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Spółki wodne obejmują swoim działaniem 575 460 ha obszaru, tj. około 74% powierzchni zmeliorowanej województwa mazowieckiego. W artykule przedstawiono sytuację spółek na tle obecnych warunków gospodarczych oraz przepisów zawartych w Prawie wodnym i innych aktach prawnych. Na zakończenie artykułu Autorzy przedstawiają problemy, które powinny być rozwiązane, aby umożliwić spółkom realizacje ich zadań statutowych.
Spółki Wodne są organizacjami na których spoczywa utrzymanie i eksploatacje szczegółowych systemów melioracyjnych. Działania te są prowadzone w imieniu i na koszt rolników, właścicieli zazwyczaj drobnej sieci rowów odwadniających. Spółki przeżywają obecnie trudny okres z uwagi na brak środków finansowych, wynikających m.in. z braku zainteresowania rolników prawidłowym utrzymaniem urządzeń wodnych. Przeprowadzona została analiza przyczyn występujących trudności i przedstawiona propozycja działań w celu poprawy sytuacji.
CPPG is a highly potent group III metabotropic glutamate receptor (mGluR4/6/7/8) antagonist with selective affi nity to mGluR4. The aim of the present study was to determine the effects of CPPG on spatial memory in the water maze, and on the activity of MMP-2 and MMP9 metalloproteases in the hippocampus of rats without and after hypoxia. Short-term hypoxia (2% O2 and 98% N2) enhances excitatory synaptic transmission and impairs spatial acquisition in the water maze. We observed that CPPG prolonged only escape latency during the fi rst day of training in water maze in group without hypoxia, while it did not infl uence escape latency, distance travelled and swim speed during training of rats after hypoxia. It did not change previously acquired escape response during free-swim trial in either group of rats. Hypoxia signifi cantly increased the activity of the proform of MMP-9 in the hippocampus. Gel zymography showed elevations of MMP-2 and MMP-9 activity in the hippocampus of rats without or after hypoxia when CPPG was administered. Concluding, CPPG has no effects on defi cits of behavioural processes induced by hypoxia in the water maze. Enhanced activity of MMP-2 and MMP9 in the hippocampus induced by CPPG does not correspond to the infl uence on acquisition in the water maze. The reconfi guration of extracellular matrix by MMP-2 and MMP-9 in hippocampus is new central effect of CPPG. Support: grant No 3-10614L from the State Committee for Scientifi c Research, Warszawa, Poland.
Elucidation of protease substrates (“proteodegradomes”) is essential for understanding the proteolytic pathways and their networks and thus their role in the regulation of cell function. Matrix metalloproteinase-9 (MMP-9) is expressed by the adult brain and released in response to enhanced neuronal activity. It is well established that MMP-9 is involved in neuronal plasticity, including long-term potentiation, learning and memory. Under pathological conditions, during excitotoxicity, stroke and traumatic brain injury, MMP-9 is detrimental to the brain tissue, probably because of its enhanced activity. MMP-9 is locally inhibited by endogenous tissue inhibitors of metalloproteinase 1 (TIMP-1). In the current studies we optimized the isolation of synaptoneurosomal fractions from the murine hippocampus. In order to induce MMP-9 activity the synaptoneurosomal fractions were treated with 50 μM of glutamate for 20 min. To identify MMP-9 substrates, we compared the synaptic fractions isolated from wild type and MMP-9 knockout mice by two-dimensional electrophoresis (2-DE). We have found the differences in the 2-D gel patterns. Further studies will be complemented by in-gel digestion of the protein spots of interest, mass spectrometry of the resultant peptides, and peptide mass fi ngerprinting to identify each protein.
Tissue plasminogen activator tPA is used for treatment of ischemic stroke patient. This thrombolytic agent resurrect blood supply to brain tissue, that is sensitive to oxygen and glucose deprivation. Administration of tPA is the only approved treatment and might be conducted up to 3 or 4.5 hours after ischemic stroke symptom onset. The benefits of it are time dependent and there is need for an improvement the timeliness of reperfusion. Some side effects of tPA is caused likely by its matrix metalloproteinase-9 (MMP-9) activation. Source and localization of MMP9 is still uncertain. This is investigated with high resolution in situ zymography. We use mouse model of in situ thromboembolic stroke and reperfusion as a clinically relevant. In this experimental set we identify oligodendrocytes and neurons but not astrocytes and microglia as a cellular source of gelatynolytic activity. Oligodendrocytes activity is most prominent. This is in opposition to literature. Activity of leukocytes is high however number of them suggest that their contribution to overall activity is negligible.
Matrix metalloproteinase-9 (MMP-9) has emerged as a physiological regulator of NMDA receptor (NMDAR)-dependent synaptic plasticity and memory. The pathways by which MMP-9 affects NMDAR signaling remain, however, not well understood. Using single Quantum Dot tracking we demonstrate that MMP-9 enzymatic activity increases NR1-NMDAR surface traffi cking but has no infl uence on AMPA receptor (AMPAR) mobility. Other extracellular protease – Cathepsin G has no effect on both NMDAR and AMPAR lateral diffusion. The mechanism of MMP-9 action on NMDAR is caused neither by change in overall extracellular matrix (ECM) structure, nor by cleavage of NMDAR subunits, but by infl uence on integrinbeta 1 signaling. These fi ndings describe a new target pathway for MMP-9 action in key physiological and pathological brain processes.
The rewiring of synaptic circuitry pertinent to memory formation in the brain has often been associated with morphological changes in dendritic spines and extracellular matrix (ECM) remodeling. Here, we linked these processes by uncovering the signaling pathway involving the serotonin 5-HT7 receptors (5 HT7R) the matrix metalloproteinase-9 (MMP-9), the hyaluronan receptor CD44, and the small GTPase Cdc42. We highlight a physical interaction between 5‑HT7R and CD44 (identified as a novel MMP 9 substrate in neurons) on the nanoscale, and find that 5-HT7R stimulation increases local MMP 9 activity triggering dendritic spines remodeling, synaptic pruning and impairment of long-term potentiation (LTP). The underlying molecular machinery involves 5-HT7R-mediated activation of MMP-9, which leads to CD44 cleavage followed by Cdc42 activation. Pharmacological/genetic suppression of this pathway rescues the 5-HT7R-induced synaptic changes and the deficit in LTP. Our results thus reveal causal interactions in a previously unknown molecular mechanism regulating neuronal plasticity. FINANCIAL SUPPORT: The work was supported by the National Science Centre (grant no. DEC-2012/06/M/ NZ3/00163), TANGO1/269352/NCBR/2015, Deutsche Forschungsgemeinschaft (grant no. PO732, excellence cluster REBIRTH), and ERA-NET Neuron/BMBF funding for the TargetECM project to E.P and A.D.
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