner G., Zelek-Molik A., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 3
3

Effect of cocaine sensitization on the expression of Galpha(q/11) proteins in rat amygdala

81%
Zelek-Molik A., Wnuk A., Nawrat D., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
4

Changed expression of apoptotic signaling-releted genes, Pmaip1 and Rock1, in the prefrontal cortex of rats treated with imipramine in chronic mild stress model of depression

71%
Bielawski A., Rafa-Zablocka K., Zelek-Molik A., Papp M., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: The chronic mild stress (CMS) procedure induces depression-like symptoms in animals. In this model, rats subjected for a prolonged time to mild stressors gradually decrease their responsiveness to rewarding stimuli. This deficit can be effectively reversed by chronic antidepressant treatment. Apoptotic changes in the prefrontal cortex were shown in animal stress models, as well as degenerative changes, which are reversed by antidepressant treatment in depressed patients. We aimed to study the apoptotic signaling-related genes in the prefrontal cortex (PFC) of rats treated with imipramine (IMI) in CMS model. METHODS: First, we used the TaqMan Low Density Arrays to indentify genes in the three groups of Wistar rats: sham-saline; stressIMI-responders and stress-IMI-nonresponders (the sucrose intake score did not return to the control level). Then, these groups of rats and two additional ones (stress-saline and sham-IMI) were assessed in the PCR reactions with one TaqMan probe for detailed mRNA analysis of the identified genes. Finally, the levels of these proteins were assessed by Western Blot in all experimental groups. RESULTS: We found that CMS decreased the expression of Pmaip1 mRNA (by 18%) and the effect remained unchanged in rats nonresponding behaviorally to IMI treatment. Furthermore, in rats nonresponding to IMI treatment, the Rock1 mRNA was decreased by 40% vs. sham and IMI responding rats. However, at the Rock1 protein level its decreased expression was observed in both groups, the IMI nonresponding and IMI responding animals (by 22% and 29%, respectively). CONCLUSION: Our results suggest the involvement of apoptotic Pmaip1 and Rock1 genes in the process of response to IMI treatment in CMS model of depression in rats. Supported by statutory funds of the Institute of Pharmacology PAS and POIG.01.01.02-12-004/09-00 grant financed by European Regional Development Fund.
5

Imipramine-reversed elevation of Hsp72 expression in the brain of rats in the chronic mild stress model of depression

71%
Bielawski A., Zelek-Molik A., Papp M., Kowalska M., Nalepa L.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
Heat shock proteins HSP70 play a protective role against stressinduced damage of cells. We assessed the expression of inducible Hsp72 in the prefrontal cortex (PFC) and hippocampus (HIP) of male Wistar rats subjected to the chronic mild stress (CMS), the procedure inducing depression-like symptoms, and subsequently Different brain areas are thought to be integrated into largescale networks. Recent approaches for investigating structural organization and functional coordination within these networks involve measures of connectivity among brain areas. Transcranial magnetic stimulation (TMS) can be used to analyze the functional state of the cerebral cortex, discovering changes in its excitability, connectivity and plasticity which may have occurred through processes such as learning or recovery from a lesion. We review studies using in vivo functional brain connectivity technologies. TMS-EEG studies have begun to describe the nature of the TMS-evoked EEG responses in order to broaden the comprehension of the activation mechanisms of TMS. Several studies have proved the power of TMS-EEG by displaying many data about the excitability or connectivity of the brain. Particularly, it has been proposed that the very first part of the TMS evoked EEG response displays the excitability of the stimulated cortex while its spatio-temporal distribution over the scalp displays the spread of activation to other cortical areas – via intra and inter-hemispheric cortico-cortical connections as well as to sub-cortical structures and spinal cord via projection fibres – that means the effective connectivity of the stimulated area. Finally effective connectivity may be considered as the union of structural and functional connectivity. These studies provide insights into the relationships between brain structure and function.
6

Effect of experimental encephalomyelitis on the alfa subunit of the Gs protein in the central nervous system

71%
Zelek-Molik A., Nalepa I., Yang J., Sanak M., Vetulani J.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
7

Changes of Galpha(q), Galpha(11) and Galpha(12) mRNA expression levels in rat prefrontal cortex and amygdala after reinstatement of cocaine-seeking behavior

71%
Zelek-Molik A., Kreiner G., Filip M., Wydra K., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Inhibition of monoamine transporters by a psychostimulant, cocaine, increases the monoamines availability at synaptic cleft and leads to the enhanced stimulation of monoaminergic postsynaptic receptors. G proteins represent the down-stream connectors from receptors to intracellular signalling. The aim of the study was to assess the expression of Gα(q), Gα(11) and Gα(12) mRNAs following reinstatement of cocaine-seeking behaviour in the prefrontal cortex (PFC) and the amygdala (AMY) of male Wistar rats using a “yoked” procedure and RT-PCR technique. We found that phases of cocaine-seeking behavior differently influenced the Gα subunits depending on the brain structure analyzed. Cocaine self-administered for 18 days induced a significant increase of mRNA levels of all Gα subunits (by ~23% for Gα12 and Gα11, and by 46% for Gαq vs yoked) in the PFC. After 10 days withdrawal from cocaine when no change in G proteins was observed, reinstatement induced by priming dose of the drug decreased G12 and Gq. The effect was more pronounced after combination of the cocaine with cue previously associated with cocaine self-administration and was noticed in G11 as well. In AMY, changes in the expression of Gα mRNAs induced by cocaine self-administration dependent on environmental cues paired with cocaine. Cocaine self-administration decreased (by ~24%) all G protein mRNAs while opposite effect was observed when cocaine self-administration was paired with cue stimulus. Withdrawal from cocaine induced 2-fold increase in mRNA level of three G proteins. On the contrary, the reinstatement induced by the cue decreased significantly Gα mRNAs to the same degree as did its combination with cocaine-priming. Our study provides the first evidence that alterations of G proteins mRNA expression can be conditioned by environmental stimuli paired with cocaine administration. Supported by statutory funds of the Institute of Pharmacology PAS.
8

Impact of fear memory consolidation and retrieval on the mRNA expression of G proteins in mice brain

61%
Zelek-Molik A., Costanzi M., Rafa-Zablocka K., Kreiner G., Roman A., Cestari V., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: Fear evoked signaling disturbances among hippocampus (HP), nuclei of amygdala (Amy) and prefrontal cortex (PFC) underlie anxiety related disorders, but their molecular mechanism remains elusive. Heterotrimeric G proteins (GP) based on intracellular activity of alpha subunit (Gα) are divided into four families: G(s) stimulating cAMP generation; G(i/o) inhibiting cAMP pathway; G(Q/11) increasing Ca++ level; G(12/13) activating monomeric GP-Rho. AIM(S): In the present study, the effects of fear memory consolidation and retrieval on the mRNA expression of Gα from all GP families were assessed in HP, Amy and PFC. METHOD(S): C57BL/6J mice were subject to 1-day fear conditioning (FC) procedure followed by contextual (CTX) or cued (Cs) retrieval test of freezing behavior. Morphine (1mg/kg/ip) injected immediately after FC was used to prevent fear consolidation process. RealTime PCR technique was adopted to measure mRNA expression of Gα subunits: 1 h after FC, 24 h later, 1 h after CTX or Cs retrieval test. RESULTS: In HP, the increased levels of Gα(s), (12) and (11) were observed 1 h after FC. The Gα(s) mRNA decreased (vs. control) when consolidation was stabilized as well after Cs retrieval. Elevated Gα(12) mRNA, as observed 1h after FC, returned to control level at fear memory stabilization and raised again with CTX retrieval. The increase in Gα(11) persisted 24 h after FC and after CTX (but not Cs) retrieval. In PFC, the CTX retrieval was accompanied by a decrease in Gα(i2) and (i3) mRNA levels. In Amy, no specific change to fear memory process was observed. CONCLUSIONS: FC evoked changes in Gα mRNA expression are observed mainly in HP and mostly connected to CTX learning. Results suggest that activated signaling pathways from Gα(s) and Gα(12) are necessary to begin fear memory consolidation process in HP while signal transduction via Gα(11) is implicated in maintenance of fear consolidation. FINANCIAL SUPPORT: Supported by statutory funds from the Institute of Pharmacology PAS.
9

Effects of bi-adrenergic receptor blockade during chronic restraint stress on the expression of selected proteins of the glutamatergic transmission in the rat prefrontal cortex

61%
Zelek-Molik A., Kowalska M., Roman A., Kusmierczyk J., Bielawski A., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: The stress impaired the structure and activity ofthe prefrontal cortical(PFC) neurons has been postulated to underlie the pathology of stress related psychiatric disorders. NMDA and AMPA glutamate receptors of PFC were shown to be affected by stress. High level of the noradrenaline release during stress is known to stimulate the β adrenergic receptors (βAR), densely expressed in PFC. The βAR can directly or indirectly, by means of Fyn kinase, regulate glutamatergic receptors activation. Also, evidence have shown that pharmacological blockade of β1AR alleviated anxiety in stress models. The aim of the study wasto evaluate the stressinduced changes in the expression of total- and phospho-(Y1472)GluN2B, (Ser845)GluA1, and (Y530)Fyn proteins in rat dorso-medial (dm) PFC and to assess whether β1AR blockade can modulate it. METHODS: Male Wistar rats underwent the chronic restraint stress procedure applied for 3 hours daily, for 14 days. During the last 7 days rats were treated with betaxolol (1 or 5 mg/kg/po) given immediately after daily stress. Next day after a completion of stress procedure, the rats were decapitated, their dmPFC was dissected and subjected to standard Western blot analysis. RESULTS: Neither stress nor betaxolol treatment changed the expression of studied NMDA and AMPA subunits. Repeated stress increased phosphorylation level of (Y530)Fyn kinase (by 25% vs. non stressed groups) and betaxolol treatment did not influence this effect. CONCLUSIONS: The Fyn kinase is a known regulator of NMDA receptors’membrane stability, on the other hand phosphorylation at Tyr 530 inactivates the kinase. Our results showing the increased phosphorylation of Fyn suggest the inhibition of Fyn activity which can be responsible for disturbed glutamatergic transmission observed in PFC after prolonged stress. This mechanism seems to be independent on β1AR activity in PFC. Supported by statutory funds of the Institute of Pharmacology PAS.
10

Changes in alfa1-adrenergic receptor subtypes in the hippocampus of rats non-responding to imipramine treatment in the chronic mild stress model of depression

61%
Rafa-Zablocka K., Zelek-Molik A., Bielawski A., Gruca P., Lason-Tyburkiewicz M., Papp M., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Despite many years of research on depression the mechanism of the disorder remains elusive. Many studies are focused on dysfunction of central monoaminergic systems and some evidence exist for the role of α1-adrenoceptor (α1-AR). There are three subtypes of this receptor - α1A, α1B and α1D, which are widely distributed in brain. The aim of this study was to assess the expression of all three α1-AR, both at the mRNA and at the protein level in the hippocampi of male Wistar rats, subjected to the chronic mild stress (CMS) procedure followed by treatment with antidepressant drug, imipramine (IMI). Five groups of animals were studied: sham-saline; stress-saline; sham-IMI; stress-IMIresponders and stress-IMI-non-responders. The latter included the stressed animals resistant to IMI treatment as indicated by anhedonia test. The mRNA level was measured using qRT-PCR and SybrGreen dye, and the protein level was assessed by Western blotting. We found that mRNA expression of all α1-AR subtypes was significantly elevated only in the IMI-non-responders group (α1A-AR by 76%; α1B-AR by 96%; α1D-AR by 50%, vs. shamsaline). Moreover, stress alone caused an increase in α1A-AR mRNA (by 41%) though the effect was statistically insignificant. Changes found in the protein level were less pronounced. The only difference between IMI-responders and non-responders was found in α1A receptor protein that was decreased by 73% vs IMIresponders. The level of α1D protein was elevated in all IMI treated groups (by about 79%, vs. sham-saline) and the change occurred independently on stress procedure. No change in the α1B protein was found. Our results indicate that although α1A-AR and α1D-AR are involved in mechanism of IMI action, only the α1A receptor seems to be engaged in the phenomenon of resistance to IMI treatment. Supported by a grant POIG.01.01.02-12-004/09-00 financed by European Regional Development Fund.
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