• MeSH
• chování zvířat účinky léků   MeSH
• chuť genetika   MeSH
• krysa rodu rattus MeSH
• plexus brachialis fyziologie   účinky léků   MeSH
• proteinkinasy závislé na vápníku a kalmodulinu fyziologie   MeSH
• učení vyhýbat se fyziologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• zvířata MeSH

• Konspekt
• Lékařské vědy. Lékařství
• NLK Obory
• neurovědy
• patologie
• fyziologie

• MeSH
• chuť k jídlu fyziologie   účinky léků   MeSH
• fosfotransferasy antagonisté a inhibitory   fyziologie   MeSH
• krátkodobá paměť MeSH
• krysa rodu rattus MeSH
• mozkový kmen účinky léků   MeSH
• poruchy chuti chemicky indukované   patofyziologie   MeSH
• tetrodotoxin farmakologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• zvířata MeSH

• MeSH
• alfa-adrenergní receptory fyziologie   MeSH
• elektrická stimulace MeSH
• kardiomyocyty MeSH
• krysa rodu rattus MeSH
• proteinkinasy závislé na vápníku a kalmodulinu fyziologie   MeSH
• techniky in vitro MeSH
• transdukce genetická MeSH
• vápníkové kanály fyziologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• zvířata MeSH

Repetitive transcranial magnetic stimulation (rTMS) was shown to have therapeutic potential for some neurological and psychiatric disorders. Previous studies reported that low-frequency rTMS (

• MeSH
• hipokampus metabolismus   ultrastruktura   MeSH
• krysa rodu rattus MeSH
• náhodné rozdělení MeSH
• neuroplasticita fyziologie   MeSH
• potkani Sprague-Dawley MeSH
• proteinkinasa závislá na vápníku a kalmodulinu typ 2 metabolismus   MeSH
• transkraniální magnetická stimulace metody   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

Agonist-induced desensitization of the transient receptor potential vanilloid receptor-1 (TRPV1) is one of the key strategies that offer a way to alleviate neuropathic and inflammatory pain. This process is initiated by TRPV1 receptor activation and the subsequent entry of extracellular Ca(2+) through the channel into sensory neurones. One of the prominent mechanisms responsible for TRPV1 desensitization is dephosphorylation of the TRPV1 protein by the Ca(2+)/calmodulin-dependent enzyme, phosphatase 2B (calcineurin). Of several consensus phosphorylation sites identified so far, the most notable are two sites for Ca(2+)/calmodulin dependent kinase II (CaMKII) at which the dynamic equilibrium between the phosphorylated and dephosphorylated states presumably regulates agonist binding. We examined the mechanisms of acute Ca(2+)-dependent desensitization using whole-cell patch-clamp techniques in human embryonic kidney (HEK) 293T cells expressing the wild type or CaMKII phosphorylation site mutants of rat TRPV1. The nonphosphorylatable mutant S502A/T704I was capsaicin-insensitive but the S502A/T704A construct was fully functional, indicating a requirement for a specific residue at position 704. A point mutation at the nearby conserved residue R701 strongly affected the heat, capsaicin and pH-evoked currents. As this residue constitutes a stringent CaMKII consensus site but is also predicted to be involved in the interaction with membrane phosphatidylinositol 4,5-bisphosphate (PIP(2)), these data suggest that in addition to dephosphorylation, or as its consequence, a short C-terminal juxtamembrane segment adjacent to the transient receptor potential box composed of R701 and T704 might be involved in the decelerated gating kinetics of the desensitized TRPV1 channel.

• MeSH
• elektrická stimulace metody   MeSH
• financování organizované MeSH
• fosfatidylinositol-4,5-difosfát farmakologie   MeSH
• kapsaicin farmakologie   MeSH
• kationtové kanály TRPV fyziologie   genetika   MeSH
• krysa rodu rattus MeSH
• lidé MeSH
• membránové potenciály MeSH
• metoda terčíkového zámku metody   MeSH
• mutace fyziologie   MeSH
• proteinkinasa závislá na vápníku a kalmodulinu typ 2 metabolismus   MeSH
• teplota MeSH
• transfekce MeSH
• transformované buněčné linie MeSH
• vápník MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• vztahy mezi strukturou a aktivitou MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• lidé MeSH
• zvířata MeSH

Activation of calmodulin dependent protein kinase (CaMK)II by exercise is beneficial in controlling membrane lipids associated with type 2 diabetes and obesity. Regulation of lipid metabolism is crucial in the improvement of type 2 diabetes and obesity associated symptoms. The role of CaMKII in membrane associated lipid metabolism was the focus of this study. Five to six weeks old male Wistar rats were used in this study. GC×GC-TOFMS technique was used to determine the levels of polyunsaturated fatty acids (linoleic acid, arachidonic acid and 11,14-eicosadienoic acid). Carnitine palmitoyltransferase (Cpt-1) and acetyl-CoA carboxylase (Acc-1) genes expression were assessed using quantitative real time PCR (qPCR). From the results, CaMKII activation by exercise increased the levels of arachidonic acid and 11,14-eicosadienoic acid while a decrease in the level of linolenic acid was observed in the skeletal muscle. The results indicated that exercise-induced CaMKII activation increased CPT-1 expression and decreased ACC-1 expression in rat skeletal muscle. All the observed increases with activation of CaMKII by exercise were aborted when KN93, an inhibitor of CaMKII was injected in exercising rats. This study demonstrated that CaMKII activation by exercise regulated lipid metabolism. This study suggests that CaMKII can be a vital target of therapeutic approach in the management of diseases such as type 2 diabetes and obesity that have increased to epidemic proportions recently.

• MeSH
• acetyl-CoA-karboxylasa genetika   metabolismus   MeSH
• aktivace enzymů MeSH
• fosforylace MeSH
• karnitin-O-palmitoyltransferasa genetika   metabolismus   MeSH
• kondiční příprava zvířat * MeSH
• kosterní svaly enzymologie   MeSH
• kyselina alfa-linolenová metabolismus   MeSH
• kyselina arachidonová metabolismus   MeSH
• mastné kyseliny metabolismus   MeSH
• messenger RNA genetika   metabolismus   MeSH
• potkani Wistar MeSH
• proteinkinasa závislá na vápníku a kalmodulinu typ 2 metabolismus   MeSH
• svalová kontrakce * MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

Central ghrelin signaling seems to play important role in addiction as well as memory processing. Antagonism of the growth hormone secretagogue receptor (GHS-R1A) has been recently proposed as a promising tool for the unsatisfactory drug addiction therapy. However, molecular aspects of GHS-R1A involvement in specific brain regions remain unclear. The present study demonstrated for the first time that acute as well as subchronic (4 days) administration of the experimental GHS-R1A antagonist JMV2959 in usual intraperitoneal doses including 3 mg/kg, had no influence on memory functions tested in the Morris Water Maze in rats as well as no significant effects on the molecular markers linked with memory processing in selected brain areas in rats, specifically on the β-actin, c-Fos, two forms of the calcium/calmodulin-dependent protein kinase II (CaMKII, p-CaMKII) and the cAMP-response element binding protein (CREB, p-CREB), within the medial prefrontal cortex (mPFC), nucleus accumbens (NAc), dorsal striatum, and hippocampus (HIPP). Furthermore, following the methamphetamine intravenous self-administration in rats, the 3 mg/kg JMV2959 pretreatment significantly reduced or prevented the methamphetamine-induced significant decrease of hippocampal β-actin and c-Fos as well as it prevented the significant decrease of CREB in the NAC and mPFC. These results imply, that the GHS-R1A antagonist/JMV2959 might reduce/prevent some of the memory-linked molecular changes elicited by methamphetamine addiction within brain structures associated with memory (HIPP), reward (NAc), and motivation (mPFC), which may contribute to the previously observed significant JMV2959-induced reduction of the methamphetamine self-administration and drug-seeking behavior in the same animals. Further research is necessary to corroborate these results.

• MeSH
• aktiny MeSH
• ghrelin farmakologie   MeSH
• krysa rodu rattus MeSH
• methamfetamin * farmakologie   MeSH
• proteinkinasa závislá na vápníku a kalmodulinu typ 2 MeSH
• receptory ghrelinu * MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Hypotonic solution alters ion channel activity, but little attention has been paid to voltage-dependent sodium channels. The aim of this study was to investigate the effects of hypotonic solution on transient sodium currents (INaT) and persistent sodium currents (INaP). We also explored whether the intracellular signal transduction systems participated in the hypotonic modifications of sodium currents. INaT and INaP were recorded by means of whole-cell patch-clamp technique in isolated rat ventricular myocytes. Our results revealed that hypotonic solution reduced INaT and simultaneously augmented INaP with the occurrence of interconversion between INaT and INaP. Hypotonic solution shifted steady-state inactivation to a more negative potential, prolonged the time of recovery from inactivation, and enhanced intermediate inactivation (IIM). Ruthenium red (RR, inhibitor of TRPV4), bisindolylmaleimide VI (BIM, inhibitor of PKC), Kn-93 (inhibitor of Ca/CaMKII) and BAPTA (Ca2+-chelator) inhibited the effects of hypotonic solution on INaT and INaP. Therefore we conclude that hypotonic solution inhibits INaT, enhances INaP and IIM with the effects being reversible. TRPV4 and intracellular Ca2+, PKC and Ca/CaMKII participate in the hypotonic modifications of sodium currents.

• MeSH
• benzylaminy farmakologie   MeSH
• chelátory farmakologie   MeSH
• EGTA analogy a deriváty   farmakologie   MeSH
• financování organizované MeSH
• hypotonické roztoky MeSH
• indoly farmakologie   MeSH
• inhibitory proteinkinas farmakologie   MeSH
• kardiomyocyty metabolismus   účinky léků   MeSH
• kationtové kanály TRPV antagonisté a inhibitory   metabolismus   MeSH
• kinetika MeSH
• krysa rodu rattus MeSH
• maleimidy farmakologie   MeSH
• membránové potenciály MeSH
• metoda terčíkového zámku MeSH
• proteinkinasa C antagonisté a inhibitory   metabolismus   MeSH
• proteinkinasa závislá na vápníku a kalmodulinu typ 2 antagonisté a inhibitory   metabolismus   MeSH
• rutheniová červeň farmakologie   MeSH
• signální transdukce účinky léků   MeSH
• sodík metabolismus   MeSH
• srdeční komory cytologie   metabolismus   účinky léků   MeSH
• sulfonamidy farmakologie   MeSH
• vápník metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• zvířata MeSH

Whole cell patch-clamp recordings from GABAergic cells of thalamic reticular nucleus (RTN) in thalamocortical slices made from postnatal day 6 (P6) to 10 (P10) were used to investigate the pattern of rebound bursts (RBs) triggered by an injection of hyperpolarizing current into RTN cells. The number of RBs in the RTN and the overlying Na+/K+ spikes changed in an agedependent manner. The generation of RBs depended largely on the amplitude of the after-hyperpolarizations (AHPs). RB patterns in response to hyperpolarizing current injection into relay cells were markedly different from RB patterns in RTN cells with an after-depolarization. GABAA receptor antagonist bicuculline methiodide (BMI) changed burst firing patterns, increasing the duration of RB and decreasing the amplitude of AHP in RTN cells. Furthermore, local puffs of NMDA in the presence of BMI induced RBs. K+ channel blocker 4-aminopyridine partially mimicked the effect of BMI on AHPs. The shapes of RBs were altered by a selective CaMKII inhibitor KN-62, but not by an inactive analog KN-04.

• MeSH
• 1-(5-isochinolinsulfonyl)-2-methylpiperazin analogy a deriváty   farmakologie   MeSH
• 4-aminopyridin farmakologie   MeSH
• akční potenciály fyziologie   účinky léků   MeSH
• antagonisté receptorů GABA-A MeSH
• bikukulin analogy a deriváty   farmakologie   MeSH
• blokátory draslíkových kanálů farmakologie   MeSH
• financování organizované MeSH
• GABA antagonisté farmakologie   MeSH
• GABA fyziologie   MeSH
• inhibitory proteinkinas farmakologie   MeSH
• jádra thalamu cytologie   fyziologie   MeSH
• myši inbrední ICR MeSH
• myši MeSH
• nervový útlum fyziologie   účinky léků   MeSH
• neurony fyziologie   MeSH
• novorozená zvířata MeSH
• orgánové kultury - kultivační techniky MeSH
• proteinkinasa závislá na vápníku a kalmodulinu typ 2 antagonisté a inhibitory   metabolismus   MeSH
• receptory GABA-A fyziologie   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH